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Can a hormone shot rescue low libido?
according to results from two small randomized controlled trials.
The data suggest that injections of kisspeptin can boost sexual desire in men and women and can increase penile rigidity in men.
Together, these two studies provide proof of concept for the development of kisspeptin-based therapeutics for men and women with distressing hypoactive sexual desire disorder (HSDD), study investigator Alexander Comninos, MD, PhD, Imperial College London, said in a news release.
One study was published online Feb. 3, 2022, in JAMA Network Open. The other was published in October 2022.
Unmet need
HSDD affects up to 10% of women and 8% of men worldwide and leads to psychological and social harm, the news release noted.
“There is a real unmet need to find new, safer, and more effective therapies for this distressing condition for both women and men seeking treatment,” Dr. Comninos said.
Kisspeptin is a naturally occurring reproductive hormone that serves as a crucial activator of the reproductive system. Emerging evidence from animal models shows that kisspeptin signaling has key roles in modulating reproductive behavior, including sexual motivation and erections.
In a double-blind, placebo-controlled, crossover study, the researchers enrolled 32 healthy heterosexual men (mean age, 37.9 years) who had HSDD.
At the first study visit, the men were given an infusion of kisspeptin-54 (1 nmol/kg per hour) or placebo (saline) over 75 minutes. The participants then crossed over to the other treatment at a second study visit at least 7 days later.
The active treatment significantly increased circulating kisspeptin levels. A steady state was reached after 30-75 minutes of infusion, the researchers reported.
Similar data in men, women
While the men viewed sexual videos, kisspeptin significantly modulated brain activity on fMRI in key structures of the sexual-processing network, compared with placebo (P = .003).
In addition, the treatment led to significant increases in penile tumescence in response to sexual stimuli (by up to 56% more than placebo; P = .02) and behavioral measures of sexual desire – most notably increased happiness about sex (P = .02).
Given the significant stimulatory effect of kisspeptin administration on penile rigidity, coupled with its demonstrated proerectile effect in rodents, future studies should examine the use of kisspeptin for patients with erectile dysfunction, the researchers wrote.
The second study included 32 women with HSDD and had the same design. Its results also showed that kisspeptin restored sexual and attraction brain processing without adverse effects.
“It is highly encouraging to see the same boosting effect in both women and men, although the precise brain pathways were slightly different, as might be expected,” coinvestigator Waljit Dhillo, PhD, Imperial College London, said in the news release.
“Collectively, the results suggest that kisspeptin may offer a safe and much-needed treatment for HSDD that affects millions of people around the world; and we look forward to taking this forward in future larger studies and in other patient groups,” Dr. Dhillo added.
The study was funded by the National Institute for Health and Care Research Imperial Biomedical Research Centre and the Medical Research Council, part of UK Research and Innovation. Dr. Comninos reported no relevant financial relationships. Dr. Dhillo reported receiving consulting fees from Myovant Sciences and KaNDy Therapeutics outside the submitted work.
A version of this article first appeared on Medscape.com.
according to results from two small randomized controlled trials.
The data suggest that injections of kisspeptin can boost sexual desire in men and women and can increase penile rigidity in men.
Together, these two studies provide proof of concept for the development of kisspeptin-based therapeutics for men and women with distressing hypoactive sexual desire disorder (HSDD), study investigator Alexander Comninos, MD, PhD, Imperial College London, said in a news release.
One study was published online Feb. 3, 2022, in JAMA Network Open. The other was published in October 2022.
Unmet need
HSDD affects up to 10% of women and 8% of men worldwide and leads to psychological and social harm, the news release noted.
“There is a real unmet need to find new, safer, and more effective therapies for this distressing condition for both women and men seeking treatment,” Dr. Comninos said.
Kisspeptin is a naturally occurring reproductive hormone that serves as a crucial activator of the reproductive system. Emerging evidence from animal models shows that kisspeptin signaling has key roles in modulating reproductive behavior, including sexual motivation and erections.
In a double-blind, placebo-controlled, crossover study, the researchers enrolled 32 healthy heterosexual men (mean age, 37.9 years) who had HSDD.
At the first study visit, the men were given an infusion of kisspeptin-54 (1 nmol/kg per hour) or placebo (saline) over 75 minutes. The participants then crossed over to the other treatment at a second study visit at least 7 days later.
The active treatment significantly increased circulating kisspeptin levels. A steady state was reached after 30-75 minutes of infusion, the researchers reported.
Similar data in men, women
While the men viewed sexual videos, kisspeptin significantly modulated brain activity on fMRI in key structures of the sexual-processing network, compared with placebo (P = .003).
In addition, the treatment led to significant increases in penile tumescence in response to sexual stimuli (by up to 56% more than placebo; P = .02) and behavioral measures of sexual desire – most notably increased happiness about sex (P = .02).
Given the significant stimulatory effect of kisspeptin administration on penile rigidity, coupled with its demonstrated proerectile effect in rodents, future studies should examine the use of kisspeptin for patients with erectile dysfunction, the researchers wrote.
The second study included 32 women with HSDD and had the same design. Its results also showed that kisspeptin restored sexual and attraction brain processing without adverse effects.
“It is highly encouraging to see the same boosting effect in both women and men, although the precise brain pathways were slightly different, as might be expected,” coinvestigator Waljit Dhillo, PhD, Imperial College London, said in the news release.
“Collectively, the results suggest that kisspeptin may offer a safe and much-needed treatment for HSDD that affects millions of people around the world; and we look forward to taking this forward in future larger studies and in other patient groups,” Dr. Dhillo added.
The study was funded by the National Institute for Health and Care Research Imperial Biomedical Research Centre and the Medical Research Council, part of UK Research and Innovation. Dr. Comninos reported no relevant financial relationships. Dr. Dhillo reported receiving consulting fees from Myovant Sciences and KaNDy Therapeutics outside the submitted work.
A version of this article first appeared on Medscape.com.
according to results from two small randomized controlled trials.
The data suggest that injections of kisspeptin can boost sexual desire in men and women and can increase penile rigidity in men.
Together, these two studies provide proof of concept for the development of kisspeptin-based therapeutics for men and women with distressing hypoactive sexual desire disorder (HSDD), study investigator Alexander Comninos, MD, PhD, Imperial College London, said in a news release.
One study was published online Feb. 3, 2022, in JAMA Network Open. The other was published in October 2022.
Unmet need
HSDD affects up to 10% of women and 8% of men worldwide and leads to psychological and social harm, the news release noted.
“There is a real unmet need to find new, safer, and more effective therapies for this distressing condition for both women and men seeking treatment,” Dr. Comninos said.
Kisspeptin is a naturally occurring reproductive hormone that serves as a crucial activator of the reproductive system. Emerging evidence from animal models shows that kisspeptin signaling has key roles in modulating reproductive behavior, including sexual motivation and erections.
In a double-blind, placebo-controlled, crossover study, the researchers enrolled 32 healthy heterosexual men (mean age, 37.9 years) who had HSDD.
At the first study visit, the men were given an infusion of kisspeptin-54 (1 nmol/kg per hour) or placebo (saline) over 75 minutes. The participants then crossed over to the other treatment at a second study visit at least 7 days later.
The active treatment significantly increased circulating kisspeptin levels. A steady state was reached after 30-75 minutes of infusion, the researchers reported.
Similar data in men, women
While the men viewed sexual videos, kisspeptin significantly modulated brain activity on fMRI in key structures of the sexual-processing network, compared with placebo (P = .003).
In addition, the treatment led to significant increases in penile tumescence in response to sexual stimuli (by up to 56% more than placebo; P = .02) and behavioral measures of sexual desire – most notably increased happiness about sex (P = .02).
Given the significant stimulatory effect of kisspeptin administration on penile rigidity, coupled with its demonstrated proerectile effect in rodents, future studies should examine the use of kisspeptin for patients with erectile dysfunction, the researchers wrote.
The second study included 32 women with HSDD and had the same design. Its results also showed that kisspeptin restored sexual and attraction brain processing without adverse effects.
“It is highly encouraging to see the same boosting effect in both women and men, although the precise brain pathways were slightly different, as might be expected,” coinvestigator Waljit Dhillo, PhD, Imperial College London, said in the news release.
“Collectively, the results suggest that kisspeptin may offer a safe and much-needed treatment for HSDD that affects millions of people around the world; and we look forward to taking this forward in future larger studies and in other patient groups,” Dr. Dhillo added.
The study was funded by the National Institute for Health and Care Research Imperial Biomedical Research Centre and the Medical Research Council, part of UK Research and Innovation. Dr. Comninos reported no relevant financial relationships. Dr. Dhillo reported receiving consulting fees from Myovant Sciences and KaNDy Therapeutics outside the submitted work.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN
Pound of flesh buys less prison time
Pound of flesh buys less prison time
We should all have more Shakespeare in our lives. Yeah, yeah, Shakespeare is meant to be played, not read, and it can be a struggle to herd teenagers through the Bard’s interesting and bloody tragedies, but even a perfunctory reading of “The Merchant of Venice” would hopefully have prevented the dystopian nightmare Massachusetts has presented us with today.
The United States has a massive shortage of donor organs. This is an unfortunate truth. So, to combat this issue, a pair of Massachusetts congresspeople have proposed HD 3822, which would allow prisoners to donate organs and/or bone marrow (a pound of flesh, so to speak) in exchange for up to a year in reduced prison time. Yes, that’s right. Give up pieces of yourself and the state of Massachusetts will deign to reduce your long prison sentence.
Oh, and before you dismiss this as typical Republican antics, the bill was sponsored by two Democrats, and in a statement one of them hoped to address racial disparities in organ donation, as people of color are much less likely to receive organs. Never mind that Black people are imprisoned at a much higher rate than Whites.
Yeah, this whole thing is what people in the business like to call an ethical disaster.
Fortunately, the bill will likely never be passed and it’s probably illegal anyway. A federal law from 1984 (how’s that for a coincidence) prevents people from donating organs for use in human transplantation in exchange for “valuable consideration.” In other words, you can’t sell your organs for profit, and in this case, reducing prison time would probably count as valuable consideration in the eyes of the courts.
Oh, and in case you’ve never read Merchant of Venice, Shylock, the character looking for the pound of flesh as payment for a debt? He’s the villain. In fact, it’s pretty safe to say that anyone looking to extract payment from human dismemberment is probably the bad guy of the story. Apparently that wasn’t clear.
How do you stop a fungi? With a deadly guy
Thanks to the new HBO series “The Last of Us,” there’s been a lot of talk about the upcoming fungi-pocalypse, as the show depicts the real-life “zombie fungus” Cordyceps turning humans into, you know, zombies.
No need to worry, ladies and gentleman, because science has discovered a way to turn back the fungal horde. A heroic, and environmentally friendly, alternative to chemical pesticides “in the fight against resistant fungi [that] are now resistant to antimycotics – partly because they are used in large quantities in agricultural fields,” investigators at the Leibniz Institute for Natural Product Research and Infection Biology in Jena, Germany, said in a written statement.
We are, of course, talking about Keanu Reeves. Wait a second. He’s not even in “The Last of Us.” Sorry folks, we are being told that it really is Keanu Reeves. Our champion in the inevitable fungal pandemic is movie star Keanu Reeves. Sort of. It’s actually keanumycin, a substance produced by bacteria of the genus Pseudomonas.
Really? Keanumycin? “The lipopeptides kill so efficiently that we named them after Keanu Reeves because he, too, is extremely deadly in his roles,” lead author Sebastian Götze, PhD, explained.
Dr. Götze and his associates had been working with pseudomonads for quite a while before they were able to isolate the toxins responsible for their ability to kill amoebae, which resemble fungi in some characteristics. When then finally tried the keanumycin against gray mold rot on hydrangea leaves, the intensely contemplative star of “The Matrix” and “John Wick” – sorry, wrong Keanu – the bacterial derivative significantly inhibited growth of the fungus, they said.
Additional testing has shown that keanumycin is not highly toxic to human cells and is effective against fungi such as Candida albicans in very low concentrations, which makes it a good candidate for future pharmaceutical development.
To that news there can be only one response from the substance’s namesake.
High fat, bye parasites
Fat. Fat. Fat. Seems like everyone is trying to avoid it these days, but fat may be good thing when it comes to weaseling out a parasite.
The parasite in this case is the whipworm, aka Trichuris trichiura. You can find this guy in the intestines of millions of people, where it causes long-lasting infections. Yikes … Researchers have found that the plan of attack to get rid of this invasive species is to boost the immune system, but instead of vitamin C and zinc it’s fat they’re pumping in. Yes, fat.
The developing countries with poor sewage that are at the highest risk for contracting parasites such as this also are among those where people ingest cheaper diets that are generally higher in fat. The investigators were interested to see how a high-fat diet would affect immune responses to the whipworms.
And, as with almost everything else, the researchers turned to mice, which were introduced to a closely related species, Trichuris muris.
A high-fat diet, rather than obesity itself, increases a molecule on T-helper cells called ST2, and this allows an increased T-helper 2 response, effectively giving eviction notices to the parasites in the intestinal lining.
To say the least, the researchers were surprised since “high-fat diets are mostly associated with increased pathology during disease,” said senior author Richard Grencis, PhD, of the University of Manchester (England), who noted that ST2 is not normally triggered with a standard diet in mice but the high-fat diet gave it a boost and an “alternate pathway” out.
Now before you start ordering extra-large fries at the drive-through to keep the whipworms away, the researchers added that they “have previously published that weight loss can aid the expulsion of a different gut parasite worm.” Figures.
Once again, though, signs are pointing to the gut for improved health.
Pound of flesh buys less prison time
We should all have more Shakespeare in our lives. Yeah, yeah, Shakespeare is meant to be played, not read, and it can be a struggle to herd teenagers through the Bard’s interesting and bloody tragedies, but even a perfunctory reading of “The Merchant of Venice” would hopefully have prevented the dystopian nightmare Massachusetts has presented us with today.
The United States has a massive shortage of donor organs. This is an unfortunate truth. So, to combat this issue, a pair of Massachusetts congresspeople have proposed HD 3822, which would allow prisoners to donate organs and/or bone marrow (a pound of flesh, so to speak) in exchange for up to a year in reduced prison time. Yes, that’s right. Give up pieces of yourself and the state of Massachusetts will deign to reduce your long prison sentence.
Oh, and before you dismiss this as typical Republican antics, the bill was sponsored by two Democrats, and in a statement one of them hoped to address racial disparities in organ donation, as people of color are much less likely to receive organs. Never mind that Black people are imprisoned at a much higher rate than Whites.
Yeah, this whole thing is what people in the business like to call an ethical disaster.
Fortunately, the bill will likely never be passed and it’s probably illegal anyway. A federal law from 1984 (how’s that for a coincidence) prevents people from donating organs for use in human transplantation in exchange for “valuable consideration.” In other words, you can’t sell your organs for profit, and in this case, reducing prison time would probably count as valuable consideration in the eyes of the courts.
Oh, and in case you’ve never read Merchant of Venice, Shylock, the character looking for the pound of flesh as payment for a debt? He’s the villain. In fact, it’s pretty safe to say that anyone looking to extract payment from human dismemberment is probably the bad guy of the story. Apparently that wasn’t clear.
How do you stop a fungi? With a deadly guy
Thanks to the new HBO series “The Last of Us,” there’s been a lot of talk about the upcoming fungi-pocalypse, as the show depicts the real-life “zombie fungus” Cordyceps turning humans into, you know, zombies.
No need to worry, ladies and gentleman, because science has discovered a way to turn back the fungal horde. A heroic, and environmentally friendly, alternative to chemical pesticides “in the fight against resistant fungi [that] are now resistant to antimycotics – partly because they are used in large quantities in agricultural fields,” investigators at the Leibniz Institute for Natural Product Research and Infection Biology in Jena, Germany, said in a written statement.
We are, of course, talking about Keanu Reeves. Wait a second. He’s not even in “The Last of Us.” Sorry folks, we are being told that it really is Keanu Reeves. Our champion in the inevitable fungal pandemic is movie star Keanu Reeves. Sort of. It’s actually keanumycin, a substance produced by bacteria of the genus Pseudomonas.
Really? Keanumycin? “The lipopeptides kill so efficiently that we named them after Keanu Reeves because he, too, is extremely deadly in his roles,” lead author Sebastian Götze, PhD, explained.
Dr. Götze and his associates had been working with pseudomonads for quite a while before they were able to isolate the toxins responsible for their ability to kill amoebae, which resemble fungi in some characteristics. When then finally tried the keanumycin against gray mold rot on hydrangea leaves, the intensely contemplative star of “The Matrix” and “John Wick” – sorry, wrong Keanu – the bacterial derivative significantly inhibited growth of the fungus, they said.
Additional testing has shown that keanumycin is not highly toxic to human cells and is effective against fungi such as Candida albicans in very low concentrations, which makes it a good candidate for future pharmaceutical development.
To that news there can be only one response from the substance’s namesake.
High fat, bye parasites
Fat. Fat. Fat. Seems like everyone is trying to avoid it these days, but fat may be good thing when it comes to weaseling out a parasite.
The parasite in this case is the whipworm, aka Trichuris trichiura. You can find this guy in the intestines of millions of people, where it causes long-lasting infections. Yikes … Researchers have found that the plan of attack to get rid of this invasive species is to boost the immune system, but instead of vitamin C and zinc it’s fat they’re pumping in. Yes, fat.
The developing countries with poor sewage that are at the highest risk for contracting parasites such as this also are among those where people ingest cheaper diets that are generally higher in fat. The investigators were interested to see how a high-fat diet would affect immune responses to the whipworms.
And, as with almost everything else, the researchers turned to mice, which were introduced to a closely related species, Trichuris muris.
A high-fat diet, rather than obesity itself, increases a molecule on T-helper cells called ST2, and this allows an increased T-helper 2 response, effectively giving eviction notices to the parasites in the intestinal lining.
To say the least, the researchers were surprised since “high-fat diets are mostly associated with increased pathology during disease,” said senior author Richard Grencis, PhD, of the University of Manchester (England), who noted that ST2 is not normally triggered with a standard diet in mice but the high-fat diet gave it a boost and an “alternate pathway” out.
Now before you start ordering extra-large fries at the drive-through to keep the whipworms away, the researchers added that they “have previously published that weight loss can aid the expulsion of a different gut parasite worm.” Figures.
Once again, though, signs are pointing to the gut for improved health.
Pound of flesh buys less prison time
We should all have more Shakespeare in our lives. Yeah, yeah, Shakespeare is meant to be played, not read, and it can be a struggle to herd teenagers through the Bard’s interesting and bloody tragedies, but even a perfunctory reading of “The Merchant of Venice” would hopefully have prevented the dystopian nightmare Massachusetts has presented us with today.
The United States has a massive shortage of donor organs. This is an unfortunate truth. So, to combat this issue, a pair of Massachusetts congresspeople have proposed HD 3822, which would allow prisoners to donate organs and/or bone marrow (a pound of flesh, so to speak) in exchange for up to a year in reduced prison time. Yes, that’s right. Give up pieces of yourself and the state of Massachusetts will deign to reduce your long prison sentence.
Oh, and before you dismiss this as typical Republican antics, the bill was sponsored by two Democrats, and in a statement one of them hoped to address racial disparities in organ donation, as people of color are much less likely to receive organs. Never mind that Black people are imprisoned at a much higher rate than Whites.
Yeah, this whole thing is what people in the business like to call an ethical disaster.
Fortunately, the bill will likely never be passed and it’s probably illegal anyway. A federal law from 1984 (how’s that for a coincidence) prevents people from donating organs for use in human transplantation in exchange for “valuable consideration.” In other words, you can’t sell your organs for profit, and in this case, reducing prison time would probably count as valuable consideration in the eyes of the courts.
Oh, and in case you’ve never read Merchant of Venice, Shylock, the character looking for the pound of flesh as payment for a debt? He’s the villain. In fact, it’s pretty safe to say that anyone looking to extract payment from human dismemberment is probably the bad guy of the story. Apparently that wasn’t clear.
How do you stop a fungi? With a deadly guy
Thanks to the new HBO series “The Last of Us,” there’s been a lot of talk about the upcoming fungi-pocalypse, as the show depicts the real-life “zombie fungus” Cordyceps turning humans into, you know, zombies.
No need to worry, ladies and gentleman, because science has discovered a way to turn back the fungal horde. A heroic, and environmentally friendly, alternative to chemical pesticides “in the fight against resistant fungi [that] are now resistant to antimycotics – partly because they are used in large quantities in agricultural fields,” investigators at the Leibniz Institute for Natural Product Research and Infection Biology in Jena, Germany, said in a written statement.
We are, of course, talking about Keanu Reeves. Wait a second. He’s not even in “The Last of Us.” Sorry folks, we are being told that it really is Keanu Reeves. Our champion in the inevitable fungal pandemic is movie star Keanu Reeves. Sort of. It’s actually keanumycin, a substance produced by bacteria of the genus Pseudomonas.
Really? Keanumycin? “The lipopeptides kill so efficiently that we named them after Keanu Reeves because he, too, is extremely deadly in his roles,” lead author Sebastian Götze, PhD, explained.
Dr. Götze and his associates had been working with pseudomonads for quite a while before they were able to isolate the toxins responsible for their ability to kill amoebae, which resemble fungi in some characteristics. When then finally tried the keanumycin against gray mold rot on hydrangea leaves, the intensely contemplative star of “The Matrix” and “John Wick” – sorry, wrong Keanu – the bacterial derivative significantly inhibited growth of the fungus, they said.
Additional testing has shown that keanumycin is not highly toxic to human cells and is effective against fungi such as Candida albicans in very low concentrations, which makes it a good candidate for future pharmaceutical development.
To that news there can be only one response from the substance’s namesake.
High fat, bye parasites
Fat. Fat. Fat. Seems like everyone is trying to avoid it these days, but fat may be good thing when it comes to weaseling out a parasite.
The parasite in this case is the whipworm, aka Trichuris trichiura. You can find this guy in the intestines of millions of people, where it causes long-lasting infections. Yikes … Researchers have found that the plan of attack to get rid of this invasive species is to boost the immune system, but instead of vitamin C and zinc it’s fat they’re pumping in. Yes, fat.
The developing countries with poor sewage that are at the highest risk for contracting parasites such as this also are among those where people ingest cheaper diets that are generally higher in fat. The investigators were interested to see how a high-fat diet would affect immune responses to the whipworms.
And, as with almost everything else, the researchers turned to mice, which were introduced to a closely related species, Trichuris muris.
A high-fat diet, rather than obesity itself, increases a molecule on T-helper cells called ST2, and this allows an increased T-helper 2 response, effectively giving eviction notices to the parasites in the intestinal lining.
To say the least, the researchers were surprised since “high-fat diets are mostly associated with increased pathology during disease,” said senior author Richard Grencis, PhD, of the University of Manchester (England), who noted that ST2 is not normally triggered with a standard diet in mice but the high-fat diet gave it a boost and an “alternate pathway” out.
Now before you start ordering extra-large fries at the drive-through to keep the whipworms away, the researchers added that they “have previously published that weight loss can aid the expulsion of a different gut parasite worm.” Figures.
Once again, though, signs are pointing to the gut for improved health.
Longer life after bariatric surgery, but suicide risk in young
Death from cardiovascular disease, cancer, and diabetes was 29%, 43%, and 72% lower, respectively, in the bariatric surgery patients versus nonsurgery peers, during a mean follow-up of 13 years (all P > .001).
However, the youngest group of bariatric surgery patients – who were 18-34 years old – had a fivefold increased risk of suicide during follow-up compared with their peers who did not undergo surgery (P = .001).
These findings are from a retrospective study in Utah that matched close to 22,000 patients with severe obesity who underwent Roux-en-Y gastric bypass, gastric banding, sleeve gastrectomy, or duodenal switch from 1982 to 2018 with an equal number of nonsurgery individuals.
The study, by Ted D. Adams, PhD, MPH, and colleagues, was published online in Obesity.
‘Impressive’ data, in men too, but psychological screening important
The overall improved survival and decreased deaths from diabetes, heart disease, and cancer over this long follow-up are “impressive,” Dr. Adams, of Intermountain Surgical Specialties/Digestive Health Clinical Program, Salt Lake City, said in an interview.
Previous studies have not shown a survival benefit from bariatric surgery versus no surgery in men, he said. However, “because we had a fair number of male patients and because of the length of follow-up, we did show that the improved mortality was not only evident for the female patients but also for the male patients,” Dr. Adams stressed.
Finding increased suicide rates among bariatric surgical patients who underwent surgery at a younger age (18-34 years) shows that “we need to try and determine who is at risk for suicide,” according to Dr. Adams.
Patients with severe obesity, especially younger ones, “may need more aggressive presurgical psychological screening and postsurgery follow-up,” wrote Dr. Adams and colleagues.
The findings may also “stimulate important research related to the discovery of physiologic and biomolecular mechanisms leading to nonsurgical treatment that results in weight loss and improved mortality similar to that achieved by bariatric surgery,” they suggested.
Close to 1 in 10 Americans has severe obesity
The prevalence of severe obesity (BMI ≥ 40 kg/m2) in the United States has increased from 4.7% during 1999-2000 to 9.2% during 2017-2018, based on National Health and Nutrition Examination Survey (NHANES) data, the researchers noted.
They previously published a study of long-term mortality in 7,925 patients who had gastric bypass surgery from 1984 to 2002 matched with patients with the same BMI who did not have bariatric surgery and were followed out to 2002.
The current study extends the follow-up through 2021, doubles the number of bypass patients, and includes three newer types of bariatric surgery.
The researchers matched 21,873 patients aged 18-80 who had Roux-en-Y gastric bypass, gastric banding, sleeve gastrectomy, or duodenal switch during 1982-2018 in Utah (from the Utah Population Database) with people of the same BMI category, age category (18-34, 35-44, 45-54, and 55-80 years), and sex (from Utah driver license data).
Most patients were women (79%) and most were White (94% and 85%). They had a mean age of 42 years and a mean BMI of 46 kg/m2.
Most patients had Roux-en-Y gastric bypass (69%), and the rest had sleeve gastrectomy (14%), gastric banding (12%), and duodenal switch (4.8%).
During follow-up, 13.5% of patients in the bariatric surgery group and 14.6% of people in the nonsurgery group died.
Overall, all-cause mortality was 16% lower in patients who had bariatric surgery versus matched nonsurgical participants; it was 14% lower in women and 21% lower in men (all P < .001).
All-cause mortality was significantly lower in patients who had bariatric surgery when they were 35-44, 45-54, and 55-80 years old compared with matched peers who did not have surgery.
However, the findings “should not imply patients necessarily postpone surgery until older age,” the researchers cautioned, “as postsurgical complications have been shown to increase with increasing age at surgery and surgical postponement may result in worsened clinical status related to certain conditions such as orthopedic joint health.”
The researchers found significantly improved all-cause mortality following either type of surgery (gastric bypass, gastric banding, and sleeve gastrectomy) compared with no surgery.
Along with fewer deaths from cardiovascular disease, cancer, and diabetes, deaths from lung disease were 39% lower in the surgery group than in the nonsurgery group.
However, in the youngest group (age 18-34), deaths from cirrhosis of the liver were significantly higher in the patients who had bariatric surgery, and rates of suicide were significantly greater for both females and males, compared with similar people who did not undergo surgery.
The study was supported by grants from Ethicon Endo-Surgery (Johnson & Johnson); the National Institute of Diabetes and Digestive and Kidney Diseases, a division of the National Institutes of Health; U.S. Public Health Service; and Intermountain Research and Medical Foundation of Intermountain Healthcare. Dr. Adams disclosed ties to Ethicon Endo-Surgery and Intermountain Healthcare. A coauthor reported ties with Biomedical Research Program at Weill Cornell Medicine in Qatar, a program funded by the Qatar Foundation. The other authors have reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Death from cardiovascular disease, cancer, and diabetes was 29%, 43%, and 72% lower, respectively, in the bariatric surgery patients versus nonsurgery peers, during a mean follow-up of 13 years (all P > .001).
However, the youngest group of bariatric surgery patients – who were 18-34 years old – had a fivefold increased risk of suicide during follow-up compared with their peers who did not undergo surgery (P = .001).
These findings are from a retrospective study in Utah that matched close to 22,000 patients with severe obesity who underwent Roux-en-Y gastric bypass, gastric banding, sleeve gastrectomy, or duodenal switch from 1982 to 2018 with an equal number of nonsurgery individuals.
The study, by Ted D. Adams, PhD, MPH, and colleagues, was published online in Obesity.
‘Impressive’ data, in men too, but psychological screening important
The overall improved survival and decreased deaths from diabetes, heart disease, and cancer over this long follow-up are “impressive,” Dr. Adams, of Intermountain Surgical Specialties/Digestive Health Clinical Program, Salt Lake City, said in an interview.
Previous studies have not shown a survival benefit from bariatric surgery versus no surgery in men, he said. However, “because we had a fair number of male patients and because of the length of follow-up, we did show that the improved mortality was not only evident for the female patients but also for the male patients,” Dr. Adams stressed.
Finding increased suicide rates among bariatric surgical patients who underwent surgery at a younger age (18-34 years) shows that “we need to try and determine who is at risk for suicide,” according to Dr. Adams.
Patients with severe obesity, especially younger ones, “may need more aggressive presurgical psychological screening and postsurgery follow-up,” wrote Dr. Adams and colleagues.
The findings may also “stimulate important research related to the discovery of physiologic and biomolecular mechanisms leading to nonsurgical treatment that results in weight loss and improved mortality similar to that achieved by bariatric surgery,” they suggested.
Close to 1 in 10 Americans has severe obesity
The prevalence of severe obesity (BMI ≥ 40 kg/m2) in the United States has increased from 4.7% during 1999-2000 to 9.2% during 2017-2018, based on National Health and Nutrition Examination Survey (NHANES) data, the researchers noted.
They previously published a study of long-term mortality in 7,925 patients who had gastric bypass surgery from 1984 to 2002 matched with patients with the same BMI who did not have bariatric surgery and were followed out to 2002.
The current study extends the follow-up through 2021, doubles the number of bypass patients, and includes three newer types of bariatric surgery.
The researchers matched 21,873 patients aged 18-80 who had Roux-en-Y gastric bypass, gastric banding, sleeve gastrectomy, or duodenal switch during 1982-2018 in Utah (from the Utah Population Database) with people of the same BMI category, age category (18-34, 35-44, 45-54, and 55-80 years), and sex (from Utah driver license data).
Most patients were women (79%) and most were White (94% and 85%). They had a mean age of 42 years and a mean BMI of 46 kg/m2.
Most patients had Roux-en-Y gastric bypass (69%), and the rest had sleeve gastrectomy (14%), gastric banding (12%), and duodenal switch (4.8%).
During follow-up, 13.5% of patients in the bariatric surgery group and 14.6% of people in the nonsurgery group died.
Overall, all-cause mortality was 16% lower in patients who had bariatric surgery versus matched nonsurgical participants; it was 14% lower in women and 21% lower in men (all P < .001).
All-cause mortality was significantly lower in patients who had bariatric surgery when they were 35-44, 45-54, and 55-80 years old compared with matched peers who did not have surgery.
However, the findings “should not imply patients necessarily postpone surgery until older age,” the researchers cautioned, “as postsurgical complications have been shown to increase with increasing age at surgery and surgical postponement may result in worsened clinical status related to certain conditions such as orthopedic joint health.”
The researchers found significantly improved all-cause mortality following either type of surgery (gastric bypass, gastric banding, and sleeve gastrectomy) compared with no surgery.
Along with fewer deaths from cardiovascular disease, cancer, and diabetes, deaths from lung disease were 39% lower in the surgery group than in the nonsurgery group.
However, in the youngest group (age 18-34), deaths from cirrhosis of the liver were significantly higher in the patients who had bariatric surgery, and rates of suicide were significantly greater for both females and males, compared with similar people who did not undergo surgery.
The study was supported by grants from Ethicon Endo-Surgery (Johnson & Johnson); the National Institute of Diabetes and Digestive and Kidney Diseases, a division of the National Institutes of Health; U.S. Public Health Service; and Intermountain Research and Medical Foundation of Intermountain Healthcare. Dr. Adams disclosed ties to Ethicon Endo-Surgery and Intermountain Healthcare. A coauthor reported ties with Biomedical Research Program at Weill Cornell Medicine in Qatar, a program funded by the Qatar Foundation. The other authors have reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Death from cardiovascular disease, cancer, and diabetes was 29%, 43%, and 72% lower, respectively, in the bariatric surgery patients versus nonsurgery peers, during a mean follow-up of 13 years (all P > .001).
However, the youngest group of bariatric surgery patients – who were 18-34 years old – had a fivefold increased risk of suicide during follow-up compared with their peers who did not undergo surgery (P = .001).
These findings are from a retrospective study in Utah that matched close to 22,000 patients with severe obesity who underwent Roux-en-Y gastric bypass, gastric banding, sleeve gastrectomy, or duodenal switch from 1982 to 2018 with an equal number of nonsurgery individuals.
The study, by Ted D. Adams, PhD, MPH, and colleagues, was published online in Obesity.
‘Impressive’ data, in men too, but psychological screening important
The overall improved survival and decreased deaths from diabetes, heart disease, and cancer over this long follow-up are “impressive,” Dr. Adams, of Intermountain Surgical Specialties/Digestive Health Clinical Program, Salt Lake City, said in an interview.
Previous studies have not shown a survival benefit from bariatric surgery versus no surgery in men, he said. However, “because we had a fair number of male patients and because of the length of follow-up, we did show that the improved mortality was not only evident for the female patients but also for the male patients,” Dr. Adams stressed.
Finding increased suicide rates among bariatric surgical patients who underwent surgery at a younger age (18-34 years) shows that “we need to try and determine who is at risk for suicide,” according to Dr. Adams.
Patients with severe obesity, especially younger ones, “may need more aggressive presurgical psychological screening and postsurgery follow-up,” wrote Dr. Adams and colleagues.
The findings may also “stimulate important research related to the discovery of physiologic and biomolecular mechanisms leading to nonsurgical treatment that results in weight loss and improved mortality similar to that achieved by bariatric surgery,” they suggested.
Close to 1 in 10 Americans has severe obesity
The prevalence of severe obesity (BMI ≥ 40 kg/m2) in the United States has increased from 4.7% during 1999-2000 to 9.2% during 2017-2018, based on National Health and Nutrition Examination Survey (NHANES) data, the researchers noted.
They previously published a study of long-term mortality in 7,925 patients who had gastric bypass surgery from 1984 to 2002 matched with patients with the same BMI who did not have bariatric surgery and were followed out to 2002.
The current study extends the follow-up through 2021, doubles the number of bypass patients, and includes three newer types of bariatric surgery.
The researchers matched 21,873 patients aged 18-80 who had Roux-en-Y gastric bypass, gastric banding, sleeve gastrectomy, or duodenal switch during 1982-2018 in Utah (from the Utah Population Database) with people of the same BMI category, age category (18-34, 35-44, 45-54, and 55-80 years), and sex (from Utah driver license data).
Most patients were women (79%) and most were White (94% and 85%). They had a mean age of 42 years and a mean BMI of 46 kg/m2.
Most patients had Roux-en-Y gastric bypass (69%), and the rest had sleeve gastrectomy (14%), gastric banding (12%), and duodenal switch (4.8%).
During follow-up, 13.5% of patients in the bariatric surgery group and 14.6% of people in the nonsurgery group died.
Overall, all-cause mortality was 16% lower in patients who had bariatric surgery versus matched nonsurgical participants; it was 14% lower in women and 21% lower in men (all P < .001).
All-cause mortality was significantly lower in patients who had bariatric surgery when they were 35-44, 45-54, and 55-80 years old compared with matched peers who did not have surgery.
However, the findings “should not imply patients necessarily postpone surgery until older age,” the researchers cautioned, “as postsurgical complications have been shown to increase with increasing age at surgery and surgical postponement may result in worsened clinical status related to certain conditions such as orthopedic joint health.”
The researchers found significantly improved all-cause mortality following either type of surgery (gastric bypass, gastric banding, and sleeve gastrectomy) compared with no surgery.
Along with fewer deaths from cardiovascular disease, cancer, and diabetes, deaths from lung disease were 39% lower in the surgery group than in the nonsurgery group.
However, in the youngest group (age 18-34), deaths from cirrhosis of the liver were significantly higher in the patients who had bariatric surgery, and rates of suicide were significantly greater for both females and males, compared with similar people who did not undergo surgery.
The study was supported by grants from Ethicon Endo-Surgery (Johnson & Johnson); the National Institute of Diabetes and Digestive and Kidney Diseases, a division of the National Institutes of Health; U.S. Public Health Service; and Intermountain Research and Medical Foundation of Intermountain Healthcare. Dr. Adams disclosed ties to Ethicon Endo-Surgery and Intermountain Healthcare. A coauthor reported ties with Biomedical Research Program at Weill Cornell Medicine in Qatar, a program funded by the Qatar Foundation. The other authors have reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
FROM OBESITY
What is the psychological cost of performing CPR?
One year ago, as the sun was setting on a late fall day, Andrés Snitcofsky, a 40-year-old designer from Buenos Aires, Argentina, heard harrowing cries for help. It was the niece and the wife of one of his neighbors: a man in his 60s who the women had found “passed out” in the bedroom. “I did CPR for 5 minutes straight until a friend of the victim came in and asked me to stop, telling me that the man had probably been dead for 2 or 3 hours already. But I had no idea because I’d never seen a dead body before,” Mr. Snitcofsky told this news organization. A few minutes later, the ambulance arrived. The doctor confirmed that there was nothing more that could be done.
Mr. Snitcofsky went home. Nobody had asked for his name or address or phone number. … And it wasn’t because they already knew who he was. In fact, there wasn’t any sort of relationship there. Mr. Snitcofsky had only known his neighbors by sight. His actions that day, however, “did not come without a cost. It took me weeks – months, actually – to put myself together again,” he said. The things he saw, the things he heard, everything about that night played over and over in his head. “I had trouble sleeping. I would play out different scenarios in my head. I questioned myself. I second-guessed myself, criticized myself. It’s like some taboo subject. There’s no one to share the experience with, no one who gets it. But with time, I was able to process the event.
“For 2 months, I talked to my psychologist about it all,” he continued. “That really helped me a lot. In addition to therapy, I reached out to a couple I know – they’re both physicians – and to a firefighter who teaches CPR. Their insight and guidance allowed me to get to a point where I was able to understand that what I did was a good thing and that what I did was all that could have been done. But anyone who finds themselves in the position of having to do CPR – they’re going to be affected in many, many ways. It goes beyond the euphoria of seeing a person come back to life. Of that, I’m quite certain.”
We’ve all seen campaigns encouraging people to learn CPR and to be prepared if the need arises. But in training the public (and even health care professionals), not much, if anything, is said about the “collateral damage”: the psychological and emotional consequences of carrying out the procedure. These especially come into play when you don’t know whether the person survived, when your efforts weren’t able to reverse the sudden cardiac arrest, or when the person you gave CPR to was a loved one – a case that may entail immediate therapeutic interventions to minimize or prevent the risk of suffering long-lasting trauma.
In May 2020, popular American activist and educator Kristin Flanary saw someone suffering cardiac arrest. She stepped in and started doing CPR. And she continued doing CPR … for 10 long minutes. The person she was trying to save was her 34-year-old husband, ophthalmologist and comedian Will Flanary. On Twitter, where she’s known as Lady Glaucomflecken, Ms. Flanary recently shared the following message, putting the topic of CPR and automated external defibrillator training front and center.
“Yes, everyone should learn #CPRandAED. But if we are going to ask people to perform such a brutal task, it’s imperative that we also provide them with the info and resources they need to process it mentally and emotionally. It’s traumatic and life changing. It’s irresponsible and unethical to ask people to help in such a brutal and traumatic way and then neglect to help them in return.” In less than a month, the tweet has racked up over 200,000 views.
Doing one’s duty
There are many people who work to promote CPR and strengthen the other links in the chain of survival for out-of-hospital sudden cardiac arrest, such as prompt access to and delivery of early defibrillation. According to them, any negative psychological impact of intervening is temporary and, when compared with the satisfaction of having done one’s duty, quite insignificant – even if the efforts to save a person’s life are not successful.
“In 99.9% of cases, people who have performed CPR feel a sense of satisfaction, even happiness, knowing that they’ve helped. The individuals I’ve spoken with, I’ve never heard any of them say that they felt worse after the event or that they needed to see a psychologist,” said Mario Fitz Maurice, MD, director of the Arrhythmia Council of the Argentine Society of Cardiology and head of Electrophysiology at Rivadavia Hospital in Buenos Aires. He went on to tell this news organization, “Of course, some degree of fear, sadness, or melancholy can remain afterward. But it seems to me, and there are reports saying as much, that, in the end, what stands out in the person’s mind is the fact that they tried to save a life. And for them, there’s joy in knowing this.”
Dr. Fitz Maurice, who is also the director of the National Arrhythmia Institute in Buenos Aires, pointed out that the kind of person who takes CPR classes “has a profile that’s going to allow them to be psychologically involved; they’re the caring person, the one who’s ready and willing to help people.” And he added that, at his hospital, if they can identify the individuals or first responders who have done CPR on a patient, the protocol is to always contact them to offer psychological care and assistance. “But in 99% of cases, they don’t even understand why we’re calling them, they’re extremely happy to have taken part.”
Some studies, though, paint a much different picture, one that shows that providing CPR can be emotionally challenging and have consequences in terms of one’s family and work life. A qualitative study published in 2016 looked into the experiences of 20 lay rescuers in Norway – five were health educated – who had provided CPR to 18 out-of-hospital cardiac arrest (OHCA) victims, 66% of whom survived. The time from experiencing the OHCA incident to participating in the interview ranged from 6 days to 13 years (median 5.5 years). Several participants reported the OHCA incident as a “shocking and terrifying” experience. Tiredness, exhaustion, confusion, and feeling alone about the OHCA experience were individual reactions that could vary in time from days to months. Anxiety and insomnia were also experienced following the incident.
Some lay rescuers described the influence on work and family life, and a few of them described deep sorrow, even several years after the incident. Overall, they reported repetitive self-criticism regarding whether they could have carried out anything else to achieve a better outcome for the cardiac arrest victim. All of them wanted to be informed about the outcome. And four of the lay rescuers needed professional counseling to process the OHCA experience.
In 2020, another qualitative study was conducted, this time in Taiwan. There were nine participants, none of whom were health professionals. Each had provided initial CPR and defibrillation with AED in public locations. Event-to-interview duration was within 1 year and 1-2 years. The major findings from the study were the following:
- The lay rescuers possessed helping traits and high motivation.
- The lay rescuers reported certain aspects of rescue reality that differed much from prior training and expectations, including difficulty in the depth of chest compression, and uncertainties in real emergency situations.
- The lay rescuers gained positive personal fulfillment in sharing their experience and receiving positive feedback from others, and were willing to help next time, although they experienced a short-term negative psychological impact from the event. “Measures should be taken to increase [a] layperson’s confidence and situation awareness, to reduce training-reality discrepancy, and to build up a support system to avoid negative psychological effects.” This was the conclusion of the study team, which was led by Matthew Huei-Ming Ma, MD, PhD. A professor in the department of emergency medicine at National Taiwan University in Taipei, he is also on the board of directors of the Resuscitation Council of Asia.
Potential trauma
In recalling his experience, Mr. Snitcofsky said, “The hardest part of it all was the moment that I stopped giving CPR, that moment of letting go. This became the image that kept coming back to me, the traumatic moment I hadn’t thought about.”
Psychiatrist Daniel Mosca, MD, is the founder and former president of the Argentine Society of Trauma Psychology. He is also the coordinator of the human factors team at the City of Buenos Aires Emergency Medical Care System. “Any event has the potential to be traumatic, all the more so when it’s an event where you come face to face with death and uncertainty. But how a rescuer reacts will depend on their psychological makeup.” Of the individuals who were held for months or years in the jungle as hostages of the Revolutionary Armed Forces of Colombia, “only” half developed symptoms of posttraumatic stress disorder.
Dr. Mosca believes that a comment by Frank Ochberg, MD, speaks to this finding. “In many cases, peritraumatic symptoms are a normal person’s normal response to an abnormal situation.” For a lot of people who have found themselves having to perform CPR, the symptoms associated with the initial acute stress reaction will resolve on their own in 30-90 days. “But if this doesn’t happen, and those symptoms persist, psychotherapeutic or pharmacological intervention will be necessary,” he noted.
“In CPR classes, it would be good for the instructors to talk about the warning signs that people should look out for in themselves and their fellow rescuers. So, for example, insomnia, anxiety, a heightened state of alertness, feeling disconnected from reality,” Dr. Mosca told this news organization.
“Another thing that can help rescuers is letting them know what happened to the person they gave CPR to. This way, they can get closure,” suggested Manlio Márquez Murillo, MD, a cardiologist and electrophysiologist in Mexico. He is also the coordinator of the Alliance Against Sudden Cardiac Death at the Interamerican Society of Cardiology.
“Medical and nursing societies would have to develop a brief protocol or performance standard. The goal would be to ensure that rescuers are asked for their contact information and that someone gets in touch to debrief them and to offer them care. Next would come the treatment part, to resolve any remaining aftereffects,” said in an interview.
For example, a three-stage Lay Responder Support Model (LRSM) was developed and implemented as part of a lay responder support program established in 2014 by the Peel Regional Council in Ontario. The LRSM identifies and engages individuals who witnessed or participated directly or indirectly in an OHCA, inviting them to participate in a debriefing session facilitated by a trained practitioner. Held 24-48 hours post event, the debriefing allows lay responders to contextualize their reaction to the event. The conversation also serves as an opportunity for them to fully articulate their concerns, questions, and thoughts. The facilitator can communicate stress reduction techniques and address psychological first aid needs as they emerge. Approximately 1 week post event, a secondary follow-up occurs. If the lay responder communicates a continuing struggle with symptoms impacting and interfering with everyday life, the facilitator offers a coordinated or facilitated referral for mental health support.
In an article published in the Journal of Cardiac Failure. Ms. Flanary speaks about the three kinds of language that anyone who was either forced to or inspired to perform CPR can use to help process their trauma: words that explain what happened, words that name (eg, “forgotten patients”), and words that validate the experience and allow the person to articulate their feelings. The tools and technologies that organizations and health care professionals provide can help the healing process. Empathy and compassion, too, have a place.
But there are virtually no standardized and proactive initiatives of this kind in much of the world, including Latin America. So, most people who just happened to be in the right place at the right time find that they have to navigate the “after” part all on their own.
Other obstacles
Dr. Márquez Murillo finds it unfortunate that countries in the region have yet to enact “Good Samaritan” laws. If individuals render aid to someone suffering cardiac arrest, then these laws would ensure that they will not be held liable in any way. This is the case in Argentina and Uruguay. So, the fear of things turning into a legal matter may be holding people back from taking action; that fear could also create additional stress for those who end up stepping in to help.
Even with the legal safeguards, exceptional circumstances may arise where rescuers find themselves facing unexpected emotional challenges. In Argentina, Virginia Pérez Antonelli, the 17-year-old who tried in vain to save the life of Fernando Báez Sosa, had to testify at the trial of the eight defendants accused of brutally beating him in January 2020. The press, the public – the attention of an entire country – was focused on her. She had to respond to the defense attorneys who were able to ask whether she was sure that she performed the CPR maneuvers correctly. And a few weeks ago, a medical examiner hired by the defense suggested that “the CPR may have made the situation worse” for the victim. An indignant Dr. Fitz Maurice responded on Twitter: “CPR SAVES LIVES!! Let’s not let a CHEAP AND BASELESS argument destroy all the work that’s been done…!”
Of course, there are consequences that are beyond our control and others that can, in fact, be anticipated and planned for. Dr. Fitz Maurice brought up a preventive approach: Make CPR second nature, teach it in schools, help people overcome their fears. “Cardiac deaths are 200 times more frequent than deaths resulting from fires – and we practice fire drills a lot more than we practice CPR,” he told this news organization. In a society where there is widespread training on the procedure, where people regularly practice the technique, those who have had the experience of giving someone CPR will feel less alone, will be better understood by others.
“On the other hand, beyond the initial impact and the lack of a formal support system, the medium- and long-term outcome for those who acted is also psychologically and emotionally favorable,” said Jorge Bombau, MD, an obstetrician/gynecologist in Buenos Aires. After Dr. Bombau’s 14-year-old son Beltrán suddenly died during a school sports tournament, Dr. Bombau became a prominent advocate spreading the word about CPR.
“I don’t know anyone who regrets doing CPR,” he told this news organization. “There may be a brief period when the person feels distressed or depressed, when they have trouble sleeping. But it’s been proven that doing a good deed improves one’s mood. And what better deed is there than trying to save someone’s life? Whether their efforts were successful or in vain, that person has, at the end of the day, done something meaningful and worthwhile.”
Mr. Snitcofsky shares this sentiment. For several months now, he’s been feeling he’s “in a good place.” And he’s been actively promoting CPR on social media. As he recently posted on Twitter, “I’m here to retweet everything that has to do with getting us all to become familiar with how to do CPR and working up the courage to do it. The training takes no more than a few hours.
“I want to know that, if I ever have an out-of-hospital sudden cardiac arrest, there will be neighbors, friends, or family members around who know how to do CPR. Every person who knows how to do CPR can persuade others, and those of us who’ve had to do CPR in real life are even better candidates for persuading others. And if one day a person ends up needing CPR, I want to step in again and make up for lost time. Here’s hoping it’ll do the job,” he concluded.
It’s the same for Matías Alonso, a journalist in Buenos Aires. On New Year’s Eve 15 years ago, he was at a family dinner when, a few minutes before midnight, he found himself giving CPR to his stepmother’s father. “Unfortunately, he passed away, but I continued doing CPR on him until the ambulance arrived. For some time, I felt a little guilty for not taking charge of the situation from the beginning, and because I had this idea in my head that more people pulled through and recovered. But afterwards, they really thanked me a lot. And that helped me realize that I’d done something. I didn’t stand still when faced with the inevitability of death. I understood that it was good to have tried,” Mr. Alonso told this news organization. “And next time … hopefully there won’t be a next time … but I’m more prepared, and I now know how I can do better.”
Mr. Alonso, Mr. Snitcofsky, Dr. Fitz Maurice, Dr. Mosca, Dr. Bombau, and Dr. Márquez Murillo disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com. This article was translated from Medscape Spanish.
One year ago, as the sun was setting on a late fall day, Andrés Snitcofsky, a 40-year-old designer from Buenos Aires, Argentina, heard harrowing cries for help. It was the niece and the wife of one of his neighbors: a man in his 60s who the women had found “passed out” in the bedroom. “I did CPR for 5 minutes straight until a friend of the victim came in and asked me to stop, telling me that the man had probably been dead for 2 or 3 hours already. But I had no idea because I’d never seen a dead body before,” Mr. Snitcofsky told this news organization. A few minutes later, the ambulance arrived. The doctor confirmed that there was nothing more that could be done.
Mr. Snitcofsky went home. Nobody had asked for his name or address or phone number. … And it wasn’t because they already knew who he was. In fact, there wasn’t any sort of relationship there. Mr. Snitcofsky had only known his neighbors by sight. His actions that day, however, “did not come without a cost. It took me weeks – months, actually – to put myself together again,” he said. The things he saw, the things he heard, everything about that night played over and over in his head. “I had trouble sleeping. I would play out different scenarios in my head. I questioned myself. I second-guessed myself, criticized myself. It’s like some taboo subject. There’s no one to share the experience with, no one who gets it. But with time, I was able to process the event.
“For 2 months, I talked to my psychologist about it all,” he continued. “That really helped me a lot. In addition to therapy, I reached out to a couple I know – they’re both physicians – and to a firefighter who teaches CPR. Their insight and guidance allowed me to get to a point where I was able to understand that what I did was a good thing and that what I did was all that could have been done. But anyone who finds themselves in the position of having to do CPR – they’re going to be affected in many, many ways. It goes beyond the euphoria of seeing a person come back to life. Of that, I’m quite certain.”
We’ve all seen campaigns encouraging people to learn CPR and to be prepared if the need arises. But in training the public (and even health care professionals), not much, if anything, is said about the “collateral damage”: the psychological and emotional consequences of carrying out the procedure. These especially come into play when you don’t know whether the person survived, when your efforts weren’t able to reverse the sudden cardiac arrest, or when the person you gave CPR to was a loved one – a case that may entail immediate therapeutic interventions to minimize or prevent the risk of suffering long-lasting trauma.
In May 2020, popular American activist and educator Kristin Flanary saw someone suffering cardiac arrest. She stepped in and started doing CPR. And she continued doing CPR … for 10 long minutes. The person she was trying to save was her 34-year-old husband, ophthalmologist and comedian Will Flanary. On Twitter, where she’s known as Lady Glaucomflecken, Ms. Flanary recently shared the following message, putting the topic of CPR and automated external defibrillator training front and center.
“Yes, everyone should learn #CPRandAED. But if we are going to ask people to perform such a brutal task, it’s imperative that we also provide them with the info and resources they need to process it mentally and emotionally. It’s traumatic and life changing. It’s irresponsible and unethical to ask people to help in such a brutal and traumatic way and then neglect to help them in return.” In less than a month, the tweet has racked up over 200,000 views.
Doing one’s duty
There are many people who work to promote CPR and strengthen the other links in the chain of survival for out-of-hospital sudden cardiac arrest, such as prompt access to and delivery of early defibrillation. According to them, any negative psychological impact of intervening is temporary and, when compared with the satisfaction of having done one’s duty, quite insignificant – even if the efforts to save a person’s life are not successful.
“In 99.9% of cases, people who have performed CPR feel a sense of satisfaction, even happiness, knowing that they’ve helped. The individuals I’ve spoken with, I’ve never heard any of them say that they felt worse after the event or that they needed to see a psychologist,” said Mario Fitz Maurice, MD, director of the Arrhythmia Council of the Argentine Society of Cardiology and head of Electrophysiology at Rivadavia Hospital in Buenos Aires. He went on to tell this news organization, “Of course, some degree of fear, sadness, or melancholy can remain afterward. But it seems to me, and there are reports saying as much, that, in the end, what stands out in the person’s mind is the fact that they tried to save a life. And for them, there’s joy in knowing this.”
Dr. Fitz Maurice, who is also the director of the National Arrhythmia Institute in Buenos Aires, pointed out that the kind of person who takes CPR classes “has a profile that’s going to allow them to be psychologically involved; they’re the caring person, the one who’s ready and willing to help people.” And he added that, at his hospital, if they can identify the individuals or first responders who have done CPR on a patient, the protocol is to always contact them to offer psychological care and assistance. “But in 99% of cases, they don’t even understand why we’re calling them, they’re extremely happy to have taken part.”
Some studies, though, paint a much different picture, one that shows that providing CPR can be emotionally challenging and have consequences in terms of one’s family and work life. A qualitative study published in 2016 looked into the experiences of 20 lay rescuers in Norway – five were health educated – who had provided CPR to 18 out-of-hospital cardiac arrest (OHCA) victims, 66% of whom survived. The time from experiencing the OHCA incident to participating in the interview ranged from 6 days to 13 years (median 5.5 years). Several participants reported the OHCA incident as a “shocking and terrifying” experience. Tiredness, exhaustion, confusion, and feeling alone about the OHCA experience were individual reactions that could vary in time from days to months. Anxiety and insomnia were also experienced following the incident.
Some lay rescuers described the influence on work and family life, and a few of them described deep sorrow, even several years after the incident. Overall, they reported repetitive self-criticism regarding whether they could have carried out anything else to achieve a better outcome for the cardiac arrest victim. All of them wanted to be informed about the outcome. And four of the lay rescuers needed professional counseling to process the OHCA experience.
In 2020, another qualitative study was conducted, this time in Taiwan. There were nine participants, none of whom were health professionals. Each had provided initial CPR and defibrillation with AED in public locations. Event-to-interview duration was within 1 year and 1-2 years. The major findings from the study were the following:
- The lay rescuers possessed helping traits and high motivation.
- The lay rescuers reported certain aspects of rescue reality that differed much from prior training and expectations, including difficulty in the depth of chest compression, and uncertainties in real emergency situations.
- The lay rescuers gained positive personal fulfillment in sharing their experience and receiving positive feedback from others, and were willing to help next time, although they experienced a short-term negative psychological impact from the event. “Measures should be taken to increase [a] layperson’s confidence and situation awareness, to reduce training-reality discrepancy, and to build up a support system to avoid negative psychological effects.” This was the conclusion of the study team, which was led by Matthew Huei-Ming Ma, MD, PhD. A professor in the department of emergency medicine at National Taiwan University in Taipei, he is also on the board of directors of the Resuscitation Council of Asia.
Potential trauma
In recalling his experience, Mr. Snitcofsky said, “The hardest part of it all was the moment that I stopped giving CPR, that moment of letting go. This became the image that kept coming back to me, the traumatic moment I hadn’t thought about.”
Psychiatrist Daniel Mosca, MD, is the founder and former president of the Argentine Society of Trauma Psychology. He is also the coordinator of the human factors team at the City of Buenos Aires Emergency Medical Care System. “Any event has the potential to be traumatic, all the more so when it’s an event where you come face to face with death and uncertainty. But how a rescuer reacts will depend on their psychological makeup.” Of the individuals who were held for months or years in the jungle as hostages of the Revolutionary Armed Forces of Colombia, “only” half developed symptoms of posttraumatic stress disorder.
Dr. Mosca believes that a comment by Frank Ochberg, MD, speaks to this finding. “In many cases, peritraumatic symptoms are a normal person’s normal response to an abnormal situation.” For a lot of people who have found themselves having to perform CPR, the symptoms associated with the initial acute stress reaction will resolve on their own in 30-90 days. “But if this doesn’t happen, and those symptoms persist, psychotherapeutic or pharmacological intervention will be necessary,” he noted.
“In CPR classes, it would be good for the instructors to talk about the warning signs that people should look out for in themselves and their fellow rescuers. So, for example, insomnia, anxiety, a heightened state of alertness, feeling disconnected from reality,” Dr. Mosca told this news organization.
“Another thing that can help rescuers is letting them know what happened to the person they gave CPR to. This way, they can get closure,” suggested Manlio Márquez Murillo, MD, a cardiologist and electrophysiologist in Mexico. He is also the coordinator of the Alliance Against Sudden Cardiac Death at the Interamerican Society of Cardiology.
“Medical and nursing societies would have to develop a brief protocol or performance standard. The goal would be to ensure that rescuers are asked for their contact information and that someone gets in touch to debrief them and to offer them care. Next would come the treatment part, to resolve any remaining aftereffects,” said in an interview.
For example, a three-stage Lay Responder Support Model (LRSM) was developed and implemented as part of a lay responder support program established in 2014 by the Peel Regional Council in Ontario. The LRSM identifies and engages individuals who witnessed or participated directly or indirectly in an OHCA, inviting them to participate in a debriefing session facilitated by a trained practitioner. Held 24-48 hours post event, the debriefing allows lay responders to contextualize their reaction to the event. The conversation also serves as an opportunity for them to fully articulate their concerns, questions, and thoughts. The facilitator can communicate stress reduction techniques and address psychological first aid needs as they emerge. Approximately 1 week post event, a secondary follow-up occurs. If the lay responder communicates a continuing struggle with symptoms impacting and interfering with everyday life, the facilitator offers a coordinated or facilitated referral for mental health support.
In an article published in the Journal of Cardiac Failure. Ms. Flanary speaks about the three kinds of language that anyone who was either forced to or inspired to perform CPR can use to help process their trauma: words that explain what happened, words that name (eg, “forgotten patients”), and words that validate the experience and allow the person to articulate their feelings. The tools and technologies that organizations and health care professionals provide can help the healing process. Empathy and compassion, too, have a place.
But there are virtually no standardized and proactive initiatives of this kind in much of the world, including Latin America. So, most people who just happened to be in the right place at the right time find that they have to navigate the “after” part all on their own.
Other obstacles
Dr. Márquez Murillo finds it unfortunate that countries in the region have yet to enact “Good Samaritan” laws. If individuals render aid to someone suffering cardiac arrest, then these laws would ensure that they will not be held liable in any way. This is the case in Argentina and Uruguay. So, the fear of things turning into a legal matter may be holding people back from taking action; that fear could also create additional stress for those who end up stepping in to help.
Even with the legal safeguards, exceptional circumstances may arise where rescuers find themselves facing unexpected emotional challenges. In Argentina, Virginia Pérez Antonelli, the 17-year-old who tried in vain to save the life of Fernando Báez Sosa, had to testify at the trial of the eight defendants accused of brutally beating him in January 2020. The press, the public – the attention of an entire country – was focused on her. She had to respond to the defense attorneys who were able to ask whether she was sure that she performed the CPR maneuvers correctly. And a few weeks ago, a medical examiner hired by the defense suggested that “the CPR may have made the situation worse” for the victim. An indignant Dr. Fitz Maurice responded on Twitter: “CPR SAVES LIVES!! Let’s not let a CHEAP AND BASELESS argument destroy all the work that’s been done…!”
Of course, there are consequences that are beyond our control and others that can, in fact, be anticipated and planned for. Dr. Fitz Maurice brought up a preventive approach: Make CPR second nature, teach it in schools, help people overcome their fears. “Cardiac deaths are 200 times more frequent than deaths resulting from fires – and we practice fire drills a lot more than we practice CPR,” he told this news organization. In a society where there is widespread training on the procedure, where people regularly practice the technique, those who have had the experience of giving someone CPR will feel less alone, will be better understood by others.
“On the other hand, beyond the initial impact and the lack of a formal support system, the medium- and long-term outcome for those who acted is also psychologically and emotionally favorable,” said Jorge Bombau, MD, an obstetrician/gynecologist in Buenos Aires. After Dr. Bombau’s 14-year-old son Beltrán suddenly died during a school sports tournament, Dr. Bombau became a prominent advocate spreading the word about CPR.
“I don’t know anyone who regrets doing CPR,” he told this news organization. “There may be a brief period when the person feels distressed or depressed, when they have trouble sleeping. But it’s been proven that doing a good deed improves one’s mood. And what better deed is there than trying to save someone’s life? Whether their efforts were successful or in vain, that person has, at the end of the day, done something meaningful and worthwhile.”
Mr. Snitcofsky shares this sentiment. For several months now, he’s been feeling he’s “in a good place.” And he’s been actively promoting CPR on social media. As he recently posted on Twitter, “I’m here to retweet everything that has to do with getting us all to become familiar with how to do CPR and working up the courage to do it. The training takes no more than a few hours.
“I want to know that, if I ever have an out-of-hospital sudden cardiac arrest, there will be neighbors, friends, or family members around who know how to do CPR. Every person who knows how to do CPR can persuade others, and those of us who’ve had to do CPR in real life are even better candidates for persuading others. And if one day a person ends up needing CPR, I want to step in again and make up for lost time. Here’s hoping it’ll do the job,” he concluded.
It’s the same for Matías Alonso, a journalist in Buenos Aires. On New Year’s Eve 15 years ago, he was at a family dinner when, a few minutes before midnight, he found himself giving CPR to his stepmother’s father. “Unfortunately, he passed away, but I continued doing CPR on him until the ambulance arrived. For some time, I felt a little guilty for not taking charge of the situation from the beginning, and because I had this idea in my head that more people pulled through and recovered. But afterwards, they really thanked me a lot. And that helped me realize that I’d done something. I didn’t stand still when faced with the inevitability of death. I understood that it was good to have tried,” Mr. Alonso told this news organization. “And next time … hopefully there won’t be a next time … but I’m more prepared, and I now know how I can do better.”
Mr. Alonso, Mr. Snitcofsky, Dr. Fitz Maurice, Dr. Mosca, Dr. Bombau, and Dr. Márquez Murillo disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com. This article was translated from Medscape Spanish.
One year ago, as the sun was setting on a late fall day, Andrés Snitcofsky, a 40-year-old designer from Buenos Aires, Argentina, heard harrowing cries for help. It was the niece and the wife of one of his neighbors: a man in his 60s who the women had found “passed out” in the bedroom. “I did CPR for 5 minutes straight until a friend of the victim came in and asked me to stop, telling me that the man had probably been dead for 2 or 3 hours already. But I had no idea because I’d never seen a dead body before,” Mr. Snitcofsky told this news organization. A few minutes later, the ambulance arrived. The doctor confirmed that there was nothing more that could be done.
Mr. Snitcofsky went home. Nobody had asked for his name or address or phone number. … And it wasn’t because they already knew who he was. In fact, there wasn’t any sort of relationship there. Mr. Snitcofsky had only known his neighbors by sight. His actions that day, however, “did not come without a cost. It took me weeks – months, actually – to put myself together again,” he said. The things he saw, the things he heard, everything about that night played over and over in his head. “I had trouble sleeping. I would play out different scenarios in my head. I questioned myself. I second-guessed myself, criticized myself. It’s like some taboo subject. There’s no one to share the experience with, no one who gets it. But with time, I was able to process the event.
“For 2 months, I talked to my psychologist about it all,” he continued. “That really helped me a lot. In addition to therapy, I reached out to a couple I know – they’re both physicians – and to a firefighter who teaches CPR. Their insight and guidance allowed me to get to a point where I was able to understand that what I did was a good thing and that what I did was all that could have been done. But anyone who finds themselves in the position of having to do CPR – they’re going to be affected in many, many ways. It goes beyond the euphoria of seeing a person come back to life. Of that, I’m quite certain.”
We’ve all seen campaigns encouraging people to learn CPR and to be prepared if the need arises. But in training the public (and even health care professionals), not much, if anything, is said about the “collateral damage”: the psychological and emotional consequences of carrying out the procedure. These especially come into play when you don’t know whether the person survived, when your efforts weren’t able to reverse the sudden cardiac arrest, or when the person you gave CPR to was a loved one – a case that may entail immediate therapeutic interventions to minimize or prevent the risk of suffering long-lasting trauma.
In May 2020, popular American activist and educator Kristin Flanary saw someone suffering cardiac arrest. She stepped in and started doing CPR. And she continued doing CPR … for 10 long minutes. The person she was trying to save was her 34-year-old husband, ophthalmologist and comedian Will Flanary. On Twitter, where she’s known as Lady Glaucomflecken, Ms. Flanary recently shared the following message, putting the topic of CPR and automated external defibrillator training front and center.
“Yes, everyone should learn #CPRandAED. But if we are going to ask people to perform such a brutal task, it’s imperative that we also provide them with the info and resources they need to process it mentally and emotionally. It’s traumatic and life changing. It’s irresponsible and unethical to ask people to help in such a brutal and traumatic way and then neglect to help them in return.” In less than a month, the tweet has racked up over 200,000 views.
Doing one’s duty
There are many people who work to promote CPR and strengthen the other links in the chain of survival for out-of-hospital sudden cardiac arrest, such as prompt access to and delivery of early defibrillation. According to them, any negative psychological impact of intervening is temporary and, when compared with the satisfaction of having done one’s duty, quite insignificant – even if the efforts to save a person’s life are not successful.
“In 99.9% of cases, people who have performed CPR feel a sense of satisfaction, even happiness, knowing that they’ve helped. The individuals I’ve spoken with, I’ve never heard any of them say that they felt worse after the event or that they needed to see a psychologist,” said Mario Fitz Maurice, MD, director of the Arrhythmia Council of the Argentine Society of Cardiology and head of Electrophysiology at Rivadavia Hospital in Buenos Aires. He went on to tell this news organization, “Of course, some degree of fear, sadness, or melancholy can remain afterward. But it seems to me, and there are reports saying as much, that, in the end, what stands out in the person’s mind is the fact that they tried to save a life. And for them, there’s joy in knowing this.”
Dr. Fitz Maurice, who is also the director of the National Arrhythmia Institute in Buenos Aires, pointed out that the kind of person who takes CPR classes “has a profile that’s going to allow them to be psychologically involved; they’re the caring person, the one who’s ready and willing to help people.” And he added that, at his hospital, if they can identify the individuals or first responders who have done CPR on a patient, the protocol is to always contact them to offer psychological care and assistance. “But in 99% of cases, they don’t even understand why we’re calling them, they’re extremely happy to have taken part.”
Some studies, though, paint a much different picture, one that shows that providing CPR can be emotionally challenging and have consequences in terms of one’s family and work life. A qualitative study published in 2016 looked into the experiences of 20 lay rescuers in Norway – five were health educated – who had provided CPR to 18 out-of-hospital cardiac arrest (OHCA) victims, 66% of whom survived. The time from experiencing the OHCA incident to participating in the interview ranged from 6 days to 13 years (median 5.5 years). Several participants reported the OHCA incident as a “shocking and terrifying” experience. Tiredness, exhaustion, confusion, and feeling alone about the OHCA experience were individual reactions that could vary in time from days to months. Anxiety and insomnia were also experienced following the incident.
Some lay rescuers described the influence on work and family life, and a few of them described deep sorrow, even several years after the incident. Overall, they reported repetitive self-criticism regarding whether they could have carried out anything else to achieve a better outcome for the cardiac arrest victim. All of them wanted to be informed about the outcome. And four of the lay rescuers needed professional counseling to process the OHCA experience.
In 2020, another qualitative study was conducted, this time in Taiwan. There were nine participants, none of whom were health professionals. Each had provided initial CPR and defibrillation with AED in public locations. Event-to-interview duration was within 1 year and 1-2 years. The major findings from the study were the following:
- The lay rescuers possessed helping traits and high motivation.
- The lay rescuers reported certain aspects of rescue reality that differed much from prior training and expectations, including difficulty in the depth of chest compression, and uncertainties in real emergency situations.
- The lay rescuers gained positive personal fulfillment in sharing their experience and receiving positive feedback from others, and were willing to help next time, although they experienced a short-term negative psychological impact from the event. “Measures should be taken to increase [a] layperson’s confidence and situation awareness, to reduce training-reality discrepancy, and to build up a support system to avoid negative psychological effects.” This was the conclusion of the study team, which was led by Matthew Huei-Ming Ma, MD, PhD. A professor in the department of emergency medicine at National Taiwan University in Taipei, he is also on the board of directors of the Resuscitation Council of Asia.
Potential trauma
In recalling his experience, Mr. Snitcofsky said, “The hardest part of it all was the moment that I stopped giving CPR, that moment of letting go. This became the image that kept coming back to me, the traumatic moment I hadn’t thought about.”
Psychiatrist Daniel Mosca, MD, is the founder and former president of the Argentine Society of Trauma Psychology. He is also the coordinator of the human factors team at the City of Buenos Aires Emergency Medical Care System. “Any event has the potential to be traumatic, all the more so when it’s an event where you come face to face with death and uncertainty. But how a rescuer reacts will depend on their psychological makeup.” Of the individuals who were held for months or years in the jungle as hostages of the Revolutionary Armed Forces of Colombia, “only” half developed symptoms of posttraumatic stress disorder.
Dr. Mosca believes that a comment by Frank Ochberg, MD, speaks to this finding. “In many cases, peritraumatic symptoms are a normal person’s normal response to an abnormal situation.” For a lot of people who have found themselves having to perform CPR, the symptoms associated with the initial acute stress reaction will resolve on their own in 30-90 days. “But if this doesn’t happen, and those symptoms persist, psychotherapeutic or pharmacological intervention will be necessary,” he noted.
“In CPR classes, it would be good for the instructors to talk about the warning signs that people should look out for in themselves and their fellow rescuers. So, for example, insomnia, anxiety, a heightened state of alertness, feeling disconnected from reality,” Dr. Mosca told this news organization.
“Another thing that can help rescuers is letting them know what happened to the person they gave CPR to. This way, they can get closure,” suggested Manlio Márquez Murillo, MD, a cardiologist and electrophysiologist in Mexico. He is also the coordinator of the Alliance Against Sudden Cardiac Death at the Interamerican Society of Cardiology.
“Medical and nursing societies would have to develop a brief protocol or performance standard. The goal would be to ensure that rescuers are asked for their contact information and that someone gets in touch to debrief them and to offer them care. Next would come the treatment part, to resolve any remaining aftereffects,” said in an interview.
For example, a three-stage Lay Responder Support Model (LRSM) was developed and implemented as part of a lay responder support program established in 2014 by the Peel Regional Council in Ontario. The LRSM identifies and engages individuals who witnessed or participated directly or indirectly in an OHCA, inviting them to participate in a debriefing session facilitated by a trained practitioner. Held 24-48 hours post event, the debriefing allows lay responders to contextualize their reaction to the event. The conversation also serves as an opportunity for them to fully articulate their concerns, questions, and thoughts. The facilitator can communicate stress reduction techniques and address psychological first aid needs as they emerge. Approximately 1 week post event, a secondary follow-up occurs. If the lay responder communicates a continuing struggle with symptoms impacting and interfering with everyday life, the facilitator offers a coordinated or facilitated referral for mental health support.
In an article published in the Journal of Cardiac Failure. Ms. Flanary speaks about the three kinds of language that anyone who was either forced to or inspired to perform CPR can use to help process their trauma: words that explain what happened, words that name (eg, “forgotten patients”), and words that validate the experience and allow the person to articulate their feelings. The tools and technologies that organizations and health care professionals provide can help the healing process. Empathy and compassion, too, have a place.
But there are virtually no standardized and proactive initiatives of this kind in much of the world, including Latin America. So, most people who just happened to be in the right place at the right time find that they have to navigate the “after” part all on their own.
Other obstacles
Dr. Márquez Murillo finds it unfortunate that countries in the region have yet to enact “Good Samaritan” laws. If individuals render aid to someone suffering cardiac arrest, then these laws would ensure that they will not be held liable in any way. This is the case in Argentina and Uruguay. So, the fear of things turning into a legal matter may be holding people back from taking action; that fear could also create additional stress for those who end up stepping in to help.
Even with the legal safeguards, exceptional circumstances may arise where rescuers find themselves facing unexpected emotional challenges. In Argentina, Virginia Pérez Antonelli, the 17-year-old who tried in vain to save the life of Fernando Báez Sosa, had to testify at the trial of the eight defendants accused of brutally beating him in January 2020. The press, the public – the attention of an entire country – was focused on her. She had to respond to the defense attorneys who were able to ask whether she was sure that she performed the CPR maneuvers correctly. And a few weeks ago, a medical examiner hired by the defense suggested that “the CPR may have made the situation worse” for the victim. An indignant Dr. Fitz Maurice responded on Twitter: “CPR SAVES LIVES!! Let’s not let a CHEAP AND BASELESS argument destroy all the work that’s been done…!”
Of course, there are consequences that are beyond our control and others that can, in fact, be anticipated and planned for. Dr. Fitz Maurice brought up a preventive approach: Make CPR second nature, teach it in schools, help people overcome their fears. “Cardiac deaths are 200 times more frequent than deaths resulting from fires – and we practice fire drills a lot more than we practice CPR,” he told this news organization. In a society where there is widespread training on the procedure, where people regularly practice the technique, those who have had the experience of giving someone CPR will feel less alone, will be better understood by others.
“On the other hand, beyond the initial impact and the lack of a formal support system, the medium- and long-term outcome for those who acted is also psychologically and emotionally favorable,” said Jorge Bombau, MD, an obstetrician/gynecologist in Buenos Aires. After Dr. Bombau’s 14-year-old son Beltrán suddenly died during a school sports tournament, Dr. Bombau became a prominent advocate spreading the word about CPR.
“I don’t know anyone who regrets doing CPR,” he told this news organization. “There may be a brief period when the person feels distressed or depressed, when they have trouble sleeping. But it’s been proven that doing a good deed improves one’s mood. And what better deed is there than trying to save someone’s life? Whether their efforts were successful or in vain, that person has, at the end of the day, done something meaningful and worthwhile.”
Mr. Snitcofsky shares this sentiment. For several months now, he’s been feeling he’s “in a good place.” And he’s been actively promoting CPR on social media. As he recently posted on Twitter, “I’m here to retweet everything that has to do with getting us all to become familiar with how to do CPR and working up the courage to do it. The training takes no more than a few hours.
“I want to know that, if I ever have an out-of-hospital sudden cardiac arrest, there will be neighbors, friends, or family members around who know how to do CPR. Every person who knows how to do CPR can persuade others, and those of us who’ve had to do CPR in real life are even better candidates for persuading others. And if one day a person ends up needing CPR, I want to step in again and make up for lost time. Here’s hoping it’ll do the job,” he concluded.
It’s the same for Matías Alonso, a journalist in Buenos Aires. On New Year’s Eve 15 years ago, he was at a family dinner when, a few minutes before midnight, he found himself giving CPR to his stepmother’s father. “Unfortunately, he passed away, but I continued doing CPR on him until the ambulance arrived. For some time, I felt a little guilty for not taking charge of the situation from the beginning, and because I had this idea in my head that more people pulled through and recovered. But afterwards, they really thanked me a lot. And that helped me realize that I’d done something. I didn’t stand still when faced with the inevitability of death. I understood that it was good to have tried,” Mr. Alonso told this news organization. “And next time … hopefully there won’t be a next time … but I’m more prepared, and I now know how I can do better.”
Mr. Alonso, Mr. Snitcofsky, Dr. Fitz Maurice, Dr. Mosca, Dr. Bombau, and Dr. Márquez Murillo disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com. This article was translated from Medscape Spanish.
Renewed Concern for Navy Conditions Following Suicides
Eight Navy sailors have died by suicide in less than a year. The most recent death was on January 23. Three sailors who died in the past 2 months have more than suicide in common: They were all stationed aboard Navy aircraft carriers undergoing refits: the USS George Washington and the USS Theodore Roosevelt.
These deaths come only a month after the Navy released a report on 3 deaths by suicide on the George Washington, all of which happened in a single week last April. Military.com reported that the ship’s commander, Capt. Brent Gaut, had said 10 sailors had died by suicide in under a year.
In November and December 2022, at least 4 sailors assigned to the Mid-Atlantic Regional Maintenance Center (MARMC) in Virginia died by suicide, multiplying concerns about a fleetwide mental health crisis. “I was inundated with the amount of hopelessness at that command,” Kayla Arestivo, a counselor brought in to help, told nbcnews.com. Sailors spoke of being overworked, undervalued, and not getting the mental health help they needed. “Part of it is toxic leadership. The sailors immediately pointed that out,” Arestivo said.
She noted that many of the people assigned to MARMC are on limited duty due to mental or physical disabilities or have personal stressors that prevent them from full unrestricted duty. Electronics technician Kody Lee Decker, for instance, was on limited duty due to mental health issues when he died by suicide on October 29, 2022, according to a friend. Those people, Arestivo suggested, should have been provided help earlier.
Disabilities are not the only potential risk factors, though. Sailors living aboard the George Washington from April 2021 until April 2022 reported difficult and noisy living conditions with shortages of power, running water, and heat, and poor ventilation. Sailors would sleep in their cars or rent rooms in town rather than stay on board.
The George Washington has been docked at Newport News [Virginia] Shipbuilding for a major overhaul and repairs since 2017 (expected to extend into 2023, nearly 2 years later than the original deadline). The Navy investigation acknowledged “overwhelming” stress and noted that the living conditions created by an “intense and complex” maintenance process were posing hardships for the sailors, including sleep deprivation. (The Theodore Roosevelt has been at the Puget Sound shipyard since August 2021, although none of the sailors live onboard.)
However, the Navy investigation concluded that the 3 April suicide deaths were not directly connected to living conditions. According to the US Fleet Forces Command, “each Sailor was experiencing unique and individualized life stressors, which were contributing factors leading to their deaths.” The 3 suicide deaths were deemed independent events, with no direct correlation among them.
But the report also charged that leaders were oblivious to the problems, and the mental health care the Navy offered was insufficient: “Multiple command members knew or should have known that MASR Mitchell-Sandor [who died by suicide] was experiencing displeasure with Navy life and could have intervened to help him better cope or seek out available support services.”
In the official response to the Navy report, Rear Adm. John Meier, Commander, Naval Air Force Atlantic, noted that he had convened a “second and broader investigation” to assess quality of life issues and other systemic issues for aircraft carriers undergoing extensive maintenance or construction in the Newport News shipyard. “It is safe to say,” he wrote, that “generations of Navy leaders had become accustomed to the reduced quality of life in the shipyard, and accepted the status quo as par for the course…”
He agreed that the general stress of the environment was not the root cause of the deaths but was “certainly a contributing factor” in at least one case. The report, he said, placed too much emphasis on the sailor’s personal decisions to not improve his own living conditions (he was offered the opportunity to change berthing) and thus placed “too much burden on him for his situation.” Senior enlisted leadership knew that the sailor was sleeping in his car and counseled him, but Meier found no evidence of follow-through. More senior sailors or an assigned mentor should have been there to support the sailor, Meier said, and help him make decisions that were in his best interests. “This was a time for intrusive leadership.”
Adm. Daryl Caudle, Commander, US Fleet Forces Command, advised revising the wording in the report to say “No one at the command knew, or had a reason to know, of MASR [Xavier] Mitchell-Sandor’s previous suicidal ideations.” He also advised modifying the wording with: “Had the Navy been aware of MASR Mitchell-Sandor’s previous suicidal ideations, existing programs and procedures were in place that make it likely that he would have been placed in a ‘do not arm’ status and received necessary care.”
Vice Admiral Kenneth Whitesell, Commander, Naval Air Force, US Pacific Fleet, also endorsed the report findings with some revisions, saying, “We cannot assume these issues are isolated to a single ship, or to shipyards alone. Rather, these 3 tragic losses brought to light the ultimate need to remain laser-focused on providing care and guidance to our sailors.”
The Navy is providing mental health support to sailors, including an embedded mental health team and 2 civilian resiliency counselors who work on the George Washington. According to an action update in the report, Commander, Naval Air Force directed all CVNs and Naval Aviation Units to have a minimum of 1 safeTALK (Suicide Alertness For Everyone; Tell, Ask, Listen and KeepSafe) trained member onboard, and 2 to 3 safeTALK trained personnel in each division no later than December 31, 2022.
At MARMC, Arestivo was brought in for several mandatory suicide prevention sessions but without systemic changes, she said, “We’re putting Band-Aids on bullet holes.”
She said she told MARMC’s commanding officer, “You will have another one.” The fourth sailor died by suicide 10 days later.
If you or someone you know is having thoughts of suicide, call or text 988 to reach the National Suicide Prevention Lifeline or contact the Veterans Crisis Line.
Eight Navy sailors have died by suicide in less than a year. The most recent death was on January 23. Three sailors who died in the past 2 months have more than suicide in common: They were all stationed aboard Navy aircraft carriers undergoing refits: the USS George Washington and the USS Theodore Roosevelt.
These deaths come only a month after the Navy released a report on 3 deaths by suicide on the George Washington, all of which happened in a single week last April. Military.com reported that the ship’s commander, Capt. Brent Gaut, had said 10 sailors had died by suicide in under a year.
In November and December 2022, at least 4 sailors assigned to the Mid-Atlantic Regional Maintenance Center (MARMC) in Virginia died by suicide, multiplying concerns about a fleetwide mental health crisis. “I was inundated with the amount of hopelessness at that command,” Kayla Arestivo, a counselor brought in to help, told nbcnews.com. Sailors spoke of being overworked, undervalued, and not getting the mental health help they needed. “Part of it is toxic leadership. The sailors immediately pointed that out,” Arestivo said.
She noted that many of the people assigned to MARMC are on limited duty due to mental or physical disabilities or have personal stressors that prevent them from full unrestricted duty. Electronics technician Kody Lee Decker, for instance, was on limited duty due to mental health issues when he died by suicide on October 29, 2022, according to a friend. Those people, Arestivo suggested, should have been provided help earlier.
Disabilities are not the only potential risk factors, though. Sailors living aboard the George Washington from April 2021 until April 2022 reported difficult and noisy living conditions with shortages of power, running water, and heat, and poor ventilation. Sailors would sleep in their cars or rent rooms in town rather than stay on board.
The George Washington has been docked at Newport News [Virginia] Shipbuilding for a major overhaul and repairs since 2017 (expected to extend into 2023, nearly 2 years later than the original deadline). The Navy investigation acknowledged “overwhelming” stress and noted that the living conditions created by an “intense and complex” maintenance process were posing hardships for the sailors, including sleep deprivation. (The Theodore Roosevelt has been at the Puget Sound shipyard since August 2021, although none of the sailors live onboard.)
However, the Navy investigation concluded that the 3 April suicide deaths were not directly connected to living conditions. According to the US Fleet Forces Command, “each Sailor was experiencing unique and individualized life stressors, which were contributing factors leading to their deaths.” The 3 suicide deaths were deemed independent events, with no direct correlation among them.
But the report also charged that leaders were oblivious to the problems, and the mental health care the Navy offered was insufficient: “Multiple command members knew or should have known that MASR Mitchell-Sandor [who died by suicide] was experiencing displeasure with Navy life and could have intervened to help him better cope or seek out available support services.”
In the official response to the Navy report, Rear Adm. John Meier, Commander, Naval Air Force Atlantic, noted that he had convened a “second and broader investigation” to assess quality of life issues and other systemic issues for aircraft carriers undergoing extensive maintenance or construction in the Newport News shipyard. “It is safe to say,” he wrote, that “generations of Navy leaders had become accustomed to the reduced quality of life in the shipyard, and accepted the status quo as par for the course…”
He agreed that the general stress of the environment was not the root cause of the deaths but was “certainly a contributing factor” in at least one case. The report, he said, placed too much emphasis on the sailor’s personal decisions to not improve his own living conditions (he was offered the opportunity to change berthing) and thus placed “too much burden on him for his situation.” Senior enlisted leadership knew that the sailor was sleeping in his car and counseled him, but Meier found no evidence of follow-through. More senior sailors or an assigned mentor should have been there to support the sailor, Meier said, and help him make decisions that were in his best interests. “This was a time for intrusive leadership.”
Adm. Daryl Caudle, Commander, US Fleet Forces Command, advised revising the wording in the report to say “No one at the command knew, or had a reason to know, of MASR [Xavier] Mitchell-Sandor’s previous suicidal ideations.” He also advised modifying the wording with: “Had the Navy been aware of MASR Mitchell-Sandor’s previous suicidal ideations, existing programs and procedures were in place that make it likely that he would have been placed in a ‘do not arm’ status and received necessary care.”
Vice Admiral Kenneth Whitesell, Commander, Naval Air Force, US Pacific Fleet, also endorsed the report findings with some revisions, saying, “We cannot assume these issues are isolated to a single ship, or to shipyards alone. Rather, these 3 tragic losses brought to light the ultimate need to remain laser-focused on providing care and guidance to our sailors.”
The Navy is providing mental health support to sailors, including an embedded mental health team and 2 civilian resiliency counselors who work on the George Washington. According to an action update in the report, Commander, Naval Air Force directed all CVNs and Naval Aviation Units to have a minimum of 1 safeTALK (Suicide Alertness For Everyone; Tell, Ask, Listen and KeepSafe) trained member onboard, and 2 to 3 safeTALK trained personnel in each division no later than December 31, 2022.
At MARMC, Arestivo was brought in for several mandatory suicide prevention sessions but without systemic changes, she said, “We’re putting Band-Aids on bullet holes.”
She said she told MARMC’s commanding officer, “You will have another one.” The fourth sailor died by suicide 10 days later.
If you or someone you know is having thoughts of suicide, call or text 988 to reach the National Suicide Prevention Lifeline or contact the Veterans Crisis Line.
Eight Navy sailors have died by suicide in less than a year. The most recent death was on January 23. Three sailors who died in the past 2 months have more than suicide in common: They were all stationed aboard Navy aircraft carriers undergoing refits: the USS George Washington and the USS Theodore Roosevelt.
These deaths come only a month after the Navy released a report on 3 deaths by suicide on the George Washington, all of which happened in a single week last April. Military.com reported that the ship’s commander, Capt. Brent Gaut, had said 10 sailors had died by suicide in under a year.
In November and December 2022, at least 4 sailors assigned to the Mid-Atlantic Regional Maintenance Center (MARMC) in Virginia died by suicide, multiplying concerns about a fleetwide mental health crisis. “I was inundated with the amount of hopelessness at that command,” Kayla Arestivo, a counselor brought in to help, told nbcnews.com. Sailors spoke of being overworked, undervalued, and not getting the mental health help they needed. “Part of it is toxic leadership. The sailors immediately pointed that out,” Arestivo said.
She noted that many of the people assigned to MARMC are on limited duty due to mental or physical disabilities or have personal stressors that prevent them from full unrestricted duty. Electronics technician Kody Lee Decker, for instance, was on limited duty due to mental health issues when he died by suicide on October 29, 2022, according to a friend. Those people, Arestivo suggested, should have been provided help earlier.
Disabilities are not the only potential risk factors, though. Sailors living aboard the George Washington from April 2021 until April 2022 reported difficult and noisy living conditions with shortages of power, running water, and heat, and poor ventilation. Sailors would sleep in their cars or rent rooms in town rather than stay on board.
The George Washington has been docked at Newport News [Virginia] Shipbuilding for a major overhaul and repairs since 2017 (expected to extend into 2023, nearly 2 years later than the original deadline). The Navy investigation acknowledged “overwhelming” stress and noted that the living conditions created by an “intense and complex” maintenance process were posing hardships for the sailors, including sleep deprivation. (The Theodore Roosevelt has been at the Puget Sound shipyard since August 2021, although none of the sailors live onboard.)
However, the Navy investigation concluded that the 3 April suicide deaths were not directly connected to living conditions. According to the US Fleet Forces Command, “each Sailor was experiencing unique and individualized life stressors, which were contributing factors leading to their deaths.” The 3 suicide deaths were deemed independent events, with no direct correlation among them.
But the report also charged that leaders were oblivious to the problems, and the mental health care the Navy offered was insufficient: “Multiple command members knew or should have known that MASR Mitchell-Sandor [who died by suicide] was experiencing displeasure with Navy life and could have intervened to help him better cope or seek out available support services.”
In the official response to the Navy report, Rear Adm. John Meier, Commander, Naval Air Force Atlantic, noted that he had convened a “second and broader investigation” to assess quality of life issues and other systemic issues for aircraft carriers undergoing extensive maintenance or construction in the Newport News shipyard. “It is safe to say,” he wrote, that “generations of Navy leaders had become accustomed to the reduced quality of life in the shipyard, and accepted the status quo as par for the course…”
He agreed that the general stress of the environment was not the root cause of the deaths but was “certainly a contributing factor” in at least one case. The report, he said, placed too much emphasis on the sailor’s personal decisions to not improve his own living conditions (he was offered the opportunity to change berthing) and thus placed “too much burden on him for his situation.” Senior enlisted leadership knew that the sailor was sleeping in his car and counseled him, but Meier found no evidence of follow-through. More senior sailors or an assigned mentor should have been there to support the sailor, Meier said, and help him make decisions that were in his best interests. “This was a time for intrusive leadership.”
Adm. Daryl Caudle, Commander, US Fleet Forces Command, advised revising the wording in the report to say “No one at the command knew, or had a reason to know, of MASR [Xavier] Mitchell-Sandor’s previous suicidal ideations.” He also advised modifying the wording with: “Had the Navy been aware of MASR Mitchell-Sandor’s previous suicidal ideations, existing programs and procedures were in place that make it likely that he would have been placed in a ‘do not arm’ status and received necessary care.”
Vice Admiral Kenneth Whitesell, Commander, Naval Air Force, US Pacific Fleet, also endorsed the report findings with some revisions, saying, “We cannot assume these issues are isolated to a single ship, or to shipyards alone. Rather, these 3 tragic losses brought to light the ultimate need to remain laser-focused on providing care and guidance to our sailors.”
The Navy is providing mental health support to sailors, including an embedded mental health team and 2 civilian resiliency counselors who work on the George Washington. According to an action update in the report, Commander, Naval Air Force directed all CVNs and Naval Aviation Units to have a minimum of 1 safeTALK (Suicide Alertness For Everyone; Tell, Ask, Listen and KeepSafe) trained member onboard, and 2 to 3 safeTALK trained personnel in each division no later than December 31, 2022.
At MARMC, Arestivo was brought in for several mandatory suicide prevention sessions but without systemic changes, she said, “We’re putting Band-Aids on bullet holes.”
She said she told MARMC’s commanding officer, “You will have another one.” The fourth sailor died by suicide 10 days later.
If you or someone you know is having thoughts of suicide, call or text 988 to reach the National Suicide Prevention Lifeline or contact the Veterans Crisis Line.
Why Did Nonventilator-Associated HAP Peak During the Pandemic?
Cases of nonventilator-associated hospital-acquired pneumonia (NV-HAP) declined by 32% between 2015 and 2020. Then, of course, COVID-19 changed the trajectory and rates began to rise. After February 2020, the incidence rate rose by 25% among veterans without COVID-19—but by 108% among those who had COVID-19.
Those are findings from a study by researchers at Rocky Mountain Regional VA Medical Center, Aurora, Colorado. They studied data on 1,567,275 veterans admitted to 135 VA facilities in acute care settings between October 2015 and March 2021, with a stay of at least 48 hours.
They say, to their knowledge, this is the first published report of changes in NV-HAP risk associated with the onset of COVID-19 among all hospitalized veterans in a national health care system.
The questions for the researchers were: What drove the increase in NV-HAP rates? Was it the elevated risk among veterans with COVID-19, reduced NV-HAP prevention measures during the extreme pandemic-related stress on the system, and/or increased patient acuity among hospitalized veterans?
They concluded that the observed increase in NV-HAP risk among all patients during the COVID-19 pandemic is “likely multifactorial.” The stresses on clinical workload may have hampered fundamental preventive nursing care, such as early mobility programs, consistent oral care, and aspiration precautions. The researchers also cite barriers including wearing personal protective equipment, which affected communication and the ability to get needed supplies to the bedside without cross-contamination.
Among patients with COVID-19 infections, the greater NV-HAP risk could be due to changes in the lower respiratory tract microbiome, disruption of the immune response, and synergism seen with COVID-19 infection. Moreover, they note, placing patients in a prone position to improve oxygenation might have raised the risk of NV-HAP.
The hospitalized veterans in the study also had a high burden of clinical comorbidities. Those with COVID-19 were more likely to have documented diagnosis of dementia in the previous year, compared with COVID-19-negative veterans or those hospitalized before the pandemic began. The researchers point out that dementia increased the risk of microaspiration, which can lead to secondary bacterial pneumonia.
In addition to reinforcing prevention efforts, the researchers suggest that NV-HAP monitoring via automated electronic surveillance could “serve as a cornerstone of a strong infection prevention program.” A system like that, installed before the pandemic, they say, might have identified the NV-HAP risk sooner.
Most importantly, they add, strategies to reduce NV-HAP risk “should be designed with resilience to significant system stress such as the COVID-19 pandemic.”
Cases of nonventilator-associated hospital-acquired pneumonia (NV-HAP) declined by 32% between 2015 and 2020. Then, of course, COVID-19 changed the trajectory and rates began to rise. After February 2020, the incidence rate rose by 25% among veterans without COVID-19—but by 108% among those who had COVID-19.
Those are findings from a study by researchers at Rocky Mountain Regional VA Medical Center, Aurora, Colorado. They studied data on 1,567,275 veterans admitted to 135 VA facilities in acute care settings between October 2015 and March 2021, with a stay of at least 48 hours.
They say, to their knowledge, this is the first published report of changes in NV-HAP risk associated with the onset of COVID-19 among all hospitalized veterans in a national health care system.
The questions for the researchers were: What drove the increase in NV-HAP rates? Was it the elevated risk among veterans with COVID-19, reduced NV-HAP prevention measures during the extreme pandemic-related stress on the system, and/or increased patient acuity among hospitalized veterans?
They concluded that the observed increase in NV-HAP risk among all patients during the COVID-19 pandemic is “likely multifactorial.” The stresses on clinical workload may have hampered fundamental preventive nursing care, such as early mobility programs, consistent oral care, and aspiration precautions. The researchers also cite barriers including wearing personal protective equipment, which affected communication and the ability to get needed supplies to the bedside without cross-contamination.
Among patients with COVID-19 infections, the greater NV-HAP risk could be due to changes in the lower respiratory tract microbiome, disruption of the immune response, and synergism seen with COVID-19 infection. Moreover, they note, placing patients in a prone position to improve oxygenation might have raised the risk of NV-HAP.
The hospitalized veterans in the study also had a high burden of clinical comorbidities. Those with COVID-19 were more likely to have documented diagnosis of dementia in the previous year, compared with COVID-19-negative veterans or those hospitalized before the pandemic began. The researchers point out that dementia increased the risk of microaspiration, which can lead to secondary bacterial pneumonia.
In addition to reinforcing prevention efforts, the researchers suggest that NV-HAP monitoring via automated electronic surveillance could “serve as a cornerstone of a strong infection prevention program.” A system like that, installed before the pandemic, they say, might have identified the NV-HAP risk sooner.
Most importantly, they add, strategies to reduce NV-HAP risk “should be designed with resilience to significant system stress such as the COVID-19 pandemic.”
Cases of nonventilator-associated hospital-acquired pneumonia (NV-HAP) declined by 32% between 2015 and 2020. Then, of course, COVID-19 changed the trajectory and rates began to rise. After February 2020, the incidence rate rose by 25% among veterans without COVID-19—but by 108% among those who had COVID-19.
Those are findings from a study by researchers at Rocky Mountain Regional VA Medical Center, Aurora, Colorado. They studied data on 1,567,275 veterans admitted to 135 VA facilities in acute care settings between October 2015 and March 2021, with a stay of at least 48 hours.
They say, to their knowledge, this is the first published report of changes in NV-HAP risk associated with the onset of COVID-19 among all hospitalized veterans in a national health care system.
The questions for the researchers were: What drove the increase in NV-HAP rates? Was it the elevated risk among veterans with COVID-19, reduced NV-HAP prevention measures during the extreme pandemic-related stress on the system, and/or increased patient acuity among hospitalized veterans?
They concluded that the observed increase in NV-HAP risk among all patients during the COVID-19 pandemic is “likely multifactorial.” The stresses on clinical workload may have hampered fundamental preventive nursing care, such as early mobility programs, consistent oral care, and aspiration precautions. The researchers also cite barriers including wearing personal protective equipment, which affected communication and the ability to get needed supplies to the bedside without cross-contamination.
Among patients with COVID-19 infections, the greater NV-HAP risk could be due to changes in the lower respiratory tract microbiome, disruption of the immune response, and synergism seen with COVID-19 infection. Moreover, they note, placing patients in a prone position to improve oxygenation might have raised the risk of NV-HAP.
The hospitalized veterans in the study also had a high burden of clinical comorbidities. Those with COVID-19 were more likely to have documented diagnosis of dementia in the previous year, compared with COVID-19-negative veterans or those hospitalized before the pandemic began. The researchers point out that dementia increased the risk of microaspiration, which can lead to secondary bacterial pneumonia.
In addition to reinforcing prevention efforts, the researchers suggest that NV-HAP monitoring via automated electronic surveillance could “serve as a cornerstone of a strong infection prevention program.” A system like that, installed before the pandemic, they say, might have identified the NV-HAP risk sooner.
Most importantly, they add, strategies to reduce NV-HAP risk “should be designed with resilience to significant system stress such as the COVID-19 pandemic.”
Keto for life? Reasons to think twice
Is the ketogenic diet the only way to lose weight? Of course not! Keep track of calories in vs. calories out and almost anyone can lose weight. The problem is keeping it off. To understand that, we need to look at metabolic adaptation and the biology of obesity.
Our bodies have a “set point” that is epigenetically latched onto the environment the brain senses, just as the fetal environment responds to the maternal environment.
If food is plentiful, our hormones force us to eat until our bodies feel that there are enough fat stores to survive. Because of environmental influences such as highly processed food, preservatives, climate change, and regulation of temperature, our brains have decided that we need more adipose tissue than we did 50-100 years ago. It could be that an element in food has caused a dysfunction of the pathways that regulate our body weight, and most of us “defend” a higher body weight in this environment.
How to counteract that? Not easily. The ketogenic diet works temporarily just like any other diet where calorie intake is lower than usual. It seems to be agreeable to many people because they say they feel full after eating protein, fat, and perhaps some vegetables. Protein and fat are certainly more satiating than simple carbohydrates.
If strictly followed, a ketogenic diet will force the body to burn fat and go into ketosis. Without a source for glucose, the brain will burn ketones from fat stores. Owen and colleagues discovered this in 1969 when they did their now-famous studies of fasting in inpatients at Brigham and Women’s hospital, using IV amino acids to protect muscle mass.
Keto for life?
Is the ketogenic diet a healthy diet for the long term? That is a different question.
Of course not – we need high-fiber carbohydrate sources such as whole grains, fruits, and vegetables to keep the colon healthy and obtain the vitamins and minerals needed to make the Krebs cycle, or citric acid cycle, work at its best.
Why, then, are we promoting ketogenic diets for those with obesity and type 2 diabetes? Ketogenic or low-carbohydrate diets are easy to teach and can rapidly help patients lose weight and return their blood glucose, blood pressure, and other metabolic parameters to normal.
The patient will be instructed to avoid all highly processed foods. Studies have shown that highly processed foods, created to maximize flavor, “coerce” people to eat more calories than when presented with the same number of calories in unprocessed foods, a way to fool the brain.
Why are we fooling the brain?
We circumvent the natural satiety mechanisms that start with the gut. When we eat, our gastric fundus and intestinal stretch receptors start the process that informs the hypothalamus about food intake. Highly processed foods are usually devoid of fiber and volume, and pack in the calories in small volumes so that the stretch receptors are not activated until more calories are ingested. The study mentioned above developed two ad lib diets with the same number of calories, sugar, fat, and carbohydrate content – one ultraprocessed and the other unprocessed.
That explanation is just the tip of the iceberg, because a lot more than primitive stretch receptors is informing the brain. There are gut hormones that are secreted before and after meals, such as ghrelin, glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and cholecystokinin (CCK), among a slew of others. These peptide hormones are all secreted from gut cells into the blood or vagus nerve, or both, and alert the brain that there is or is not enough food to maintain body weight at its set point.
It’s a highly regulated and precise system that regulates body weight for survival of the species in this environment. However, the environment has changed over the past 100 years but our genetic makeup for survival of the fittest has not. The mechanism of action for defense of a higher body weight set point in this new environment has not been elucidated as yet. Most likely, there are many players or instigators involved, such as food-supply changes, sedentary lifestyle, ambient temperature, fetal programming, air quality, and global warming and climate change, to name a few.
The goal of obesity researchers is to investigate the underlying mechanisms of the increased prevalence of obesity over the past 100 years. The goal of obesity medicine specialists is to treat obesity in adults and children, and to prevent obesity as much as possible with lifestyle change and medications that have been shown to help “reverse” the metabolic adaptation to this environment. Our newest GLP-1/GIP receptor agonists have been shown in animal models to hit several pathways that lead to obesity. They are not just appetite suppressants. Yes, they do modulate appetite and satiety, but they also affect energy expenditure. The body’s normal reaction to a lack of calorie intake is to reduce resting energy expenditure until body weight increases back to “set point levels.” These agonists prevent that metabolic adaptation. That is why they are true agents that can treat obesity – the disease.
Back to the ketogenic diet. The ketogenic diet can fool the brain temporarily by using protein and fat to elicit satiety with less food intake in calories. After a while, however, gut hormones and other factors begin to counteract the weight loss with a reduction in resting energy and total energy expenditure, and other metabolic measures, to get the body back to a certain body weight set point.
The ketogenic diet also can help dieters avoid ultra- and highly processed foods. In the end, any type of diet that lowers caloric intake will work for weight loss, but it’s the maintenance of that weight loss that makes a long-term difference, and that involves closing the metabolic gap that the body generates to defend fat mass. Understanding this pathophysiology will allow obesity medicine specialists to assist patients with obesity to lose weight and keep it off.
Dr. Apovian is in the department of medicine, division of endocrinology, diabetes, and hypertension, and codirector, Center for Weight Management and Wellness, Harvard Medical School, Boston. She disclosed ties with Altimmune, Cowen and Company, Currax Pharmaceuticals, EPG Communication Holdings, Gelesis Srl, L-Nutra, NeuroBo Pharmaceuticals, National Institutes of Health, Patient-Centered Outcomes Research Institute, GI Dynamics, and Novo Nordisk. A version of this article first appeared on Medscape.com.
Is the ketogenic diet the only way to lose weight? Of course not! Keep track of calories in vs. calories out and almost anyone can lose weight. The problem is keeping it off. To understand that, we need to look at metabolic adaptation and the biology of obesity.
Our bodies have a “set point” that is epigenetically latched onto the environment the brain senses, just as the fetal environment responds to the maternal environment.
If food is plentiful, our hormones force us to eat until our bodies feel that there are enough fat stores to survive. Because of environmental influences such as highly processed food, preservatives, climate change, and regulation of temperature, our brains have decided that we need more adipose tissue than we did 50-100 years ago. It could be that an element in food has caused a dysfunction of the pathways that regulate our body weight, and most of us “defend” a higher body weight in this environment.
How to counteract that? Not easily. The ketogenic diet works temporarily just like any other diet where calorie intake is lower than usual. It seems to be agreeable to many people because they say they feel full after eating protein, fat, and perhaps some vegetables. Protein and fat are certainly more satiating than simple carbohydrates.
If strictly followed, a ketogenic diet will force the body to burn fat and go into ketosis. Without a source for glucose, the brain will burn ketones from fat stores. Owen and colleagues discovered this in 1969 when they did their now-famous studies of fasting in inpatients at Brigham and Women’s hospital, using IV amino acids to protect muscle mass.
Keto for life?
Is the ketogenic diet a healthy diet for the long term? That is a different question.
Of course not – we need high-fiber carbohydrate sources such as whole grains, fruits, and vegetables to keep the colon healthy and obtain the vitamins and minerals needed to make the Krebs cycle, or citric acid cycle, work at its best.
Why, then, are we promoting ketogenic diets for those with obesity and type 2 diabetes? Ketogenic or low-carbohydrate diets are easy to teach and can rapidly help patients lose weight and return their blood glucose, blood pressure, and other metabolic parameters to normal.
The patient will be instructed to avoid all highly processed foods. Studies have shown that highly processed foods, created to maximize flavor, “coerce” people to eat more calories than when presented with the same number of calories in unprocessed foods, a way to fool the brain.
Why are we fooling the brain?
We circumvent the natural satiety mechanisms that start with the gut. When we eat, our gastric fundus and intestinal stretch receptors start the process that informs the hypothalamus about food intake. Highly processed foods are usually devoid of fiber and volume, and pack in the calories in small volumes so that the stretch receptors are not activated until more calories are ingested. The study mentioned above developed two ad lib diets with the same number of calories, sugar, fat, and carbohydrate content – one ultraprocessed and the other unprocessed.
That explanation is just the tip of the iceberg, because a lot more than primitive stretch receptors is informing the brain. There are gut hormones that are secreted before and after meals, such as ghrelin, glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and cholecystokinin (CCK), among a slew of others. These peptide hormones are all secreted from gut cells into the blood or vagus nerve, or both, and alert the brain that there is or is not enough food to maintain body weight at its set point.
It’s a highly regulated and precise system that regulates body weight for survival of the species in this environment. However, the environment has changed over the past 100 years but our genetic makeup for survival of the fittest has not. The mechanism of action for defense of a higher body weight set point in this new environment has not been elucidated as yet. Most likely, there are many players or instigators involved, such as food-supply changes, sedentary lifestyle, ambient temperature, fetal programming, air quality, and global warming and climate change, to name a few.
The goal of obesity researchers is to investigate the underlying mechanisms of the increased prevalence of obesity over the past 100 years. The goal of obesity medicine specialists is to treat obesity in adults and children, and to prevent obesity as much as possible with lifestyle change and medications that have been shown to help “reverse” the metabolic adaptation to this environment. Our newest GLP-1/GIP receptor agonists have been shown in animal models to hit several pathways that lead to obesity. They are not just appetite suppressants. Yes, they do modulate appetite and satiety, but they also affect energy expenditure. The body’s normal reaction to a lack of calorie intake is to reduce resting energy expenditure until body weight increases back to “set point levels.” These agonists prevent that metabolic adaptation. That is why they are true agents that can treat obesity – the disease.
Back to the ketogenic diet. The ketogenic diet can fool the brain temporarily by using protein and fat to elicit satiety with less food intake in calories. After a while, however, gut hormones and other factors begin to counteract the weight loss with a reduction in resting energy and total energy expenditure, and other metabolic measures, to get the body back to a certain body weight set point.
The ketogenic diet also can help dieters avoid ultra- and highly processed foods. In the end, any type of diet that lowers caloric intake will work for weight loss, but it’s the maintenance of that weight loss that makes a long-term difference, and that involves closing the metabolic gap that the body generates to defend fat mass. Understanding this pathophysiology will allow obesity medicine specialists to assist patients with obesity to lose weight and keep it off.
Dr. Apovian is in the department of medicine, division of endocrinology, diabetes, and hypertension, and codirector, Center for Weight Management and Wellness, Harvard Medical School, Boston. She disclosed ties with Altimmune, Cowen and Company, Currax Pharmaceuticals, EPG Communication Holdings, Gelesis Srl, L-Nutra, NeuroBo Pharmaceuticals, National Institutes of Health, Patient-Centered Outcomes Research Institute, GI Dynamics, and Novo Nordisk. A version of this article first appeared on Medscape.com.
Is the ketogenic diet the only way to lose weight? Of course not! Keep track of calories in vs. calories out and almost anyone can lose weight. The problem is keeping it off. To understand that, we need to look at metabolic adaptation and the biology of obesity.
Our bodies have a “set point” that is epigenetically latched onto the environment the brain senses, just as the fetal environment responds to the maternal environment.
If food is plentiful, our hormones force us to eat until our bodies feel that there are enough fat stores to survive. Because of environmental influences such as highly processed food, preservatives, climate change, and regulation of temperature, our brains have decided that we need more adipose tissue than we did 50-100 years ago. It could be that an element in food has caused a dysfunction of the pathways that regulate our body weight, and most of us “defend” a higher body weight in this environment.
How to counteract that? Not easily. The ketogenic diet works temporarily just like any other diet where calorie intake is lower than usual. It seems to be agreeable to many people because they say they feel full after eating protein, fat, and perhaps some vegetables. Protein and fat are certainly more satiating than simple carbohydrates.
If strictly followed, a ketogenic diet will force the body to burn fat and go into ketosis. Without a source for glucose, the brain will burn ketones from fat stores. Owen and colleagues discovered this in 1969 when they did their now-famous studies of fasting in inpatients at Brigham and Women’s hospital, using IV amino acids to protect muscle mass.
Keto for life?
Is the ketogenic diet a healthy diet for the long term? That is a different question.
Of course not – we need high-fiber carbohydrate sources such as whole grains, fruits, and vegetables to keep the colon healthy and obtain the vitamins and minerals needed to make the Krebs cycle, or citric acid cycle, work at its best.
Why, then, are we promoting ketogenic diets for those with obesity and type 2 diabetes? Ketogenic or low-carbohydrate diets are easy to teach and can rapidly help patients lose weight and return their blood glucose, blood pressure, and other metabolic parameters to normal.
The patient will be instructed to avoid all highly processed foods. Studies have shown that highly processed foods, created to maximize flavor, “coerce” people to eat more calories than when presented with the same number of calories in unprocessed foods, a way to fool the brain.
Why are we fooling the brain?
We circumvent the natural satiety mechanisms that start with the gut. When we eat, our gastric fundus and intestinal stretch receptors start the process that informs the hypothalamus about food intake. Highly processed foods are usually devoid of fiber and volume, and pack in the calories in small volumes so that the stretch receptors are not activated until more calories are ingested. The study mentioned above developed two ad lib diets with the same number of calories, sugar, fat, and carbohydrate content – one ultraprocessed and the other unprocessed.
That explanation is just the tip of the iceberg, because a lot more than primitive stretch receptors is informing the brain. There are gut hormones that are secreted before and after meals, such as ghrelin, glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and cholecystokinin (CCK), among a slew of others. These peptide hormones are all secreted from gut cells into the blood or vagus nerve, or both, and alert the brain that there is or is not enough food to maintain body weight at its set point.
It’s a highly regulated and precise system that regulates body weight for survival of the species in this environment. However, the environment has changed over the past 100 years but our genetic makeup for survival of the fittest has not. The mechanism of action for defense of a higher body weight set point in this new environment has not been elucidated as yet. Most likely, there are many players or instigators involved, such as food-supply changes, sedentary lifestyle, ambient temperature, fetal programming, air quality, and global warming and climate change, to name a few.
The goal of obesity researchers is to investigate the underlying mechanisms of the increased prevalence of obesity over the past 100 years. The goal of obesity medicine specialists is to treat obesity in adults and children, and to prevent obesity as much as possible with lifestyle change and medications that have been shown to help “reverse” the metabolic adaptation to this environment. Our newest GLP-1/GIP receptor agonists have been shown in animal models to hit several pathways that lead to obesity. They are not just appetite suppressants. Yes, they do modulate appetite and satiety, but they also affect energy expenditure. The body’s normal reaction to a lack of calorie intake is to reduce resting energy expenditure until body weight increases back to “set point levels.” These agonists prevent that metabolic adaptation. That is why they are true agents that can treat obesity – the disease.
Back to the ketogenic diet. The ketogenic diet can fool the brain temporarily by using protein and fat to elicit satiety with less food intake in calories. After a while, however, gut hormones and other factors begin to counteract the weight loss with a reduction in resting energy and total energy expenditure, and other metabolic measures, to get the body back to a certain body weight set point.
The ketogenic diet also can help dieters avoid ultra- and highly processed foods. In the end, any type of diet that lowers caloric intake will work for weight loss, but it’s the maintenance of that weight loss that makes a long-term difference, and that involves closing the metabolic gap that the body generates to defend fat mass. Understanding this pathophysiology will allow obesity medicine specialists to assist patients with obesity to lose weight and keep it off.
Dr. Apovian is in the department of medicine, division of endocrinology, diabetes, and hypertension, and codirector, Center for Weight Management and Wellness, Harvard Medical School, Boston. She disclosed ties with Altimmune, Cowen and Company, Currax Pharmaceuticals, EPG Communication Holdings, Gelesis Srl, L-Nutra, NeuroBo Pharmaceuticals, National Institutes of Health, Patient-Centered Outcomes Research Institute, GI Dynamics, and Novo Nordisk. A version of this article first appeared on Medscape.com.
Systemic sclerosis antibodies show link to interstitial lung disease in RA
Adults with rheumatoid arthritis or primary Sjogren’s syndrome plus interstitial lung disease had higher levels of systemic sclerosis–specific antibodies than those without lung disease, based on data from 101 individuals.
Systemic sclerosis (SSc) has been associated with the development of interstitial lung disease (ILD), but the prevalence of SSc autoantibodies in patients with rheumatoid arthritis (RA) and primary Sjogren’s syndrome (SS) has not been explored, wrote Vasilike Koulouri, MD, of Kapodistrian University of Athens, and colleagues.
In a study published in the Journal of Translational Autoimmunity, the researchers reviewed serum data from patients with RA and SS using immunoblot assays to determine the prevalence of SSc-specific and anti-Ro52 autoantibodies, both of which have been associated with ILD in SSc patients.
The study population included 28 RA patients with ILD, 32 RA patients without ILD, 9 primary SS patients with ILD, and 32 primary SS patients with no ILD. The mean age of the RA participants was 63.4 years, 70% were women, and the mean age at RA diagnosis was 50.2 years. The mean age of the primary SS group was 60.3 years, 87.8% were female, and the mean age at diagnosis was 52.7 years.
Overall, SSc-specific antibodies across all titers were detected more frequently in RA patients with ILD compared with those with no ILD, though not statistically significant (42.9% vs. 21.9%, P = .08). However, “This trend was mainly attributed to the statistically significant difference between the two groups at strong titers (25% vs. 3.1%, P = .01),” the researchers wrote. Notably, they added.
No significant differences appeared in the prevalence of SSc-specific or Ro52 autoantibodies between primary SS patients with and without ILD, which might be attributable in part to the increased prevalence of anticentromere antibodies in primary SS, the researchers said.
RA patients who were positive for SSc-specific antibodies at strong titers were significantly more likely to have respiratory abnormalities than those who were negative (87.5% vs. 47.2%, P = .04), but no such differences appeared in primary SS patients.
“Early detection of SSc antibodies could be important in clinical practice as it may mandate further diagnostic (for example, screening for pulmonary hypertension) and therapeutic approaches of these patients,” the researchers wrote in their discussion.
The study findings were limited by several factors, mainly the small sample size, but also the potential for false-positive results on antibody titers, lack of data on the clinical significance of medium autoantibody titers, and the lack of long-term follow-up data, the researchers noted.
However, the results suggest that many seropositive RA patients with evidence of ILD “may evolve to a clinically evident overlap of RA and SSc” that would benefit from targeted treatment, they concluded.
The study was supported by a grant from Novartis AG and by the Molecular Immunology and Clinical Applications Unit, Department of Physiology, School of Medicine, National and Kapodistrian University of Athens. The researchers had no financial conflicts to disclose.
Adults with rheumatoid arthritis or primary Sjogren’s syndrome plus interstitial lung disease had higher levels of systemic sclerosis–specific antibodies than those without lung disease, based on data from 101 individuals.
Systemic sclerosis (SSc) has been associated with the development of interstitial lung disease (ILD), but the prevalence of SSc autoantibodies in patients with rheumatoid arthritis (RA) and primary Sjogren’s syndrome (SS) has not been explored, wrote Vasilike Koulouri, MD, of Kapodistrian University of Athens, and colleagues.
In a study published in the Journal of Translational Autoimmunity, the researchers reviewed serum data from patients with RA and SS using immunoblot assays to determine the prevalence of SSc-specific and anti-Ro52 autoantibodies, both of which have been associated with ILD in SSc patients.
The study population included 28 RA patients with ILD, 32 RA patients without ILD, 9 primary SS patients with ILD, and 32 primary SS patients with no ILD. The mean age of the RA participants was 63.4 years, 70% were women, and the mean age at RA diagnosis was 50.2 years. The mean age of the primary SS group was 60.3 years, 87.8% were female, and the mean age at diagnosis was 52.7 years.
Overall, SSc-specific antibodies across all titers were detected more frequently in RA patients with ILD compared with those with no ILD, though not statistically significant (42.9% vs. 21.9%, P = .08). However, “This trend was mainly attributed to the statistically significant difference between the two groups at strong titers (25% vs. 3.1%, P = .01),” the researchers wrote. Notably, they added.
No significant differences appeared in the prevalence of SSc-specific or Ro52 autoantibodies between primary SS patients with and without ILD, which might be attributable in part to the increased prevalence of anticentromere antibodies in primary SS, the researchers said.
RA patients who were positive for SSc-specific antibodies at strong titers were significantly more likely to have respiratory abnormalities than those who were negative (87.5% vs. 47.2%, P = .04), but no such differences appeared in primary SS patients.
“Early detection of SSc antibodies could be important in clinical practice as it may mandate further diagnostic (for example, screening for pulmonary hypertension) and therapeutic approaches of these patients,” the researchers wrote in their discussion.
The study findings were limited by several factors, mainly the small sample size, but also the potential for false-positive results on antibody titers, lack of data on the clinical significance of medium autoantibody titers, and the lack of long-term follow-up data, the researchers noted.
However, the results suggest that many seropositive RA patients with evidence of ILD “may evolve to a clinically evident overlap of RA and SSc” that would benefit from targeted treatment, they concluded.
The study was supported by a grant from Novartis AG and by the Molecular Immunology and Clinical Applications Unit, Department of Physiology, School of Medicine, National and Kapodistrian University of Athens. The researchers had no financial conflicts to disclose.
Adults with rheumatoid arthritis or primary Sjogren’s syndrome plus interstitial lung disease had higher levels of systemic sclerosis–specific antibodies than those without lung disease, based on data from 101 individuals.
Systemic sclerosis (SSc) has been associated with the development of interstitial lung disease (ILD), but the prevalence of SSc autoantibodies in patients with rheumatoid arthritis (RA) and primary Sjogren’s syndrome (SS) has not been explored, wrote Vasilike Koulouri, MD, of Kapodistrian University of Athens, and colleagues.
In a study published in the Journal of Translational Autoimmunity, the researchers reviewed serum data from patients with RA and SS using immunoblot assays to determine the prevalence of SSc-specific and anti-Ro52 autoantibodies, both of which have been associated with ILD in SSc patients.
The study population included 28 RA patients with ILD, 32 RA patients without ILD, 9 primary SS patients with ILD, and 32 primary SS patients with no ILD. The mean age of the RA participants was 63.4 years, 70% were women, and the mean age at RA diagnosis was 50.2 years. The mean age of the primary SS group was 60.3 years, 87.8% were female, and the mean age at diagnosis was 52.7 years.
Overall, SSc-specific antibodies across all titers were detected more frequently in RA patients with ILD compared with those with no ILD, though not statistically significant (42.9% vs. 21.9%, P = .08). However, “This trend was mainly attributed to the statistically significant difference between the two groups at strong titers (25% vs. 3.1%, P = .01),” the researchers wrote. Notably, they added.
No significant differences appeared in the prevalence of SSc-specific or Ro52 autoantibodies between primary SS patients with and without ILD, which might be attributable in part to the increased prevalence of anticentromere antibodies in primary SS, the researchers said.
RA patients who were positive for SSc-specific antibodies at strong titers were significantly more likely to have respiratory abnormalities than those who were negative (87.5% vs. 47.2%, P = .04), but no such differences appeared in primary SS patients.
“Early detection of SSc antibodies could be important in clinical practice as it may mandate further diagnostic (for example, screening for pulmonary hypertension) and therapeutic approaches of these patients,” the researchers wrote in their discussion.
The study findings were limited by several factors, mainly the small sample size, but also the potential for false-positive results on antibody titers, lack of data on the clinical significance of medium autoantibody titers, and the lack of long-term follow-up data, the researchers noted.
However, the results suggest that many seropositive RA patients with evidence of ILD “may evolve to a clinically evident overlap of RA and SSc” that would benefit from targeted treatment, they concluded.
The study was supported by a grant from Novartis AG and by the Molecular Immunology and Clinical Applications Unit, Department of Physiology, School of Medicine, National and Kapodistrian University of Athens. The researchers had no financial conflicts to disclose.
FROM THE JOURNAL OF TRANSLATIONAL AUTOIMMUNITY
The challenge of incidentally detected interstitial lung abnormalities
Clinicians working within the U.S. health care system order CTs; it’s just what we do, and we do it a lot. This isn’t necessarily bad, but an inevitable byproduct is the pandemic of incidental findings. One underrecognized but frequent “incidentaloma” on CT is an interstitial lung abnormality (ILA). The Fleischner Society defines an ILA as honeycombing, traction bronchiectasis, parenchymal distortions, and reticular abnormalities that take up more than 5% of a particular lung zone in a patient without a clinical diagnosis of interstitial lung disease (ILD). In essence, ILAs are both a radiographic and a clinical diagnosis.
ILAs are common. With the advent of lung cancer screening and advances in CT technology, we’re now inundated with detailed images of lung parenchyma in older smokers who are at high risk for respiratory disease. The resulting opportunity for early identification of disease is as exciting as the risk for overdiagnosis, excessive testing, and unnecessary treatment is frightening. Early diagnosis remains critical for preventing irreversible respiratory disease. But as with any disease process, when we attempt to detect pathology before it has become apparent, the line between benign change and true abnormality is blurred.
Such is the challenge with ILAs. Past studies have shown an association between ILAs and morbidity and mortality, but considerable uncertainty persists over what the ILAs represent and how they should be managed. A recent study published in the American Journal of Respiratory and Critical Care Medicine provides some clarity. The authors used data from the COPDGene cohort to correlate ILAs with lung testing, and functional and respiratory outcomes. As with other studies, they found that approximately 10% of the COPDGene patients that they examined had ILAs on CT and half of those met their criteria for “suspected ILD.” Suspected ILD was defined radiographically (definite fibrosis) and on lung function testing (abnormal forced vital capacity [FVC] or diffusing capacity of the lungs for carbon monoxide [DLCO]). The patients with suspected ILD had worse clinical outcomes; being a Black individual, pack-years of smoking, and GOLD stage on spirometry were independently associated with suspected ILD.
This type of study is urgently needed. Given their high prevalence, we’re in dire need of a valid model for risk stratifying ILAs. The authors of this study have moved us closer, but we’ve still got a long way to go. The study has significant limitations. First, although patients with previous documentation of ILD were excluded from COPDGene, no formal, multidisciplinary assessment was performed; therefore, some of the patients labeled as having ILA probably had diagnosable ILD. Their possible inclusion would falsely increase the prevalence of clinically important ILAs and exaggerate the relationship between ILAs and clinical outcomes.
The rhetorical gymnastics performed throughout the paper are necessary yet problematic. “Suspected ILD” is not a recognized diagnosis and the definition is therefore arbitrary. To the extent that “suspected ILD” requires an abnormality on spirometry or DLCO, one could argue it’s the lung function changes and not the radiographic findings that are driving the differences. In fact, “suspected ILD” was defined by lung function more often than radiographic criteria (16% had definite fibrosis on CT, 57% had an abnormal FVC, and 67% had an abnormal DLCO). Patients with ILAs without suspected ILD had outcomes that weren’t statistically different from those with no ILAs at all, implying that the lung testing and not the ILA is the better discriminator. Regardless, this leads us back to where we started before this paper was published: ILAs require lung function testing and referral to a pulmonologist for proper risk stratification. An accompanying editorial highlights these and other limitations.
One particular problem that isn’t addressed by the authors or the editorial is their findings on race. The authors concluded that Black persons with ILAs are more likely to have “suspected ILD.” However, their definition suffers from an insidious form of incorporation bias generated by the way they handled their DLCO reference values. The Global Lung Function Initiative equations they used were derived exclusively from White persons. In accordance with the recent American Thoracic Society/European Respiratory Society (ATS/ERS) statement on lung testing, the authors did not apply a fixed correction factor to adjust for race. Without such an adjustment, Black persons would be biased toward having lower percent predicted values for DLCO. In short, self-identified Black individuals would be more likely to have a predicted DLCO of less than 70% and to therefore meet criteria for “suspected ILD.” The resulting effects on biologic plausibility, causal inference, and the strength of the relationship between “suspected ILD” and clinical outcomes will vary by whether the association between race and lung function is considered a product of inherent biologic variability or a result of external (socioeconomic and environmental) effects.
In summary, ILAs remain a challenge for radiologists, primary care providers, pulmonologists, and anyone else who orders a CT of the lungs. Despite its limitations, I believe the recently published paper pushes us forward conceptually. Perhaps its most important contribution is showing that 50% of ILAs are clinically insignificant by definition. This offers further reassurance that a subset of ILAs can be dismissed. Now, all we need is an easy, cost-effective, and efficient way to identify this subset.
Dr. Holley is professor of medicine at Uniformed Services University in Bethesda, Md., and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center in Washington. He covers a wide range of topics in pulmonary, critical care, and sleep medicine. He disclosed ties to Metapharm Inc., CHEST College, and WebMD. A version of this article originally appeared on Medscape.com.
Clinicians working within the U.S. health care system order CTs; it’s just what we do, and we do it a lot. This isn’t necessarily bad, but an inevitable byproduct is the pandemic of incidental findings. One underrecognized but frequent “incidentaloma” on CT is an interstitial lung abnormality (ILA). The Fleischner Society defines an ILA as honeycombing, traction bronchiectasis, parenchymal distortions, and reticular abnormalities that take up more than 5% of a particular lung zone in a patient without a clinical diagnosis of interstitial lung disease (ILD). In essence, ILAs are both a radiographic and a clinical diagnosis.
ILAs are common. With the advent of lung cancer screening and advances in CT technology, we’re now inundated with detailed images of lung parenchyma in older smokers who are at high risk for respiratory disease. The resulting opportunity for early identification of disease is as exciting as the risk for overdiagnosis, excessive testing, and unnecessary treatment is frightening. Early diagnosis remains critical for preventing irreversible respiratory disease. But as with any disease process, when we attempt to detect pathology before it has become apparent, the line between benign change and true abnormality is blurred.
Such is the challenge with ILAs. Past studies have shown an association between ILAs and morbidity and mortality, but considerable uncertainty persists over what the ILAs represent and how they should be managed. A recent study published in the American Journal of Respiratory and Critical Care Medicine provides some clarity. The authors used data from the COPDGene cohort to correlate ILAs with lung testing, and functional and respiratory outcomes. As with other studies, they found that approximately 10% of the COPDGene patients that they examined had ILAs on CT and half of those met their criteria for “suspected ILD.” Suspected ILD was defined radiographically (definite fibrosis) and on lung function testing (abnormal forced vital capacity [FVC] or diffusing capacity of the lungs for carbon monoxide [DLCO]). The patients with suspected ILD had worse clinical outcomes; being a Black individual, pack-years of smoking, and GOLD stage on spirometry were independently associated with suspected ILD.
This type of study is urgently needed. Given their high prevalence, we’re in dire need of a valid model for risk stratifying ILAs. The authors of this study have moved us closer, but we’ve still got a long way to go. The study has significant limitations. First, although patients with previous documentation of ILD were excluded from COPDGene, no formal, multidisciplinary assessment was performed; therefore, some of the patients labeled as having ILA probably had diagnosable ILD. Their possible inclusion would falsely increase the prevalence of clinically important ILAs and exaggerate the relationship between ILAs and clinical outcomes.
The rhetorical gymnastics performed throughout the paper are necessary yet problematic. “Suspected ILD” is not a recognized diagnosis and the definition is therefore arbitrary. To the extent that “suspected ILD” requires an abnormality on spirometry or DLCO, one could argue it’s the lung function changes and not the radiographic findings that are driving the differences. In fact, “suspected ILD” was defined by lung function more often than radiographic criteria (16% had definite fibrosis on CT, 57% had an abnormal FVC, and 67% had an abnormal DLCO). Patients with ILAs without suspected ILD had outcomes that weren’t statistically different from those with no ILAs at all, implying that the lung testing and not the ILA is the better discriminator. Regardless, this leads us back to where we started before this paper was published: ILAs require lung function testing and referral to a pulmonologist for proper risk stratification. An accompanying editorial highlights these and other limitations.
One particular problem that isn’t addressed by the authors or the editorial is their findings on race. The authors concluded that Black persons with ILAs are more likely to have “suspected ILD.” However, their definition suffers from an insidious form of incorporation bias generated by the way they handled their DLCO reference values. The Global Lung Function Initiative equations they used were derived exclusively from White persons. In accordance with the recent American Thoracic Society/European Respiratory Society (ATS/ERS) statement on lung testing, the authors did not apply a fixed correction factor to adjust for race. Without such an adjustment, Black persons would be biased toward having lower percent predicted values for DLCO. In short, self-identified Black individuals would be more likely to have a predicted DLCO of less than 70% and to therefore meet criteria for “suspected ILD.” The resulting effects on biologic plausibility, causal inference, and the strength of the relationship between “suspected ILD” and clinical outcomes will vary by whether the association between race and lung function is considered a product of inherent biologic variability or a result of external (socioeconomic and environmental) effects.
In summary, ILAs remain a challenge for radiologists, primary care providers, pulmonologists, and anyone else who orders a CT of the lungs. Despite its limitations, I believe the recently published paper pushes us forward conceptually. Perhaps its most important contribution is showing that 50% of ILAs are clinically insignificant by definition. This offers further reassurance that a subset of ILAs can be dismissed. Now, all we need is an easy, cost-effective, and efficient way to identify this subset.
Dr. Holley is professor of medicine at Uniformed Services University in Bethesda, Md., and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center in Washington. He covers a wide range of topics in pulmonary, critical care, and sleep medicine. He disclosed ties to Metapharm Inc., CHEST College, and WebMD. A version of this article originally appeared on Medscape.com.
Clinicians working within the U.S. health care system order CTs; it’s just what we do, and we do it a lot. This isn’t necessarily bad, but an inevitable byproduct is the pandemic of incidental findings. One underrecognized but frequent “incidentaloma” on CT is an interstitial lung abnormality (ILA). The Fleischner Society defines an ILA as honeycombing, traction bronchiectasis, parenchymal distortions, and reticular abnormalities that take up more than 5% of a particular lung zone in a patient without a clinical diagnosis of interstitial lung disease (ILD). In essence, ILAs are both a radiographic and a clinical diagnosis.
ILAs are common. With the advent of lung cancer screening and advances in CT technology, we’re now inundated with detailed images of lung parenchyma in older smokers who are at high risk for respiratory disease. The resulting opportunity for early identification of disease is as exciting as the risk for overdiagnosis, excessive testing, and unnecessary treatment is frightening. Early diagnosis remains critical for preventing irreversible respiratory disease. But as with any disease process, when we attempt to detect pathology before it has become apparent, the line between benign change and true abnormality is blurred.
Such is the challenge with ILAs. Past studies have shown an association between ILAs and morbidity and mortality, but considerable uncertainty persists over what the ILAs represent and how they should be managed. A recent study published in the American Journal of Respiratory and Critical Care Medicine provides some clarity. The authors used data from the COPDGene cohort to correlate ILAs with lung testing, and functional and respiratory outcomes. As with other studies, they found that approximately 10% of the COPDGene patients that they examined had ILAs on CT and half of those met their criteria for “suspected ILD.” Suspected ILD was defined radiographically (definite fibrosis) and on lung function testing (abnormal forced vital capacity [FVC] or diffusing capacity of the lungs for carbon monoxide [DLCO]). The patients with suspected ILD had worse clinical outcomes; being a Black individual, pack-years of smoking, and GOLD stage on spirometry were independently associated with suspected ILD.
This type of study is urgently needed. Given their high prevalence, we’re in dire need of a valid model for risk stratifying ILAs. The authors of this study have moved us closer, but we’ve still got a long way to go. The study has significant limitations. First, although patients with previous documentation of ILD were excluded from COPDGene, no formal, multidisciplinary assessment was performed; therefore, some of the patients labeled as having ILA probably had diagnosable ILD. Their possible inclusion would falsely increase the prevalence of clinically important ILAs and exaggerate the relationship between ILAs and clinical outcomes.
The rhetorical gymnastics performed throughout the paper are necessary yet problematic. “Suspected ILD” is not a recognized diagnosis and the definition is therefore arbitrary. To the extent that “suspected ILD” requires an abnormality on spirometry or DLCO, one could argue it’s the lung function changes and not the radiographic findings that are driving the differences. In fact, “suspected ILD” was defined by lung function more often than radiographic criteria (16% had definite fibrosis on CT, 57% had an abnormal FVC, and 67% had an abnormal DLCO). Patients with ILAs without suspected ILD had outcomes that weren’t statistically different from those with no ILAs at all, implying that the lung testing and not the ILA is the better discriminator. Regardless, this leads us back to where we started before this paper was published: ILAs require lung function testing and referral to a pulmonologist for proper risk stratification. An accompanying editorial highlights these and other limitations.
One particular problem that isn’t addressed by the authors or the editorial is their findings on race. The authors concluded that Black persons with ILAs are more likely to have “suspected ILD.” However, their definition suffers from an insidious form of incorporation bias generated by the way they handled their DLCO reference values. The Global Lung Function Initiative equations they used were derived exclusively from White persons. In accordance with the recent American Thoracic Society/European Respiratory Society (ATS/ERS) statement on lung testing, the authors did not apply a fixed correction factor to adjust for race. Without such an adjustment, Black persons would be biased toward having lower percent predicted values for DLCO. In short, self-identified Black individuals would be more likely to have a predicted DLCO of less than 70% and to therefore meet criteria for “suspected ILD.” The resulting effects on biologic plausibility, causal inference, and the strength of the relationship between “suspected ILD” and clinical outcomes will vary by whether the association between race and lung function is considered a product of inherent biologic variability or a result of external (socioeconomic and environmental) effects.
In summary, ILAs remain a challenge for radiologists, primary care providers, pulmonologists, and anyone else who orders a CT of the lungs. Despite its limitations, I believe the recently published paper pushes us forward conceptually. Perhaps its most important contribution is showing that 50% of ILAs are clinically insignificant by definition. This offers further reassurance that a subset of ILAs can be dismissed. Now, all we need is an easy, cost-effective, and efficient way to identify this subset.
Dr. Holley is professor of medicine at Uniformed Services University in Bethesda, Md., and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center in Washington. He covers a wide range of topics in pulmonary, critical care, and sleep medicine. He disclosed ties to Metapharm Inc., CHEST College, and WebMD. A version of this article originally appeared on Medscape.com.
‘Ozempic face’: Accepting wrinkles for improved health
This transcript has been edited for clarity.
Last week, a number of patients emailed me regarding their concerns about this phenomenon known as Ozempic face. I went on to read about what this meant. I live in Los Angeles, where most people appear to be on semaglutide (Ozempic). It’s the phenomenon where people lose weight relatively rapidly, making their faces thin out. Then what happens, apparently, is they look older because their face is more wrinkled and baggier. They might have to have further plastic surgery. I say that with slight sarcasm because of where I live.
I want to talk about what I think about this, living here where there’s a great pressure to prescribe semaglutide off label, and what I think about it for my patients with diabetes.
Historically, we haven’t had much in terms of effective medication for treating obesity, and frankly, now we do. We now have agents that are effective, that have relatively few side effects, and that have become part of what’s out there. People now want to use these agents, semaglutide, and there’s been a great need for these agents.
The problem, however, is twofold. One, as we all know, is that it has basically caused a shortage of medication for treating our patients who actually have type 2 diabetes and really need these medications to manage their disease. Then we have people who want these medications who can’t pay for them. Insurance doesn’t cover obesity medications, which is problematic and actually quite frustrating for people who, I think, really would benefit from using these medications.
What I tell people, frankly, is that until I have enough supply for my patients with type 2 diabetes, who need these agents to control their blood sugars, I want to keep this class of drugs available to them. I also hope we’re able to expand it more and more with improving insurance coverage – and that’s a big if, if you ask me – both for people who have prediabetes and for patients who are overweight and obese, because I think it’s really hard for people to lose weight.
It’s frustrating, and for many people, being overweight and obese causes all sorts of other health issues, not only diabetes. I believe that these drugs are both safe and effective and should be more available. I do think we need to be careful in terms of who we prescribe them to, at least at the moment. Hopefully, we’ll be able to expand their use.
Anything that can encourage our population to lose weight and maintain that weight loss is very important. We need to couple weight loss medications with lifestyle interventions. I think people can out-eat any medication; therefore, it’s very important to encourage our patients to eat better, to exercise more, and to do all the other things they need to do to reduce their risks for other comorbidities.
I am incredibly happy to have these newer agents on the market. I tell my patients – at least those who have diabetes – that they have to accept looking a little bit too thin for the benefits that we can see in using these medications.
Thank you.
Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts, and three books, on diabetes, and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations. She has ties with Abbott Diabetes Care, AstraZeneca Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen. A version of this article originally appeared on Medscape.com.
This transcript has been edited for clarity.
Last week, a number of patients emailed me regarding their concerns about this phenomenon known as Ozempic face. I went on to read about what this meant. I live in Los Angeles, where most people appear to be on semaglutide (Ozempic). It’s the phenomenon where people lose weight relatively rapidly, making their faces thin out. Then what happens, apparently, is they look older because their face is more wrinkled and baggier. They might have to have further plastic surgery. I say that with slight sarcasm because of where I live.
I want to talk about what I think about this, living here where there’s a great pressure to prescribe semaglutide off label, and what I think about it for my patients with diabetes.
Historically, we haven’t had much in terms of effective medication for treating obesity, and frankly, now we do. We now have agents that are effective, that have relatively few side effects, and that have become part of what’s out there. People now want to use these agents, semaglutide, and there’s been a great need for these agents.
The problem, however, is twofold. One, as we all know, is that it has basically caused a shortage of medication for treating our patients who actually have type 2 diabetes and really need these medications to manage their disease. Then we have people who want these medications who can’t pay for them. Insurance doesn’t cover obesity medications, which is problematic and actually quite frustrating for people who, I think, really would benefit from using these medications.
What I tell people, frankly, is that until I have enough supply for my patients with type 2 diabetes, who need these agents to control their blood sugars, I want to keep this class of drugs available to them. I also hope we’re able to expand it more and more with improving insurance coverage – and that’s a big if, if you ask me – both for people who have prediabetes and for patients who are overweight and obese, because I think it’s really hard for people to lose weight.
It’s frustrating, and for many people, being overweight and obese causes all sorts of other health issues, not only diabetes. I believe that these drugs are both safe and effective and should be more available. I do think we need to be careful in terms of who we prescribe them to, at least at the moment. Hopefully, we’ll be able to expand their use.
Anything that can encourage our population to lose weight and maintain that weight loss is very important. We need to couple weight loss medications with lifestyle interventions. I think people can out-eat any medication; therefore, it’s very important to encourage our patients to eat better, to exercise more, and to do all the other things they need to do to reduce their risks for other comorbidities.
I am incredibly happy to have these newer agents on the market. I tell my patients – at least those who have diabetes – that they have to accept looking a little bit too thin for the benefits that we can see in using these medications.
Thank you.
Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts, and three books, on diabetes, and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations. She has ties with Abbott Diabetes Care, AstraZeneca Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen. A version of this article originally appeared on Medscape.com.
This transcript has been edited for clarity.
Last week, a number of patients emailed me regarding their concerns about this phenomenon known as Ozempic face. I went on to read about what this meant. I live in Los Angeles, where most people appear to be on semaglutide (Ozempic). It’s the phenomenon where people lose weight relatively rapidly, making their faces thin out. Then what happens, apparently, is they look older because their face is more wrinkled and baggier. They might have to have further plastic surgery. I say that with slight sarcasm because of where I live.
I want to talk about what I think about this, living here where there’s a great pressure to prescribe semaglutide off label, and what I think about it for my patients with diabetes.
Historically, we haven’t had much in terms of effective medication for treating obesity, and frankly, now we do. We now have agents that are effective, that have relatively few side effects, and that have become part of what’s out there. People now want to use these agents, semaglutide, and there’s been a great need for these agents.
The problem, however, is twofold. One, as we all know, is that it has basically caused a shortage of medication for treating our patients who actually have type 2 diabetes and really need these medications to manage their disease. Then we have people who want these medications who can’t pay for them. Insurance doesn’t cover obesity medications, which is problematic and actually quite frustrating for people who, I think, really would benefit from using these medications.
What I tell people, frankly, is that until I have enough supply for my patients with type 2 diabetes, who need these agents to control their blood sugars, I want to keep this class of drugs available to them. I also hope we’re able to expand it more and more with improving insurance coverage – and that’s a big if, if you ask me – both for people who have prediabetes and for patients who are overweight and obese, because I think it’s really hard for people to lose weight.
It’s frustrating, and for many people, being overweight and obese causes all sorts of other health issues, not only diabetes. I believe that these drugs are both safe and effective and should be more available. I do think we need to be careful in terms of who we prescribe them to, at least at the moment. Hopefully, we’ll be able to expand their use.
Anything that can encourage our population to lose weight and maintain that weight loss is very important. We need to couple weight loss medications with lifestyle interventions. I think people can out-eat any medication; therefore, it’s very important to encourage our patients to eat better, to exercise more, and to do all the other things they need to do to reduce their risks for other comorbidities.
I am incredibly happy to have these newer agents on the market. I tell my patients – at least those who have diabetes – that they have to accept looking a little bit too thin for the benefits that we can see in using these medications.
Thank you.
Dr. Peters is professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts, and three books, on diabetes, and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations. She has ties with Abbott Diabetes Care, AstraZeneca Becton Dickinson, Boehringer Ingelheim Pharmaceuticals, Dexcom, Eli Lilly, Lexicon Pharmaceuticals, Livongo, MannKind Corporation, Medscape, Merck, Novo Nordisk, Omada Health, OptumHealth, Sanofi, and Zafgen. A version of this article originally appeared on Medscape.com.