Clinical Endocrinology News

Intake of salt is a biological necessity, inextricably woven into physiologic systems. However, excessive salt intake is associated with high blood pressure. Hypertension is linked to increased cardiovascular morbidity and mortality, and it is estimated that excessive salt intake causes approximately 5 million deaths per year worldwide. Reducing salt intake lowers blood pressure, but processed foods contain “hidden” salt, which makes dietary control of salt difficult. This problem is compounded by growing inequalities in food systems, which present another hurdle to sustaining individual dietary control of salt intake.

Krisana Antharith / EyeEm / Getty Images

Of the 87 risk factors included in the Global Burden of Diseases, Injuries, and Risk Factors Study 2019, high systolic blood pressure was identified as the leading risk factor for disease burden at the global level and for its effect on human health. A range of strategies, including primary care management and reduction in sodium intake, are known to reduce the burden of this critical risk factor. Two questions remain unanswered: “What is the relationship between mortality and adding salt to foods?” and “How much does a reduction in salt intake influence people’s health?”
 

Cardiovascular disease and death

Because dietary sodium intake has been identified as a risk factor for cardiovascular disease and premature death, high sodium intake can be expected to curtail life span. A study tested this hypothesis by analyzing the relationship between sodium intake and life expectancy and survival in 181 countries. Sodium intake correlated positively with life expectancy and inversely with all-cause mortality worldwide and in high-income countries, which argues against dietary sodium intake curtailing life span or a being risk factor for premature death. These results help fuel a scientific debate about sodium intake, life expectancy, and mortality. The debate requires interpreting composite data of positive linear, J-shaped, or inverse linear correlations, which underscores the uncertainty regarding this issue.

In a prospective study of 501,379 participants from the UK Biobank, researchers found that higher frequency of adding salt to foods was significantly associated with a higher risk of premature mortality and lower life expectancy independently of diet, lifestyle, socioeconomic level, and preexisting diseases. They found that the positive association appeared to be attenuated with increasing intake of high-potassium foods (vegetables and fruits).

In addition, the researchers made the following observations:

• For cause-specific premature mortality, they found that higher frequency of adding salt to foods was significantly associated with a higher risk of cardiovascular disease mortality and cancer mortality (P-trend < .001 and P-trend < .001, respectively).
• Always adding salt to foods was associated with the lower life expectancy at the age of 50 years by 1.50 (95% confidence interval, 0.72-2.30) and 2.28 (95% CI, 1.66-2.90) years for women and men, respectively, compared with participants who never or rarely added salt to foods.

The researchers noted that adding salt to foods (usually at the table) is common and is directly related to an individual’s long-term preference for salty foods and habitual salt intake. Indeed, in the Western diet, adding salt at the table accounts for 6%-20% of total salt intake. In addition, commonly used table salt contains 97%-99% sodium chloride, minimizing the potential confounding effects of other dietary factors, including potassium. Therefore, adding salt to foods provides a way to evaluate the association between habitual sodium intake and mortality – something that is relevant, given that it has been estimated that in 2010, a total of 1.65 million deaths from cardiovascular causes were attributable to consumption of more than 2.0 g of sodium per day.
 

Salt sensitivity

Current evidence supports a recommendation for moderate sodium intake in the general population (3-5 g/day). Persons with hypertension should consume salt at the lower end of that range. Some dietary guidelines recommend consuming less than 2,300 mg dietary sodium per day for persons aged 14 years or older and less for persons aged 2-13 years. Although low sodium intake (< 2.0 g/day) has been achieved in short-term clinical trials, sustained low sodium intake has not been achieved in any of the longer-term clinical trials (duration > 6 months).

The controversy continues as to the relationship between low sodium intake and blood pressure or cardiovascular diseases. Most studies show that both in individuals with hypertension and those without, blood pressure is reduced by consuming less sodium. However, it is not necessarily lowered by reducing sodium intake (< 3-5 g/day). With a sodium-rich diet, most normotensive individuals experienced a minimal change in mean arterial pressure; for many individuals with hypertension, the values increased by about 4 mm Hg. In addition, among individuals with hypertension who are “salt sensitive,” arterial pressure can increase by > 10 mm Hg in response to high sodium intake.
 

The effect of potassium

Replacing some of the sodium chloride in regular salt with potassium chloride may mitigate some of salt’s harmful cardiovascular effects. Indeed, salt substitutes that have reduced sodium levels and increased potassium levels have been shown to lower blood pressure.

In one trial, researchers enrolled over 20,000 persons from 600 villages in rural China and compared the use of regular salt (100% sodium chloride) with the use of a salt substitute (75% sodium chloride and 25% potassium chloride by mass).

The participants were at high risk for stroke, cardiovascular events, and death. The mean duration of follow-up was 4.74 years. The results were surprising. The rate of stroke was lower with the salt substitute than with regular salt (29.14 events vs. 33.65 events per 1,000 person-years; rate ratio, 0.86; 95% CI, 0.77-0.96; P = .006), as were the rates of major cardiovascular events and death from any cause. The rate of serious adverse events attributed to hyperkalemia was not significantly higher with the salt substitute than with regular salt.

Although there is an ongoing debate about the extent of salt’s effects on the cardiovascular system, there is no doubt that in most places in the world, people are consuming more salt than the body needs.

A lot depends upon the kind of diet consumed by a particular population. Processed food is rarely used in rural areas, such as those involved in the above-mentioned trial, with dietary sodium chloride being added while preparing food at home. This is a determining factor with regard to cardiovascular outcomes, but it cannot be generalized to other social-environmental settings.

In much of the world, commercial food preservation introduces a lot of sodium chloride into the diet, and most salt intake could not be fully attributed to the use of salt substitutes. Indeed, by comparing the sodium content of cereal-based products currently sold on the Italian market with the respective benchmarks proposed by the World Health Organization, researchers found that for most items, the sodium content is much higher than the benchmarks, especially with flatbreads, leavened breads, and crackers/savory biscuits. This shows that there is work to be done to achieve the World Health Organization/United Nations objective of a 30% global reduction in sodium intake by 2025.

This article was translated from Univadis Italy. A version of this article first appeared on Medscape.com.

Intake of salt is a biological necessity, inextricably woven into physiologic systems. However, excessive salt intake is associated with high blood pressure. Hypertension is linked to increased cardiovascular morbidity and mortality, and it is estimated that excessive salt intake causes approximately 5 million deaths per year worldwide. Reducing salt intake lowers blood pressure, but processed foods contain “hidden” salt, which makes dietary control of salt difficult. This problem is compounded by growing inequalities in food systems, which present another hurdle to sustaining individual dietary control of salt intake.

Krisana Antharith / EyeEm / Getty Images

Of the 87 risk factors included in the Global Burden of Diseases, Injuries, and Risk Factors Study 2019, high systolic blood pressure was identified as the leading risk factor for disease burden at the global level and for its effect on human health. A range of strategies, including primary care management and reduction in sodium intake, are known to reduce the burden of this critical risk factor. Two questions remain unanswered: “What is the relationship between mortality and adding salt to foods?” and “How much does a reduction in salt intake influence people’s health?”
 

Cardiovascular disease and death

Because dietary sodium intake has been identified as a risk factor for cardiovascular disease and premature death, high sodium intake can be expected to curtail life span. A study tested this hypothesis by analyzing the relationship between sodium intake and life expectancy and survival in 181 countries. Sodium intake correlated positively with life expectancy and inversely with all-cause mortality worldwide and in high-income countries, which argues against dietary sodium intake curtailing life span or a being risk factor for premature death. These results help fuel a scientific debate about sodium intake, life expectancy, and mortality. The debate requires interpreting composite data of positive linear, J-shaped, or inverse linear correlations, which underscores the uncertainty regarding this issue.

In a prospective study of 501,379 participants from the UK Biobank, researchers found that higher frequency of adding salt to foods was significantly associated with a higher risk of premature mortality and lower life expectancy independently of diet, lifestyle, socioeconomic level, and preexisting diseases. They found that the positive association appeared to be attenuated with increasing intake of high-potassium foods (vegetables and fruits).

In addition, the researchers made the following observations:

• For cause-specific premature mortality, they found that higher frequency of adding salt to foods was significantly associated with a higher risk of cardiovascular disease mortality and cancer mortality (P-trend < .001 and P-trend < .001, respectively).
• Always adding salt to foods was associated with the lower life expectancy at the age of 50 years by 1.50 (95% confidence interval, 0.72-2.30) and 2.28 (95% CI, 1.66-2.90) years for women and men, respectively, compared with participants who never or rarely added salt to foods.

The researchers noted that adding salt to foods (usually at the table) is common and is directly related to an individual’s long-term preference for salty foods and habitual salt intake. Indeed, in the Western diet, adding salt at the table accounts for 6%-20% of total salt intake. In addition, commonly used table salt contains 97%-99% sodium chloride, minimizing the potential confounding effects of other dietary factors, including potassium. Therefore, adding salt to foods provides a way to evaluate the association between habitual sodium intake and mortality – something that is relevant, given that it has been estimated that in 2010, a total of 1.65 million deaths from cardiovascular causes were attributable to consumption of more than 2.0 g of sodium per day.
 

Salt sensitivity

Current evidence supports a recommendation for moderate sodium intake in the general population (3-5 g/day). Persons with hypertension should consume salt at the lower end of that range. Some dietary guidelines recommend consuming less than 2,300 mg dietary sodium per day for persons aged 14 years or older and less for persons aged 2-13 years. Although low sodium intake (< 2.0 g/day) has been achieved in short-term clinical trials, sustained low sodium intake has not been achieved in any of the longer-term clinical trials (duration > 6 months).

The controversy continues as to the relationship between low sodium intake and blood pressure or cardiovascular diseases. Most studies show that both in individuals with hypertension and those without, blood pressure is reduced by consuming less sodium. However, it is not necessarily lowered by reducing sodium intake (< 3-5 g/day). With a sodium-rich diet, most normotensive individuals experienced a minimal change in mean arterial pressure; for many individuals with hypertension, the values increased by about 4 mm Hg. In addition, among individuals with hypertension who are “salt sensitive,” arterial pressure can increase by > 10 mm Hg in response to high sodium intake.
 

The effect of potassium

Replacing some of the sodium chloride in regular salt with potassium chloride may mitigate some of salt’s harmful cardiovascular effects. Indeed, salt substitutes that have reduced sodium levels and increased potassium levels have been shown to lower blood pressure.

In one trial, researchers enrolled over 20,000 persons from 600 villages in rural China and compared the use of regular salt (100% sodium chloride) with the use of a salt substitute (75% sodium chloride and 25% potassium chloride by mass).

The participants were at high risk for stroke, cardiovascular events, and death. The mean duration of follow-up was 4.74 years. The results were surprising. The rate of stroke was lower with the salt substitute than with regular salt (29.14 events vs. 33.65 events per 1,000 person-years; rate ratio, 0.86; 95% CI, 0.77-0.96; P = .006), as were the rates of major cardiovascular events and death from any cause. The rate of serious adverse events attributed to hyperkalemia was not significantly higher with the salt substitute than with regular salt.

Although there is an ongoing debate about the extent of salt’s effects on the cardiovascular system, there is no doubt that in most places in the world, people are consuming more salt than the body needs.

A lot depends upon the kind of diet consumed by a particular population. Processed food is rarely used in rural areas, such as those involved in the above-mentioned trial, with dietary sodium chloride being added while preparing food at home. This is a determining factor with regard to cardiovascular outcomes, but it cannot be generalized to other social-environmental settings.

In much of the world, commercial food preservation introduces a lot of sodium chloride into the diet, and most salt intake could not be fully attributed to the use of salt substitutes. Indeed, by comparing the sodium content of cereal-based products currently sold on the Italian market with the respective benchmarks proposed by the World Health Organization, researchers found that for most items, the sodium content is much higher than the benchmarks, especially with flatbreads, leavened breads, and crackers/savory biscuits. This shows that there is work to be done to achieve the World Health Organization/United Nations objective of a 30% global reduction in sodium intake by 2025.

This article was translated from Univadis Italy. A version of this article first appeared on Medscape.com.

Intake of salt is a biological necessity, inextricably woven into physiologic systems. However, excessive salt intake is associated with high blood pressure. Hypertension is linked to increased cardiovascular morbidity and mortality, and it is estimated that excessive salt intake causes approximately 5 million deaths per year worldwide. Reducing salt intake lowers blood pressure, but processed foods contain “hidden” salt, which makes dietary control of salt difficult. This problem is compounded by growing inequalities in food systems, which present another hurdle to sustaining individual dietary control of salt intake.

Krisana Antharith / EyeEm / Getty Images

Of the 87 risk factors included in the Global Burden of Diseases, Injuries, and Risk Factors Study 2019, high systolic blood pressure was identified as the leading risk factor for disease burden at the global level and for its effect on human health. A range of strategies, including primary care management and reduction in sodium intake, are known to reduce the burden of this critical risk factor. Two questions remain unanswered: “What is the relationship between mortality and adding salt to foods?” and “How much does a reduction in salt intake influence people’s health?”
 

Cardiovascular disease and death

Because dietary sodium intake has been identified as a risk factor for cardiovascular disease and premature death, high sodium intake can be expected to curtail life span. A study tested this hypothesis by analyzing the relationship between sodium intake and life expectancy and survival in 181 countries. Sodium intake correlated positively with life expectancy and inversely with all-cause mortality worldwide and in high-income countries, which argues against dietary sodium intake curtailing life span or a being risk factor for premature death. These results help fuel a scientific debate about sodium intake, life expectancy, and mortality. The debate requires interpreting composite data of positive linear, J-shaped, or inverse linear correlations, which underscores the uncertainty regarding this issue.

In a prospective study of 501,379 participants from the UK Biobank, researchers found that higher frequency of adding salt to foods was significantly associated with a higher risk of premature mortality and lower life expectancy independently of diet, lifestyle, socioeconomic level, and preexisting diseases. They found that the positive association appeared to be attenuated with increasing intake of high-potassium foods (vegetables and fruits).

In addition, the researchers made the following observations:

• For cause-specific premature mortality, they found that higher frequency of adding salt to foods was significantly associated with a higher risk of cardiovascular disease mortality and cancer mortality (P-trend < .001 and P-trend < .001, respectively).
• Always adding salt to foods was associated with the lower life expectancy at the age of 50 years by 1.50 (95% confidence interval, 0.72-2.30) and 2.28 (95% CI, 1.66-2.90) years for women and men, respectively, compared with participants who never or rarely added salt to foods.

The researchers noted that adding salt to foods (usually at the table) is common and is directly related to an individual’s long-term preference for salty foods and habitual salt intake. Indeed, in the Western diet, adding salt at the table accounts for 6%-20% of total salt intake. In addition, commonly used table salt contains 97%-99% sodium chloride, minimizing the potential confounding effects of other dietary factors, including potassium. Therefore, adding salt to foods provides a way to evaluate the association between habitual sodium intake and mortality – something that is relevant, given that it has been estimated that in 2010, a total of 1.65 million deaths from cardiovascular causes were attributable to consumption of more than 2.0 g of sodium per day.
 

Salt sensitivity

Current evidence supports a recommendation for moderate sodium intake in the general population (3-5 g/day). Persons with hypertension should consume salt at the lower end of that range. Some dietary guidelines recommend consuming less than 2,300 mg dietary sodium per day for persons aged 14 years or older and less for persons aged 2-13 years. Although low sodium intake (< 2.0 g/day) has been achieved in short-term clinical trials, sustained low sodium intake has not been achieved in any of the longer-term clinical trials (duration > 6 months).

The controversy continues as to the relationship between low sodium intake and blood pressure or cardiovascular diseases. Most studies show that both in individuals with hypertension and those without, blood pressure is reduced by consuming less sodium. However, it is not necessarily lowered by reducing sodium intake (< 3-5 g/day). With a sodium-rich diet, most normotensive individuals experienced a minimal change in mean arterial pressure; for many individuals with hypertension, the values increased by about 4 mm Hg. In addition, among individuals with hypertension who are “salt sensitive,” arterial pressure can increase by > 10 mm Hg in response to high sodium intake.
 

The effect of potassium

Replacing some of the sodium chloride in regular salt with potassium chloride may mitigate some of salt’s harmful cardiovascular effects. Indeed, salt substitutes that have reduced sodium levels and increased potassium levels have been shown to lower blood pressure.

In one trial, researchers enrolled over 20,000 persons from 600 villages in rural China and compared the use of regular salt (100% sodium chloride) with the use of a salt substitute (75% sodium chloride and 25% potassium chloride by mass).

The participants were at high risk for stroke, cardiovascular events, and death. The mean duration of follow-up was 4.74 years. The results were surprising. The rate of stroke was lower with the salt substitute than with regular salt (29.14 events vs. 33.65 events per 1,000 person-years; rate ratio, 0.86; 95% CI, 0.77-0.96; P = .006), as were the rates of major cardiovascular events and death from any cause. The rate of serious adverse events attributed to hyperkalemia was not significantly higher with the salt substitute than with regular salt.

Although there is an ongoing debate about the extent of salt’s effects on the cardiovascular system, there is no doubt that in most places in the world, people are consuming more salt than the body needs.

A lot depends upon the kind of diet consumed by a particular population. Processed food is rarely used in rural areas, such as those involved in the above-mentioned trial, with dietary sodium chloride being added while preparing food at home. This is a determining factor with regard to cardiovascular outcomes, but it cannot be generalized to other social-environmental settings.

In much of the world, commercial food preservation introduces a lot of sodium chloride into the diet, and most salt intake could not be fully attributed to the use of salt substitutes. Indeed, by comparing the sodium content of cereal-based products currently sold on the Italian market with the respective benchmarks proposed by the World Health Organization, researchers found that for most items, the sodium content is much higher than the benchmarks, especially with flatbreads, leavened breads, and crackers/savory biscuits. This shows that there is work to be done to achieve the World Health Organization/United Nations objective of a 30% global reduction in sodium intake by 2025.

This article was translated from Univadis Italy. A version of this article first appeared on Medscape.com.

Comments from the White House this week suggesting a once-a-year COVID-19 shot for most Americans, “just like your annual flu shot,” were met with backlash from many who say COVID and influenza come from different viruses and need different schedules.

Remarks, from “capitulation” to too few data, hit the airwaves and social media.

Some, however, agree with the White House vision and say that asking people to get one shot in the fall instead of periodic pushes for boosters will raise public confidence and buy-in and reduce consumer confusion.  

Health leaders, including Bob Wachter, MD, chair of the department of medicine at the University of California, San Francisco, say they like the framing of the concept – that people who are not high-risk should plan each year for a COVID shot and a flu shot.

“Doesn’t mean we KNOW shot will prevent transmission for a year. DOES mean it’ll likely lower odds of SEVERE case for a year & we need strategy to bump uptake,” Dr. Wachter tweeted this week.

But the numbers of Americans seeking boosters remain low. Only one-third of all eligible people 50 years and older have gotten a second COVID booster, according to the Centers for Disease Control and Prevention. About half of those who got the original two shots got a first booster.

Meanwhile, the United States is still averaging about 70,000 new COVID cases and more than 300 deaths every day.

The suggested change in approach comes as Pfizer/BioNTech and Moderna roll out their new boosters that target Omicron subvariants BA.4 and BA.5 after the CDC recommended their use and the U.S. Food and Drug Administration approved emergency use authorization. 

“As the virus continues to change, we will now be able to update our vaccines annually to target the dominant variant,” President Joe Biden said in a statement promoting the yearly approach.
 

Some say annual shot premature

Other experts say it’s too soon to tell whether an annual approach will work.

“We have no data to support that current vaccines, including the new BA.5 booster, will provide durable protection beyond 4-6 months. It would be good to aspire to this objective, and much longer duration or protection, but that will likely require next generation and nasal vaccines,” said Eric Topol, MD, Medscape’s editor-in-chief and founder and director of the Scripps Research Translational Institute.

A report in Nature Reviews Immunology states, “Mucosal vaccines offer the potential to trigger robust protective immune responses at the predominant sites of pathogen infection” and potentially “can prevent an infection from becoming established in the first place, rather than only curtailing infection and protecting against the development of disease symptoms.”

Dr. Topol tweeted after the White House statements, “[An annual vaccine] has the ring of Covid capitulation.”

William Schaffner, MD, an infectious disease expert at Vanderbilt University, Nashville, Tenn., told this news organization that he cautions against interpreting the White House comments as official policy.

“This is the difficulty of having public health announcements come out of Washington,” he said. “They ought to come out of the CDC.”

He says there is a reasonable analogy between COVID and influenza, but warns, “don’t push the analogy.”

They are both serious respiratory viruses that can cause much illness and death in essentially the same populations, he notes. These are the older, frail people, people who have underlying illnesses or are immunocompromised.

Both viruses also mutate. But there the paths diverge.

“We’ve gotten into a pattern of annually updating the influenza vaccine because it is such a singularly seasonal virus,” Dr. Schaffner said. “Basically it disappears during the summer. We’ve had plenty of COVID during the summers.”

For COVID, he said, “We will need a periodic booster. Could this be annually? That would certainly make it easier.” But it’s too soon to tell, he said.

Dr. Schaffner noted that several manufacturers are working on a combined flu/COVID vaccine.
 

Just a ‘first step’ toward annual shot

The currently updated COVID vaccine may be the first step toward an annual vaccine, but it’s only the first step, Dr. Schaffner said. “We haven’t committed to further steps yet because we’re watching this virus.”

Syra Madad, DHSc, MSc, an infectious disease epidemiologist at Harvard University’s Belfer Center for Science and International Affairs, Cambridge, Mass., and the New York City hospital system, told this news organization that arguments on both sides make sense.

Having a single message once a year can help eliminate the considerable confusion involving people on individual timelines with different levels of immunity and separate campaigns for COVID and flu shots coming at different times of the year.

“Communication around vaccines is very muddled and that shows in our overall vaccination rates, particularly booster rates,” she says. “The overall strategy is hopeful and makes sense if we’re going to progress that way based on data.”

However, she said that the data are just not there yet to show it’s time for an annual vaccine. First, scientists will need to see how long protection lasts with the Omicron-specific vaccine and how well and how long it protects against severe disease and death as well as infection.

COVID is less predictable than influenza and the influenza vaccine has been around for decades, Dr. Madad noted. With influenza, the patterns are more easily anticipated with their “ladder-like pattern,” she said. “COVID-19 is not like that.”

What is hopeful, she said, “is that we’ve been in the Omicron dynasty since November of 2021. I’m hopeful that we’ll stick with that particular variant.”

Dr. Topol, Dr. Schaffner, and Dr. Madad declared no relevant financial relationships.

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

Comments from the White House this week suggesting a once-a-year COVID-19 shot for most Americans, “just like your annual flu shot,” were met with backlash from many who say COVID and influenza come from different viruses and need different schedules.

Remarks, from “capitulation” to too few data, hit the airwaves and social media.

Some, however, agree with the White House vision and say that asking people to get one shot in the fall instead of periodic pushes for boosters will raise public confidence and buy-in and reduce consumer confusion.  

Health leaders, including Bob Wachter, MD, chair of the department of medicine at the University of California, San Francisco, say they like the framing of the concept – that people who are not high-risk should plan each year for a COVID shot and a flu shot.

“Doesn’t mean we KNOW shot will prevent transmission for a year. DOES mean it’ll likely lower odds of SEVERE case for a year & we need strategy to bump uptake,” Dr. Wachter tweeted this week.

But the numbers of Americans seeking boosters remain low. Only one-third of all eligible people 50 years and older have gotten a second COVID booster, according to the Centers for Disease Control and Prevention. About half of those who got the original two shots got a first booster.

Meanwhile, the United States is still averaging about 70,000 new COVID cases and more than 300 deaths every day.

The suggested change in approach comes as Pfizer/BioNTech and Moderna roll out their new boosters that target Omicron subvariants BA.4 and BA.5 after the CDC recommended their use and the U.S. Food and Drug Administration approved emergency use authorization. 

“As the virus continues to change, we will now be able to update our vaccines annually to target the dominant variant,” President Joe Biden said in a statement promoting the yearly approach.
 

Some say annual shot premature

Other experts say it’s too soon to tell whether an annual approach will work.

“We have no data to support that current vaccines, including the new BA.5 booster, will provide durable protection beyond 4-6 months. It would be good to aspire to this objective, and much longer duration or protection, but that will likely require next generation and nasal vaccines,” said Eric Topol, MD, Medscape’s editor-in-chief and founder and director of the Scripps Research Translational Institute.

A report in Nature Reviews Immunology states, “Mucosal vaccines offer the potential to trigger robust protective immune responses at the predominant sites of pathogen infection” and potentially “can prevent an infection from becoming established in the first place, rather than only curtailing infection and protecting against the development of disease symptoms.”

Dr. Topol tweeted after the White House statements, “[An annual vaccine] has the ring of Covid capitulation.”

William Schaffner, MD, an infectious disease expert at Vanderbilt University, Nashville, Tenn., told this news organization that he cautions against interpreting the White House comments as official policy.

“This is the difficulty of having public health announcements come out of Washington,” he said. “They ought to come out of the CDC.”

He says there is a reasonable analogy between COVID and influenza, but warns, “don’t push the analogy.”

They are both serious respiratory viruses that can cause much illness and death in essentially the same populations, he notes. These are the older, frail people, people who have underlying illnesses or are immunocompromised.

Both viruses also mutate. But there the paths diverge.

“We’ve gotten into a pattern of annually updating the influenza vaccine because it is such a singularly seasonal virus,” Dr. Schaffner said. “Basically it disappears during the summer. We’ve had plenty of COVID during the summers.”

For COVID, he said, “We will need a periodic booster. Could this be annually? That would certainly make it easier.” But it’s too soon to tell, he said.

Dr. Schaffner noted that several manufacturers are working on a combined flu/COVID vaccine.
 

Just a ‘first step’ toward annual shot

The currently updated COVID vaccine may be the first step toward an annual vaccine, but it’s only the first step, Dr. Schaffner said. “We haven’t committed to further steps yet because we’re watching this virus.”

Syra Madad, DHSc, MSc, an infectious disease epidemiologist at Harvard University’s Belfer Center for Science and International Affairs, Cambridge, Mass., and the New York City hospital system, told this news organization that arguments on both sides make sense.

Having a single message once a year can help eliminate the considerable confusion involving people on individual timelines with different levels of immunity and separate campaigns for COVID and flu shots coming at different times of the year.

“Communication around vaccines is very muddled and that shows in our overall vaccination rates, particularly booster rates,” she says. “The overall strategy is hopeful and makes sense if we’re going to progress that way based on data.”

However, she said that the data are just not there yet to show it’s time for an annual vaccine. First, scientists will need to see how long protection lasts with the Omicron-specific vaccine and how well and how long it protects against severe disease and death as well as infection.

COVID is less predictable than influenza and the influenza vaccine has been around for decades, Dr. Madad noted. With influenza, the patterns are more easily anticipated with their “ladder-like pattern,” she said. “COVID-19 is not like that.”

What is hopeful, she said, “is that we’ve been in the Omicron dynasty since November of 2021. I’m hopeful that we’ll stick with that particular variant.”

Dr. Topol, Dr. Schaffner, and Dr. Madad declared no relevant financial relationships.

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

Comments from the White House this week suggesting a once-a-year COVID-19 shot for most Americans, “just like your annual flu shot,” were met with backlash from many who say COVID and influenza come from different viruses and need different schedules.

Remarks, from “capitulation” to too few data, hit the airwaves and social media.

Some, however, agree with the White House vision and say that asking people to get one shot in the fall instead of periodic pushes for boosters will raise public confidence and buy-in and reduce consumer confusion.  

Health leaders, including Bob Wachter, MD, chair of the department of medicine at the University of California, San Francisco, say they like the framing of the concept – that people who are not high-risk should plan each year for a COVID shot and a flu shot.

“Doesn’t mean we KNOW shot will prevent transmission for a year. DOES mean it’ll likely lower odds of SEVERE case for a year & we need strategy to bump uptake,” Dr. Wachter tweeted this week.

But the numbers of Americans seeking boosters remain low. Only one-third of all eligible people 50 years and older have gotten a second COVID booster, according to the Centers for Disease Control and Prevention. About half of those who got the original two shots got a first booster.

Meanwhile, the United States is still averaging about 70,000 new COVID cases and more than 300 deaths every day.

The suggested change in approach comes as Pfizer/BioNTech and Moderna roll out their new boosters that target Omicron subvariants BA.4 and BA.5 after the CDC recommended their use and the U.S. Food and Drug Administration approved emergency use authorization. 

“As the virus continues to change, we will now be able to update our vaccines annually to target the dominant variant,” President Joe Biden said in a statement promoting the yearly approach.
 

Some say annual shot premature

Other experts say it’s too soon to tell whether an annual approach will work.

“We have no data to support that current vaccines, including the new BA.5 booster, will provide durable protection beyond 4-6 months. It would be good to aspire to this objective, and much longer duration or protection, but that will likely require next generation and nasal vaccines,” said Eric Topol, MD, Medscape’s editor-in-chief and founder and director of the Scripps Research Translational Institute.

A report in Nature Reviews Immunology states, “Mucosal vaccines offer the potential to trigger robust protective immune responses at the predominant sites of pathogen infection” and potentially “can prevent an infection from becoming established in the first place, rather than only curtailing infection and protecting against the development of disease symptoms.”

Dr. Topol tweeted after the White House statements, “[An annual vaccine] has the ring of Covid capitulation.”

William Schaffner, MD, an infectious disease expert at Vanderbilt University, Nashville, Tenn., told this news organization that he cautions against interpreting the White House comments as official policy.

“This is the difficulty of having public health announcements come out of Washington,” he said. “They ought to come out of the CDC.”

He says there is a reasonable analogy between COVID and influenza, but warns, “don’t push the analogy.”

They are both serious respiratory viruses that can cause much illness and death in essentially the same populations, he notes. These are the older, frail people, people who have underlying illnesses or are immunocompromised.

Both viruses also mutate. But there the paths diverge.

“We’ve gotten into a pattern of annually updating the influenza vaccine because it is such a singularly seasonal virus,” Dr. Schaffner said. “Basically it disappears during the summer. We’ve had plenty of COVID during the summers.”

For COVID, he said, “We will need a periodic booster. Could this be annually? That would certainly make it easier.” But it’s too soon to tell, he said.

Dr. Schaffner noted that several manufacturers are working on a combined flu/COVID vaccine.
 

Just a ‘first step’ toward annual shot

The currently updated COVID vaccine may be the first step toward an annual vaccine, but it’s only the first step, Dr. Schaffner said. “We haven’t committed to further steps yet because we’re watching this virus.”

Syra Madad, DHSc, MSc, an infectious disease epidemiologist at Harvard University’s Belfer Center for Science and International Affairs, Cambridge, Mass., and the New York City hospital system, told this news organization that arguments on both sides make sense.

Having a single message once a year can help eliminate the considerable confusion involving people on individual timelines with different levels of immunity and separate campaigns for COVID and flu shots coming at different times of the year.

“Communication around vaccines is very muddled and that shows in our overall vaccination rates, particularly booster rates,” she says. “The overall strategy is hopeful and makes sense if we’re going to progress that way based on data.”

However, she said that the data are just not there yet to show it’s time for an annual vaccine. First, scientists will need to see how long protection lasts with the Omicron-specific vaccine and how well and how long it protects against severe disease and death as well as infection.

COVID is less predictable than influenza and the influenza vaccine has been around for decades, Dr. Madad noted. With influenza, the patterns are more easily anticipated with their “ladder-like pattern,” she said. “COVID-19 is not like that.”

What is hopeful, she said, “is that we’ve been in the Omicron dynasty since November of 2021. I’m hopeful that we’ll stick with that particular variant.”

Dr. Topol, Dr. Schaffner, and Dr. Madad declared no relevant financial relationships.

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

During a medical malpractice trial in New Jersey, jurors waited nearly 4 hours for the physician defendant to show up. When he did arrive, the body-building surgeon was sporting two thick gold chains and a diamond pinky ring, and had the top buttons of his shirt open enough to reveal his chest hair.

“This trial was in a very rural, farming community,” recalls medical liability defense attorney Catherine Flynn, of Flynn Watts LLC, based in Parsippany, N.J. “Many of the jurors were wearing flannel shirts and jeans. The doctor’s wife walked in wearing a five-carat diamond ring and other jewelry.”

Ms. Flynn took the couple aside and asked them to remove the jewelry. She explained that the opulent accessories could damage the jury’s view of the physician. The surgeon and his wife, however, refused to remove their jewelry, she said. They didn’t think it was a big deal.

The case against the surgeon involved intraoperative damage to a patient when the physician inadvertently removed a portion of nerve in the area of the procedure. After repair of the nerve, the patient had a positive result. However, the patient alleged the surgeon’s negligence resulted in permanent damage despite the successful repair.

Jurors ultimately found the physician negligent in the case and awarded the plaintiff $1.2 million. Ms. Flynn believes that physician’s flamboyant attire and arrogant nature tainted the jury’s decision.

“In certain counties in New Jersey, his attire would not have been a problem,” she said. “In this rural, farming county, it was a huge problem. You have to know your audience. There are a lot of other things that come into play in a medical malpractice case, but when it comes to damages in a case, you don’t want to be sending the message that supports what somebody’s bias may already be telling them about a doctor.”

The surgeon appealed the verdict, and the case ultimately settled for a lesser amount, according to Ms. Flynn.

An over-the-top wardrobe is just one way that physicians can negatively influence jurors during legal trials. From subtle facial expressions to sudden outbursts to downright rudeness, attorneys have witnessed countless examples of physicians sabotaging their own trials. Legal experts say the cringeworthy experiences are good reminders that jurors are often judging more than just evidence.  

“The minute you enter the courthouse, jurors or potential jurors are sizing you up,” says health law attorney Michael Clark, of Womble Bond Dickinson (US) LLP, based in Houston. “The same phenomenon occurs in a deposition. Awareness of how you are being assessed at all times, and the image that is needed, is important since a negative impression by jurors can have a detrimental effect on a physician’s case.”
 

Juror: We didn’t like the doctor’s shoes

In another case, attorneys warned a physician defendant against dressing in his signature wardrobe during his trial. Against their advice, the doctor showed up daily to his trial in bright pastel, monochromatic suits with matching Gucci-brand shoes, said medical liability defense attorney Meredith C. Lander, of Kaufman Borgeest & Ryan LLP, based in Connecticut. On the witness stand, the doctor was long-winded and wasn’t “terribly likable,” Ms. Lander said.

However, the evidence weighed in the physician’s favor, and there was strong testimony by defense experts. The physician won the case, Ms. Lander said, but after the verdict, the jury foreperson approached the trial attorney and made some disparaging remarks about the defendant.

“The foreperson said the jury didn’t like the doctor or his ‘Gucci suits and shoes,’ but they believed the experts,” Ms. Lander said.

Disruptive behavior can also harm jurors’ perception of physicians, Ms. Flynn adds. During one instance, a surgeon insisted on sitting next to Ms. Flynn, although she generally requests clients sit in the first row so that jurors are not so focused on their reactions during testimony. The surgeon loudly peppered Ms. Flynn with questions as witnesses testified, prompting a reprimand from the judge.

“The judge admonished the doctor several times and said, ‘Doctor, you’re raising your voice. You’ll get a chance to speak with your attorney during the break,’ ” Ms. Flynn recalled. “The doctor refused to stop talking, and the judge told him in front of the jury to go sit in the back of the courtroom. His reaction was, ‘Why do I have to move?! I need to sit here!’ ”

The surgeon eventually moved to the back of the courtroom and a sheriff’s deputy stood next to him. Testimony continued until a note in the form of a paper airplane landed on the table in front of Ms. Flynn. She carefully crumpled the note and tossed it in the wastebasket. Luckily, this drew a laugh from jurors, she said. 

But things got worse when the surgeon testified. Rather than answer the questions, he interrupted and started telling jurors his own version of events.

“The judge finally said, ‘Doctor, if you don’t listen to your attorney and answer her questions, I’m going to make you get off the stand,’ ” Ms. Flynn said. “That was the most unbelievable, egregious self-sabotage trial moment I’ve ever experienced.”

Fortunately, the physician’s legal case was strong, and the experts who testified drove the defense’s side home, Ms. Flynn said. The surgeon won the case.
 

Attorney: Watch what you say in the elevator

Other, more subtle behaviors – while often unintentional – can also be damaging.

Physicians often let their guard down while outside the courtroom and can unknowingly wind up next to a juror in an elevator or standing in a hallway, said Laura Postilion, a partner at Quintairos, Prieto, Wood & Boyer, P.A., based in Chicago.

“For instance, a doctor is in an elevator and feels that some witness on the stand was lying,” Ms. Postilion said. “They might be very upset about it and start ranting about a witness lying, not realizing there is a juror is in the elevator with you.”

Physicians should also be cautious when speaking on the phone to their family or friends during a trial break.

“At the Daley Center in downtown Chicago, there are these long corridors and long line of windows; a lot of people will stand there during breaks. A doctor may be talking to his or her spouse and saying, ‘Yeah, this juror is sleeping!’ Jurors are [often] looking for drama. They’re looking for somebody letting their guard down. Hearing a doctor speak badly about them would certainly give them a reason to dislike the physician.”

Ms. Postilion warns against talking about jurors in or outside of the courtroom. This includes parking structures, she said.

Physicians can take additional steps to save themselves from negative judgment from jurors, attorneys say. Even before the trial starts, Ms. Postilion advises clients to make their social media accounts private. Some curious jurors may look up a physician’s social media accounts to learn more about their personal life, political leanings, or social beliefs, which could prejudice them against the doctor, she said.

Once on the stand, the words and tone used are key. The last thing a physician defendant wants is to come across as arrogant or condescending to jurors, said medical liability defense attorney Michael Moroney, of Flynn Watts LLC.

“For instance, a defendant might say, ‘Well, let me make this simple for you,’ as if they’re talking to a bunch of schoolchildren,” he said. “You don’t know who’s on the jury. That type of language can be offensive.”

Ms. Lander counsels her clients to refrain from using the common phrase, “honestly,” before answering questions on the stand.

“Everything you’re saying on the stand is presumed to be honest,” she said. “When you start an answer with, ‘Honestly…’ out of habit, it really does undercut everything that follows and everything else that’s already been said. It suggests that you were not being honest in your other answers.”
 

Attitude, body language speak volumes

Keep in mind that plaintiffs’ attorneys will try their best to rattle physicians on the stand and get them to appear unlikeable, says Mr. Clark, the Houston-based health law attorney. Physicians who lose their cool and begin arguing with attorneys play into their strategy.

“Plaintiffs’ attorneys have been trained in ways to get under their skin,” he said. “Righteous indignation and annoyance are best left for a rare occasion. Think about how you feel in a social setting when people are bickering in front of you. It’s uncomfortable at best. That’s how a jury feels too.”

Body language is also important, Mr. Clark notes. Physicians should avoid crossed arms, leaning back and rocking, or putting a hand on their mouth while testifying, he said. Many attorneys have practice sessions with their clients and record the interaction so that doctors can watch it and see how they look.

“Know your strengths and weaknesses,” he said. “Get help from your lawyer and perhaps consultants about how to improve these skills. Practice and preparation are important.”

Ms. Postilion goes over courtroom clothing with physician clients before trial. Anything “too flashy, too high-end, or too dumpy” should be avoided, she said. Getting accustomed to the courtroom and practicing in an empty courtroom are good ways to ensure that a physician’s voice is loud enough and projecting far enough in the courtroom, she adds.

“The doctor should try to be the best version of him- or herself to jurors,” she said. “A jury can pick up someone who’s trying to be something they’re not. A good attorney can help the doctor find the best version of themselves and capitalize on it. What is it that you want the jury to know about your care of the patient? Take that overall feeling and make sure it’s clearly expressed to the jury.”

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

During a medical malpractice trial in New Jersey, jurors waited nearly 4 hours for the physician defendant to show up. When he did arrive, the body-building surgeon was sporting two thick gold chains and a diamond pinky ring, and had the top buttons of his shirt open enough to reveal his chest hair.

“This trial was in a very rural, farming community,” recalls medical liability defense attorney Catherine Flynn, of Flynn Watts LLC, based in Parsippany, N.J. “Many of the jurors were wearing flannel shirts and jeans. The doctor’s wife walked in wearing a five-carat diamond ring and other jewelry.”

Ms. Flynn took the couple aside and asked them to remove the jewelry. She explained that the opulent accessories could damage the jury’s view of the physician. The surgeon and his wife, however, refused to remove their jewelry, she said. They didn’t think it was a big deal.

The case against the surgeon involved intraoperative damage to a patient when the physician inadvertently removed a portion of nerve in the area of the procedure. After repair of the nerve, the patient had a positive result. However, the patient alleged the surgeon’s negligence resulted in permanent damage despite the successful repair.

Jurors ultimately found the physician negligent in the case and awarded the plaintiff $1.2 million. Ms. Flynn believes that physician’s flamboyant attire and arrogant nature tainted the jury’s decision.

“In certain counties in New Jersey, his attire would not have been a problem,” she said. “In this rural, farming county, it was a huge problem. You have to know your audience. There are a lot of other things that come into play in a medical malpractice case, but when it comes to damages in a case, you don’t want to be sending the message that supports what somebody’s bias may already be telling them about a doctor.”

The surgeon appealed the verdict, and the case ultimately settled for a lesser amount, according to Ms. Flynn.

An over-the-top wardrobe is just one way that physicians can negatively influence jurors during legal trials. From subtle facial expressions to sudden outbursts to downright rudeness, attorneys have witnessed countless examples of physicians sabotaging their own trials. Legal experts say the cringeworthy experiences are good reminders that jurors are often judging more than just evidence.  

“The minute you enter the courthouse, jurors or potential jurors are sizing you up,” says health law attorney Michael Clark, of Womble Bond Dickinson (US) LLP, based in Houston. “The same phenomenon occurs in a deposition. Awareness of how you are being assessed at all times, and the image that is needed, is important since a negative impression by jurors can have a detrimental effect on a physician’s case.”
 

Juror: We didn’t like the doctor’s shoes

In another case, attorneys warned a physician defendant against dressing in his signature wardrobe during his trial. Against their advice, the doctor showed up daily to his trial in bright pastel, monochromatic suits with matching Gucci-brand shoes, said medical liability defense attorney Meredith C. Lander, of Kaufman Borgeest & Ryan LLP, based in Connecticut. On the witness stand, the doctor was long-winded and wasn’t “terribly likable,” Ms. Lander said.

However, the evidence weighed in the physician’s favor, and there was strong testimony by defense experts. The physician won the case, Ms. Lander said, but after the verdict, the jury foreperson approached the trial attorney and made some disparaging remarks about the defendant.

“The foreperson said the jury didn’t like the doctor or his ‘Gucci suits and shoes,’ but they believed the experts,” Ms. Lander said.

Disruptive behavior can also harm jurors’ perception of physicians, Ms. Flynn adds. During one instance, a surgeon insisted on sitting next to Ms. Flynn, although she generally requests clients sit in the first row so that jurors are not so focused on their reactions during testimony. The surgeon loudly peppered Ms. Flynn with questions as witnesses testified, prompting a reprimand from the judge.

“The judge admonished the doctor several times and said, ‘Doctor, you’re raising your voice. You’ll get a chance to speak with your attorney during the break,’ ” Ms. Flynn recalled. “The doctor refused to stop talking, and the judge told him in front of the jury to go sit in the back of the courtroom. His reaction was, ‘Why do I have to move?! I need to sit here!’ ”

The surgeon eventually moved to the back of the courtroom and a sheriff’s deputy stood next to him. Testimony continued until a note in the form of a paper airplane landed on the table in front of Ms. Flynn. She carefully crumpled the note and tossed it in the wastebasket. Luckily, this drew a laugh from jurors, she said. 

But things got worse when the surgeon testified. Rather than answer the questions, he interrupted and started telling jurors his own version of events.

“The judge finally said, ‘Doctor, if you don’t listen to your attorney and answer her questions, I’m going to make you get off the stand,’ ” Ms. Flynn said. “That was the most unbelievable, egregious self-sabotage trial moment I’ve ever experienced.”

Fortunately, the physician’s legal case was strong, and the experts who testified drove the defense’s side home, Ms. Flynn said. The surgeon won the case.
 

Attorney: Watch what you say in the elevator

Other, more subtle behaviors – while often unintentional – can also be damaging.

Physicians often let their guard down while outside the courtroom and can unknowingly wind up next to a juror in an elevator or standing in a hallway, said Laura Postilion, a partner at Quintairos, Prieto, Wood & Boyer, P.A., based in Chicago.

“For instance, a doctor is in an elevator and feels that some witness on the stand was lying,” Ms. Postilion said. “They might be very upset about it and start ranting about a witness lying, not realizing there is a juror is in the elevator with you.”

Physicians should also be cautious when speaking on the phone to their family or friends during a trial break.

“At the Daley Center in downtown Chicago, there are these long corridors and long line of windows; a lot of people will stand there during breaks. A doctor may be talking to his or her spouse and saying, ‘Yeah, this juror is sleeping!’ Jurors are [often] looking for drama. They’re looking for somebody letting their guard down. Hearing a doctor speak badly about them would certainly give them a reason to dislike the physician.”

Ms. Postilion warns against talking about jurors in or outside of the courtroom. This includes parking structures, she said.

Physicians can take additional steps to save themselves from negative judgment from jurors, attorneys say. Even before the trial starts, Ms. Postilion advises clients to make their social media accounts private. Some curious jurors may look up a physician’s social media accounts to learn more about their personal life, political leanings, or social beliefs, which could prejudice them against the doctor, she said.

Once on the stand, the words and tone used are key. The last thing a physician defendant wants is to come across as arrogant or condescending to jurors, said medical liability defense attorney Michael Moroney, of Flynn Watts LLC.

“For instance, a defendant might say, ‘Well, let me make this simple for you,’ as if they’re talking to a bunch of schoolchildren,” he said. “You don’t know who’s on the jury. That type of language can be offensive.”

Ms. Lander counsels her clients to refrain from using the common phrase, “honestly,” before answering questions on the stand.

“Everything you’re saying on the stand is presumed to be honest,” she said. “When you start an answer with, ‘Honestly…’ out of habit, it really does undercut everything that follows and everything else that’s already been said. It suggests that you were not being honest in your other answers.”
 

Attitude, body language speak volumes

Keep in mind that plaintiffs’ attorneys will try their best to rattle physicians on the stand and get them to appear unlikeable, says Mr. Clark, the Houston-based health law attorney. Physicians who lose their cool and begin arguing with attorneys play into their strategy.

“Plaintiffs’ attorneys have been trained in ways to get under their skin,” he said. “Righteous indignation and annoyance are best left for a rare occasion. Think about how you feel in a social setting when people are bickering in front of you. It’s uncomfortable at best. That’s how a jury feels too.”

Body language is also important, Mr. Clark notes. Physicians should avoid crossed arms, leaning back and rocking, or putting a hand on their mouth while testifying, he said. Many attorneys have practice sessions with their clients and record the interaction so that doctors can watch it and see how they look.

“Know your strengths and weaknesses,” he said. “Get help from your lawyer and perhaps consultants about how to improve these skills. Practice and preparation are important.”

Ms. Postilion goes over courtroom clothing with physician clients before trial. Anything “too flashy, too high-end, or too dumpy” should be avoided, she said. Getting accustomed to the courtroom and practicing in an empty courtroom are good ways to ensure that a physician’s voice is loud enough and projecting far enough in the courtroom, she adds.

“The doctor should try to be the best version of him- or herself to jurors,” she said. “A jury can pick up someone who’s trying to be something they’re not. A good attorney can help the doctor find the best version of themselves and capitalize on it. What is it that you want the jury to know about your care of the patient? Take that overall feeling and make sure it’s clearly expressed to the jury.”

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

During a medical malpractice trial in New Jersey, jurors waited nearly 4 hours for the physician defendant to show up. When he did arrive, the body-building surgeon was sporting two thick gold chains and a diamond pinky ring, and had the top buttons of his shirt open enough to reveal his chest hair.

“This trial was in a very rural, farming community,” recalls medical liability defense attorney Catherine Flynn, of Flynn Watts LLC, based in Parsippany, N.J. “Many of the jurors were wearing flannel shirts and jeans. The doctor’s wife walked in wearing a five-carat diamond ring and other jewelry.”

Ms. Flynn took the couple aside and asked them to remove the jewelry. She explained that the opulent accessories could damage the jury’s view of the physician. The surgeon and his wife, however, refused to remove their jewelry, she said. They didn’t think it was a big deal.

The case against the surgeon involved intraoperative damage to a patient when the physician inadvertently removed a portion of nerve in the area of the procedure. After repair of the nerve, the patient had a positive result. However, the patient alleged the surgeon’s negligence resulted in permanent damage despite the successful repair.

Jurors ultimately found the physician negligent in the case and awarded the plaintiff $1.2 million. Ms. Flynn believes that physician’s flamboyant attire and arrogant nature tainted the jury’s decision.

“In certain counties in New Jersey, his attire would not have been a problem,” she said. “In this rural, farming county, it was a huge problem. You have to know your audience. There are a lot of other things that come into play in a medical malpractice case, but when it comes to damages in a case, you don’t want to be sending the message that supports what somebody’s bias may already be telling them about a doctor.”

The surgeon appealed the verdict, and the case ultimately settled for a lesser amount, according to Ms. Flynn.

An over-the-top wardrobe is just one way that physicians can negatively influence jurors during legal trials. From subtle facial expressions to sudden outbursts to downright rudeness, attorneys have witnessed countless examples of physicians sabotaging their own trials. Legal experts say the cringeworthy experiences are good reminders that jurors are often judging more than just evidence.  

“The minute you enter the courthouse, jurors or potential jurors are sizing you up,” says health law attorney Michael Clark, of Womble Bond Dickinson (US) LLP, based in Houston. “The same phenomenon occurs in a deposition. Awareness of how you are being assessed at all times, and the image that is needed, is important since a negative impression by jurors can have a detrimental effect on a physician’s case.”
 

Juror: We didn’t like the doctor’s shoes

In another case, attorneys warned a physician defendant against dressing in his signature wardrobe during his trial. Against their advice, the doctor showed up daily to his trial in bright pastel, monochromatic suits with matching Gucci-brand shoes, said medical liability defense attorney Meredith C. Lander, of Kaufman Borgeest & Ryan LLP, based in Connecticut. On the witness stand, the doctor was long-winded and wasn’t “terribly likable,” Ms. Lander said.

However, the evidence weighed in the physician’s favor, and there was strong testimony by defense experts. The physician won the case, Ms. Lander said, but after the verdict, the jury foreperson approached the trial attorney and made some disparaging remarks about the defendant.

“The foreperson said the jury didn’t like the doctor or his ‘Gucci suits and shoes,’ but they believed the experts,” Ms. Lander said.

Disruptive behavior can also harm jurors’ perception of physicians, Ms. Flynn adds. During one instance, a surgeon insisted on sitting next to Ms. Flynn, although she generally requests clients sit in the first row so that jurors are not so focused on their reactions during testimony. The surgeon loudly peppered Ms. Flynn with questions as witnesses testified, prompting a reprimand from the judge.

“The judge admonished the doctor several times and said, ‘Doctor, you’re raising your voice. You’ll get a chance to speak with your attorney during the break,’ ” Ms. Flynn recalled. “The doctor refused to stop talking, and the judge told him in front of the jury to go sit in the back of the courtroom. His reaction was, ‘Why do I have to move?! I need to sit here!’ ”

The surgeon eventually moved to the back of the courtroom and a sheriff’s deputy stood next to him. Testimony continued until a note in the form of a paper airplane landed on the table in front of Ms. Flynn. She carefully crumpled the note and tossed it in the wastebasket. Luckily, this drew a laugh from jurors, she said. 

But things got worse when the surgeon testified. Rather than answer the questions, he interrupted and started telling jurors his own version of events.

“The judge finally said, ‘Doctor, if you don’t listen to your attorney and answer her questions, I’m going to make you get off the stand,’ ” Ms. Flynn said. “That was the most unbelievable, egregious self-sabotage trial moment I’ve ever experienced.”

Fortunately, the physician’s legal case was strong, and the experts who testified drove the defense’s side home, Ms. Flynn said. The surgeon won the case.
 

Attorney: Watch what you say in the elevator

Other, more subtle behaviors – while often unintentional – can also be damaging.

Physicians often let their guard down while outside the courtroom and can unknowingly wind up next to a juror in an elevator or standing in a hallway, said Laura Postilion, a partner at Quintairos, Prieto, Wood & Boyer, P.A., based in Chicago.

“For instance, a doctor is in an elevator and feels that some witness on the stand was lying,” Ms. Postilion said. “They might be very upset about it and start ranting about a witness lying, not realizing there is a juror is in the elevator with you.”

Physicians should also be cautious when speaking on the phone to their family or friends during a trial break.

“At the Daley Center in downtown Chicago, there are these long corridors and long line of windows; a lot of people will stand there during breaks. A doctor may be talking to his or her spouse and saying, ‘Yeah, this juror is sleeping!’ Jurors are [often] looking for drama. They’re looking for somebody letting their guard down. Hearing a doctor speak badly about them would certainly give them a reason to dislike the physician.”

Ms. Postilion warns against talking about jurors in or outside of the courtroom. This includes parking structures, she said.

Physicians can take additional steps to save themselves from negative judgment from jurors, attorneys say. Even before the trial starts, Ms. Postilion advises clients to make their social media accounts private. Some curious jurors may look up a physician’s social media accounts to learn more about their personal life, political leanings, or social beliefs, which could prejudice them against the doctor, she said.

Once on the stand, the words and tone used are key. The last thing a physician defendant wants is to come across as arrogant or condescending to jurors, said medical liability defense attorney Michael Moroney, of Flynn Watts LLC.

“For instance, a defendant might say, ‘Well, let me make this simple for you,’ as if they’re talking to a bunch of schoolchildren,” he said. “You don’t know who’s on the jury. That type of language can be offensive.”

Ms. Lander counsels her clients to refrain from using the common phrase, “honestly,” before answering questions on the stand.

“Everything you’re saying on the stand is presumed to be honest,” she said. “When you start an answer with, ‘Honestly…’ out of habit, it really does undercut everything that follows and everything else that’s already been said. It suggests that you were not being honest in your other answers.”
 

Attitude, body language speak volumes

Keep in mind that plaintiffs’ attorneys will try their best to rattle physicians on the stand and get them to appear unlikeable, says Mr. Clark, the Houston-based health law attorney. Physicians who lose their cool and begin arguing with attorneys play into their strategy.

“Plaintiffs’ attorneys have been trained in ways to get under their skin,” he said. “Righteous indignation and annoyance are best left for a rare occasion. Think about how you feel in a social setting when people are bickering in front of you. It’s uncomfortable at best. That’s how a jury feels too.”

Body language is also important, Mr. Clark notes. Physicians should avoid crossed arms, leaning back and rocking, or putting a hand on their mouth while testifying, he said. Many attorneys have practice sessions with their clients and record the interaction so that doctors can watch it and see how they look.

“Know your strengths and weaknesses,” he said. “Get help from your lawyer and perhaps consultants about how to improve these skills. Practice and preparation are important.”

Ms. Postilion goes over courtroom clothing with physician clients before trial. Anything “too flashy, too high-end, or too dumpy” should be avoided, she said. Getting accustomed to the courtroom and practicing in an empty courtroom are good ways to ensure that a physician’s voice is loud enough and projecting far enough in the courtroom, she adds.

“The doctor should try to be the best version of him- or herself to jurors,” she said. “A jury can pick up someone who’s trying to be something they’re not. A good attorney can help the doctor find the best version of themselves and capitalize on it. What is it that you want the jury to know about your care of the patient? Take that overall feeling and make sure it’s clearly expressed to the jury.”

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

Lipoprotein(a) (Lp[a]) levels should be measured in clinical practice to refine risk prediction for atherosclerotic cardiovascular disease (ASCVD) and inform treatment decisions, even if they cannot yet be lowered directly, recommends the National Lipid Association (NLA) in a scientific statement.

The statement was published in the Journal of Clinical Lipidology.

Don P. Wilson, MD, department of pediatric endocrinology and diabetes, Cook Children’s Medical Center, Fort Worth, Tex., told this news organization that lipoprotein(a) is a “very timely subject.”

“The question in the scientific community is: What role does that particular biomarker play in terms of causing serious heart disease, stroke, and calcification of the aortic valve?”

“It’s pretty clear that, in and of itself, it actually can contribute and or cause any of those conditions,” he added. “The thing that’s then sort of problematic is that we don’t have a specific treatment to lower” Lp(a).

However, Dr. Wilson said that the statement underlines it is “still worth knowing” an individual’s Lp(a) concentrations because the risk with increased levels is “even higher for those people who have other conditions, such as metabolic disease or diabetes or high cholesterol.”

There are nevertheless several drugs in phase 2 and 3 clinical trials that appear to have the potential to significantly lower Lp(a) levels.

“I’m very excited,” said Dr. Wilson, noting that, so far, the drugs seem to be “quite safe,” and the currently available data suggest that they can “reduce Lp(a) levels by about 90%, which is huge.”

“That’s better than any drug we’ve got on the market.”

He cautioned, however, that it is going to take time after the drugs are approved to see the real benefits and risks once they start being used in very large populations, given that raised Lp(a) concentrations are present in about 20% of the world population.

The publication of the NLA statement coincides with a similar one from the European Atherosclerosis Society presented at the European Society of Cardiology Congress 2022 on Aug. 29, and published simultaneously in the European Heart Journal.

Coauthor of the EAS statement, Alberico L. Catapano, MD, PhD, professor of pharmacology at the University of Milan, and past president of the EAS, said that there are many areas in which the two statements are “in complete agreement.”

“However, the spirit of the documents is different,” he continued, chief among them being that the EAS statement focuses on the “global risk” of ASCVD and provides a risk calculator to help balance the risk increase with Lp(a) with that from other factors.

Another is that increased Lp(a) levels are recognized as being on a continuum in terms of their risk, such that there is no level at which raised concentrations can be deemed safe.

Dr. Wilson agreed with Dr. Capatano’s assessment, saying that the EAS statement takes current scientific observations “a step further,” in part by emphasizing that Lp(a) is “only one piece of the puzzle” for determining an individuals’ cardiovascular risk.

This will have huge implications for the conversations clinicians have with patients over shared decision-making, Dr. Wilson added.

Nevertheless, Dr. Catapano underlined to this news organization that “both documents are very important” in terms of the need to “raise awareness about a causal risk factor” for cardiovascular disease as well as that modifying Lp(a) concentrations “will probably reduce the risk.”

The statement from the NLA builds on the association’s prior Recommendations for the Patient-Centered Management of Dyslipidemia, published in two parts in 2014 and 2015, and comes to many of the same conclusions as the EAS statement.

It explains that apolipoprotein A, a component of Lp(a) attached to apolipoprotein B, has “unique” properties that promote the “initiation and progression of atherosclerosis and calcific valvular aortic stenosis, through endothelial dysfunction and proinflammatory responses, and pro-osteogenic effects promoting calcification.”

This, in turn, has the potential to cause myocardial infarction and ischemic stroke, the authors note.

This has been confirmed in meta-analyses of prospective, population-based studies showing a high risk for MI, coronary heart disease, and ischemic stroke with high Lp(a) levels, the statement adds.

Moreover, large genetic studies have confirmed that Lp(a) is a causal factor, independent of low-density lipoprotein cholesterol levels, for MI, ischemic stroke, valvular aortic stenosis, coronary artery stenosis, carotid stenosis, femoral artery stenosis, heart failure, cardiovascular mortality, and all-cause mortality.

Like the authors of the EAS statement, the NLA statement authors underline that the measurement of Lp(a) is “currently not standardized or harmonized,” and there is insufficient evidence on the utility of different cut-offs for risk based on age, gender, ethnicity, or the presence of comorbid conditions.

However, they do suggest that Lp(a) levels greater than 50 mg/dL (> 100 nmol/L) may be considered as a risk-enhancing factor favoring the initiation of statin therapy, although they note that the threshold could be threefold higher in African American individuals.

Despite these reservations, the authors say that Lp(a) testing “is reasonable” for refining the risk assessment of ASCVD in the first-degree relatives of people with premature ASCVD and those with a personal history of premature disease as well as in individuals with primary severe hypercholesterolemia.

Testing also “may be reasonable” to “aid in the clinician-patient discussion about whether to prescribe a statin” in people aged 40-75 years with borderline 10-year ASCVD risk, defined as 5%-7.4%, as well as in other equivocal clinical situations.

In terms of what to do in an individual with raised Lp(a) levels, the statement notes that lifestyle therapy and statins do not decrease Lp(a).

Although lomitapide (Juxtapid) and proprotein convertase subtilisin–kexin type 9 (PCSK9) inhibitors both lower levels of the lipoprotein, the former is “not recommended for ASCVD risk reduction,” whereas the impact of the latter on ASCVD risk reduction via Lp(a) reduction “remains undetermined.”

Several experimental agents are currently under investigation to reduce Lp(a) levels, including SLN360 (Silence Therapeutics), and AKCEA-APO(a)-LRX (Akcea Therapeutics/Ionis Pharmaceuticals).

In the meantime, the authors say it is reasonable to use Lp(a) as a “risk-enhancing factor” for the initiation of moderate- or high-intensity statins in the primary prevention of ASCVD and to consider the addition of ezetimibe and/or PCSK9 inhibitors in high- and very high–risk patients already on maximally tolerated statin therapy.

Finally, the authors recognize the need for “additional evidence” to support clinical practice. In the absence of a randomized clinical trial of Lp(a) lowering in those who are at risk for ASCVD, they note that “several important unanswered questions remain.”

These include: “Is it reasonable to recommend universal testing of Lp(a) in everyone regardless of family history or health status at least once to help encourage healthy habits and inform clinical decision-making?” “Will earlier testing and effective interventions help to improve outcomes?”

Alongside more evidence in children, the authors also emphasize that “additional data are urgently needed in Blacks, South Asians, and those of Hispanic descent.”

No funding declared. Dr. Wilson declares relationships with Osler Institute, Merck Sharp & Dohm, Novo Nordisk, and Alexion Pharmaceuticals. Other authors also declare numerous relationships. Dr. Catapano declares a relationship with Novartis.

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

Lipoprotein(a) (Lp[a]) levels should be measured in clinical practice to refine risk prediction for atherosclerotic cardiovascular disease (ASCVD) and inform treatment decisions, even if they cannot yet be lowered directly, recommends the National Lipid Association (NLA) in a scientific statement.

The statement was published in the Journal of Clinical Lipidology.

Don P. Wilson, MD, department of pediatric endocrinology and diabetes, Cook Children’s Medical Center, Fort Worth, Tex., told this news organization that lipoprotein(a) is a “very timely subject.”

“The question in the scientific community is: What role does that particular biomarker play in terms of causing serious heart disease, stroke, and calcification of the aortic valve?”

“It’s pretty clear that, in and of itself, it actually can contribute and or cause any of those conditions,” he added. “The thing that’s then sort of problematic is that we don’t have a specific treatment to lower” Lp(a).

However, Dr. Wilson said that the statement underlines it is “still worth knowing” an individual’s Lp(a) concentrations because the risk with increased levels is “even higher for those people who have other conditions, such as metabolic disease or diabetes or high cholesterol.”

There are nevertheless several drugs in phase 2 and 3 clinical trials that appear to have the potential to significantly lower Lp(a) levels.

“I’m very excited,” said Dr. Wilson, noting that, so far, the drugs seem to be “quite safe,” and the currently available data suggest that they can “reduce Lp(a) levels by about 90%, which is huge.”

“That’s better than any drug we’ve got on the market.”

He cautioned, however, that it is going to take time after the drugs are approved to see the real benefits and risks once they start being used in very large populations, given that raised Lp(a) concentrations are present in about 20% of the world population.

The publication of the NLA statement coincides with a similar one from the European Atherosclerosis Society presented at the European Society of Cardiology Congress 2022 on Aug. 29, and published simultaneously in the European Heart Journal.

Coauthor of the EAS statement, Alberico L. Catapano, MD, PhD, professor of pharmacology at the University of Milan, and past president of the EAS, said that there are many areas in which the two statements are “in complete agreement.”

“However, the spirit of the documents is different,” he continued, chief among them being that the EAS statement focuses on the “global risk” of ASCVD and provides a risk calculator to help balance the risk increase with Lp(a) with that from other factors.

Another is that increased Lp(a) levels are recognized as being on a continuum in terms of their risk, such that there is no level at which raised concentrations can be deemed safe.

Dr. Wilson agreed with Dr. Capatano’s assessment, saying that the EAS statement takes current scientific observations “a step further,” in part by emphasizing that Lp(a) is “only one piece of the puzzle” for determining an individuals’ cardiovascular risk.

This will have huge implications for the conversations clinicians have with patients over shared decision-making, Dr. Wilson added.

Nevertheless, Dr. Catapano underlined to this news organization that “both documents are very important” in terms of the need to “raise awareness about a causal risk factor” for cardiovascular disease as well as that modifying Lp(a) concentrations “will probably reduce the risk.”

The statement from the NLA builds on the association’s prior Recommendations for the Patient-Centered Management of Dyslipidemia, published in two parts in 2014 and 2015, and comes to many of the same conclusions as the EAS statement.

It explains that apolipoprotein A, a component of Lp(a) attached to apolipoprotein B, has “unique” properties that promote the “initiation and progression of atherosclerosis and calcific valvular aortic stenosis, through endothelial dysfunction and proinflammatory responses, and pro-osteogenic effects promoting calcification.”

This, in turn, has the potential to cause myocardial infarction and ischemic stroke, the authors note.

This has been confirmed in meta-analyses of prospective, population-based studies showing a high risk for MI, coronary heart disease, and ischemic stroke with high Lp(a) levels, the statement adds.

Moreover, large genetic studies have confirmed that Lp(a) is a causal factor, independent of low-density lipoprotein cholesterol levels, for MI, ischemic stroke, valvular aortic stenosis, coronary artery stenosis, carotid stenosis, femoral artery stenosis, heart failure, cardiovascular mortality, and all-cause mortality.

Like the authors of the EAS statement, the NLA statement authors underline that the measurement of Lp(a) is “currently not standardized or harmonized,” and there is insufficient evidence on the utility of different cut-offs for risk based on age, gender, ethnicity, or the presence of comorbid conditions.

However, they do suggest that Lp(a) levels greater than 50 mg/dL (> 100 nmol/L) may be considered as a risk-enhancing factor favoring the initiation of statin therapy, although they note that the threshold could be threefold higher in African American individuals.

Despite these reservations, the authors say that Lp(a) testing “is reasonable” for refining the risk assessment of ASCVD in the first-degree relatives of people with premature ASCVD and those with a personal history of premature disease as well as in individuals with primary severe hypercholesterolemia.

Testing also “may be reasonable” to “aid in the clinician-patient discussion about whether to prescribe a statin” in people aged 40-75 years with borderline 10-year ASCVD risk, defined as 5%-7.4%, as well as in other equivocal clinical situations.

In terms of what to do in an individual with raised Lp(a) levels, the statement notes that lifestyle therapy and statins do not decrease Lp(a).

Although lomitapide (Juxtapid) and proprotein convertase subtilisin–kexin type 9 (PCSK9) inhibitors both lower levels of the lipoprotein, the former is “not recommended for ASCVD risk reduction,” whereas the impact of the latter on ASCVD risk reduction via Lp(a) reduction “remains undetermined.”

Several experimental agents are currently under investigation to reduce Lp(a) levels, including SLN360 (Silence Therapeutics), and AKCEA-APO(a)-LRX (Akcea Therapeutics/Ionis Pharmaceuticals).

In the meantime, the authors say it is reasonable to use Lp(a) as a “risk-enhancing factor” for the initiation of moderate- or high-intensity statins in the primary prevention of ASCVD and to consider the addition of ezetimibe and/or PCSK9 inhibitors in high- and very high–risk patients already on maximally tolerated statin therapy.

Finally, the authors recognize the need for “additional evidence” to support clinical practice. In the absence of a randomized clinical trial of Lp(a) lowering in those who are at risk for ASCVD, they note that “several important unanswered questions remain.”

These include: “Is it reasonable to recommend universal testing of Lp(a) in everyone regardless of family history or health status at least once to help encourage healthy habits and inform clinical decision-making?” “Will earlier testing and effective interventions help to improve outcomes?”

Alongside more evidence in children, the authors also emphasize that “additional data are urgently needed in Blacks, South Asians, and those of Hispanic descent.”

No funding declared. Dr. Wilson declares relationships with Osler Institute, Merck Sharp & Dohm, Novo Nordisk, and Alexion Pharmaceuticals. Other authors also declare numerous relationships. Dr. Catapano declares a relationship with Novartis.

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

Lipoprotein(a) (Lp[a]) levels should be measured in clinical practice to refine risk prediction for atherosclerotic cardiovascular disease (ASCVD) and inform treatment decisions, even if they cannot yet be lowered directly, recommends the National Lipid Association (NLA) in a scientific statement.

The statement was published in the Journal of Clinical Lipidology.

Don P. Wilson, MD, department of pediatric endocrinology and diabetes, Cook Children’s Medical Center, Fort Worth, Tex., told this news organization that lipoprotein(a) is a “very timely subject.”

“The question in the scientific community is: What role does that particular biomarker play in terms of causing serious heart disease, stroke, and calcification of the aortic valve?”

“It’s pretty clear that, in and of itself, it actually can contribute and or cause any of those conditions,” he added. “The thing that’s then sort of problematic is that we don’t have a specific treatment to lower” Lp(a).

However, Dr. Wilson said that the statement underlines it is “still worth knowing” an individual’s Lp(a) concentrations because the risk with increased levels is “even higher for those people who have other conditions, such as metabolic disease or diabetes or high cholesterol.”

There are nevertheless several drugs in phase 2 and 3 clinical trials that appear to have the potential to significantly lower Lp(a) levels.

“I’m very excited,” said Dr. Wilson, noting that, so far, the drugs seem to be “quite safe,” and the currently available data suggest that they can “reduce Lp(a) levels by about 90%, which is huge.”

“That’s better than any drug we’ve got on the market.”

He cautioned, however, that it is going to take time after the drugs are approved to see the real benefits and risks once they start being used in very large populations, given that raised Lp(a) concentrations are present in about 20% of the world population.

The publication of the NLA statement coincides with a similar one from the European Atherosclerosis Society presented at the European Society of Cardiology Congress 2022 on Aug. 29, and published simultaneously in the European Heart Journal.

Coauthor of the EAS statement, Alberico L. Catapano, MD, PhD, professor of pharmacology at the University of Milan, and past president of the EAS, said that there are many areas in which the two statements are “in complete agreement.”

“However, the spirit of the documents is different,” he continued, chief among them being that the EAS statement focuses on the “global risk” of ASCVD and provides a risk calculator to help balance the risk increase with Lp(a) with that from other factors.

Another is that increased Lp(a) levels are recognized as being on a continuum in terms of their risk, such that there is no level at which raised concentrations can be deemed safe.

Dr. Wilson agreed with Dr. Capatano’s assessment, saying that the EAS statement takes current scientific observations “a step further,” in part by emphasizing that Lp(a) is “only one piece of the puzzle” for determining an individuals’ cardiovascular risk.

This will have huge implications for the conversations clinicians have with patients over shared decision-making, Dr. Wilson added.

Nevertheless, Dr. Catapano underlined to this news organization that “both documents are very important” in terms of the need to “raise awareness about a causal risk factor” for cardiovascular disease as well as that modifying Lp(a) concentrations “will probably reduce the risk.”

The statement from the NLA builds on the association’s prior Recommendations for the Patient-Centered Management of Dyslipidemia, published in two parts in 2014 and 2015, and comes to many of the same conclusions as the EAS statement.

It explains that apolipoprotein A, a component of Lp(a) attached to apolipoprotein B, has “unique” properties that promote the “initiation and progression of atherosclerosis and calcific valvular aortic stenosis, through endothelial dysfunction and proinflammatory responses, and pro-osteogenic effects promoting calcification.”

This, in turn, has the potential to cause myocardial infarction and ischemic stroke, the authors note.

This has been confirmed in meta-analyses of prospective, population-based studies showing a high risk for MI, coronary heart disease, and ischemic stroke with high Lp(a) levels, the statement adds.

Moreover, large genetic studies have confirmed that Lp(a) is a causal factor, independent of low-density lipoprotein cholesterol levels, for MI, ischemic stroke, valvular aortic stenosis, coronary artery stenosis, carotid stenosis, femoral artery stenosis, heart failure, cardiovascular mortality, and all-cause mortality.

Like the authors of the EAS statement, the NLA statement authors underline that the measurement of Lp(a) is “currently not standardized or harmonized,” and there is insufficient evidence on the utility of different cut-offs for risk based on age, gender, ethnicity, or the presence of comorbid conditions.

However, they do suggest that Lp(a) levels greater than 50 mg/dL (> 100 nmol/L) may be considered as a risk-enhancing factor favoring the initiation of statin therapy, although they note that the threshold could be threefold higher in African American individuals.

Despite these reservations, the authors say that Lp(a) testing “is reasonable” for refining the risk assessment of ASCVD in the first-degree relatives of people with premature ASCVD and those with a personal history of premature disease as well as in individuals with primary severe hypercholesterolemia.

Testing also “may be reasonable” to “aid in the clinician-patient discussion about whether to prescribe a statin” in people aged 40-75 years with borderline 10-year ASCVD risk, defined as 5%-7.4%, as well as in other equivocal clinical situations.

In terms of what to do in an individual with raised Lp(a) levels, the statement notes that lifestyle therapy and statins do not decrease Lp(a).

Although lomitapide (Juxtapid) and proprotein convertase subtilisin–kexin type 9 (PCSK9) inhibitors both lower levels of the lipoprotein, the former is “not recommended for ASCVD risk reduction,” whereas the impact of the latter on ASCVD risk reduction via Lp(a) reduction “remains undetermined.”

Several experimental agents are currently under investigation to reduce Lp(a) levels, including SLN360 (Silence Therapeutics), and AKCEA-APO(a)-LRX (Akcea Therapeutics/Ionis Pharmaceuticals).

In the meantime, the authors say it is reasonable to use Lp(a) as a “risk-enhancing factor” for the initiation of moderate- or high-intensity statins in the primary prevention of ASCVD and to consider the addition of ezetimibe and/or PCSK9 inhibitors in high- and very high–risk patients already on maximally tolerated statin therapy.

Finally, the authors recognize the need for “additional evidence” to support clinical practice. In the absence of a randomized clinical trial of Lp(a) lowering in those who are at risk for ASCVD, they note that “several important unanswered questions remain.”

These include: “Is it reasonable to recommend universal testing of Lp(a) in everyone regardless of family history or health status at least once to help encourage healthy habits and inform clinical decision-making?” “Will earlier testing and effective interventions help to improve outcomes?”

Alongside more evidence in children, the authors also emphasize that “additional data are urgently needed in Blacks, South Asians, and those of Hispanic descent.”

No funding declared. Dr. Wilson declares relationships with Osler Institute, Merck Sharp & Dohm, Novo Nordisk, and Alexion Pharmaceuticals. Other authors also declare numerous relationships. Dr. Catapano declares a relationship with Novartis.

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

A trip to the cath lab for possible revascularization after a positive stress test, compared with a wait-and-see approach backed by optimal medications, did not improve 5-year survival for patients with advanced chronic kidney disease (CKD) in the ISCHEMIA-CKD trial’s extension study, ISCHEMIA-CKD EXTEND.

The long-term results, from the same 777 patients followed for an average of 2.2 years in the main trial, are consistent with the overall findings of no survival advantage with an initially invasive strategy, compared with one that is initially conservative. The finding applies to patients like those in the trial who had moderate to severe ischemia at stress testing and whose CKD put them in an especially high-risk and little-studied coronary artery disease (CAD) category.

Indeed, in a reflection of that high-risk status, 5-year all-cause mortality reached about 40% and cardiovascular (CV) mortality approached 30%, with no significant differences between patients in the invasive- and conservative-strategy groups.

MDedge News/Mitchel L. Zoler

Those numbers arguably put CKD’s effect on CAD survival in about the same league as an ejection fraction (EF) of 35% or less. For context, all-cause mortality over 3-4 years was about 32% in the REVIVED-BCIS2 trial of such patients with ischemic reduced-EF cardiomyopathy, whether or not they were revascularized, observed Sripal Bangalore, MD, MHA.

Yet in ISCHEMIA-CKD EXTEND, “you’re seeing in a group of patients, with largely preserved EF but advanced CKD, a mortality rate close to 40% at 5 years,” said Dr. Bangalore of New York University.

Although the study doesn’t show benefit from the initially invasive approach in CKD patients with stable CAD, for those with acute coronary syndromes (ACS), it seems to suggest that “at least the invasive strategy is safe,” Dr. Bangalore said during a press conference preceding his presentation of the study Aug. 29 at the annual congress of the European Society of Cardiology, held in Barcelona.

REVIVED-BCIS2 was also presented at the ESC sessions on Aug. 27, as reported by this news organization.

ISCHEMIA-CKD EXTEND “is a large trial and a very well-done trial. The results are robust, and they should influence clinical practice,” Deepak L. Bhatt, MD, MPH, Brigham and Women’s Hospital Heart & Vascular Center, Boston, said as the invited discussant after Dr. Bangalore’s presentation.

“The main message here, really, is don’t just go looking for ischemia, at least with the modalities used in this trial, in your CKD patients as a routine practice, and then try to stomp out that ischemia with revascularization,” Dr. Bhatt said. “The right thing to do in these high-risk patients is to focus on lifestyle modification and intensive medical therapy.”

A caveat, he said, is that the trial’s results don’t apply to the types of patients excluded from it, including those with recent ACS and those who are highly symptomatic or have an EF of less than 35%.

“Those CKD patients likely benefit from an invasive strategy with anatomically appropriate revascularization,” whether percutaneous coronary intervention (PCI) or coronary bypass surgery, Dr. Bhatt said.

At a median follow-up of 5 years in the extension study, the rates of death from any cause were 40.6% for patients in the invasive-strategy group and 37.4% for those in the conservative-strategy group. That yielded a hazard ratio of 1.12 (95% confidence interval, 0.89-1.41; P = .32) after adjustment for age, sex, diabetes status, EF, dialysis status, and – for patients not on dialysis – baseline estimated glomerular filtration rate.

The rates of CV death were 29% for patients managed invasively and 27% for those initially managed conservatively, for a similarly adjusted HR of 1.04 (95% CI, 0.80-1.37; P = .75).

In subgroup analyses, Dr. Bangalore reported, there were no significant differences in all-cause or CV mortality by diabetes status, by severity of baseline ischemia, or by whether the patient had recently experienced new or more frequent angina at study entry, was on guideline-directed medical therapy at baseline, or was on dialysis.

Among the contributions of ISCHEMIA-CKD and its 5-year extension study, Dr. Bangalore told this news organization, is that the relative safety of revascularization they showed may help to counter “renalism,” that is, the aversion to invasive intervention in patients with advanced CKD in clinical practice.

For example, if a patient with advanced CKD presents with an acute myocardial infarction, “people are hesitant to take them to the cath lab,” Dr. Bangalore said. But “if you follow protocols, if you follow strategies to minimize the risk, you can safely go ahead and do it.”

But in patients with stable CAD, as the ISCHEMIA-CKD studies show, “routinely revascularizing them may not have significant benefits.”

ISCHEMIC-CKD and its extension study were funded by the National Heart, Lung, and Blood Institute. Dr. Bangalore discloses receiving research grants from NHLBI and serving as a consultant for Abbott Vascular, Biotronik, Boston Scientific, Amgen, Pfizer, Merck, and Reata. Dr. Bhatt has disclosed grants and/or personal fees from many companies; personal fees from WebMD and other publications or organizations; and having other relationships with Medscape Cardiology and other publications or organizations.

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

A trip to the cath lab for possible revascularization after a positive stress test, compared with a wait-and-see approach backed by optimal medications, did not improve 5-year survival for patients with advanced chronic kidney disease (CKD) in the ISCHEMIA-CKD trial’s extension study, ISCHEMIA-CKD EXTEND.

The long-term results, from the same 777 patients followed for an average of 2.2 years in the main trial, are consistent with the overall findings of no survival advantage with an initially invasive strategy, compared with one that is initially conservative. The finding applies to patients like those in the trial who had moderate to severe ischemia at stress testing and whose CKD put them in an especially high-risk and little-studied coronary artery disease (CAD) category.

Indeed, in a reflection of that high-risk status, 5-year all-cause mortality reached about 40% and cardiovascular (CV) mortality approached 30%, with no significant differences between patients in the invasive- and conservative-strategy groups.

MDedge News/Mitchel L. Zoler

Those numbers arguably put CKD’s effect on CAD survival in about the same league as an ejection fraction (EF) of 35% or less. For context, all-cause mortality over 3-4 years was about 32% in the REVIVED-BCIS2 trial of such patients with ischemic reduced-EF cardiomyopathy, whether or not they were revascularized, observed Sripal Bangalore, MD, MHA.

Yet in ISCHEMIA-CKD EXTEND, “you’re seeing in a group of patients, with largely preserved EF but advanced CKD, a mortality rate close to 40% at 5 years,” said Dr. Bangalore of New York University.

Although the study doesn’t show benefit from the initially invasive approach in CKD patients with stable CAD, for those with acute coronary syndromes (ACS), it seems to suggest that “at least the invasive strategy is safe,” Dr. Bangalore said during a press conference preceding his presentation of the study Aug. 29 at the annual congress of the European Society of Cardiology, held in Barcelona.

REVIVED-BCIS2 was also presented at the ESC sessions on Aug. 27, as reported by this news organization.

ISCHEMIA-CKD EXTEND “is a large trial and a very well-done trial. The results are robust, and they should influence clinical practice,” Deepak L. Bhatt, MD, MPH, Brigham and Women’s Hospital Heart & Vascular Center, Boston, said as the invited discussant after Dr. Bangalore’s presentation.

“The main message here, really, is don’t just go looking for ischemia, at least with the modalities used in this trial, in your CKD patients as a routine practice, and then try to stomp out that ischemia with revascularization,” Dr. Bhatt said. “The right thing to do in these high-risk patients is to focus on lifestyle modification and intensive medical therapy.”

A caveat, he said, is that the trial’s results don’t apply to the types of patients excluded from it, including those with recent ACS and those who are highly symptomatic or have an EF of less than 35%.

“Those CKD patients likely benefit from an invasive strategy with anatomically appropriate revascularization,” whether percutaneous coronary intervention (PCI) or coronary bypass surgery, Dr. Bhatt said.

At a median follow-up of 5 years in the extension study, the rates of death from any cause were 40.6% for patients in the invasive-strategy group and 37.4% for those in the conservative-strategy group. That yielded a hazard ratio of 1.12 (95% confidence interval, 0.89-1.41; P = .32) after adjustment for age, sex, diabetes status, EF, dialysis status, and – for patients not on dialysis – baseline estimated glomerular filtration rate.

The rates of CV death were 29% for patients managed invasively and 27% for those initially managed conservatively, for a similarly adjusted HR of 1.04 (95% CI, 0.80-1.37; P = .75).

In subgroup analyses, Dr. Bangalore reported, there were no significant differences in all-cause or CV mortality by diabetes status, by severity of baseline ischemia, or by whether the patient had recently experienced new or more frequent angina at study entry, was on guideline-directed medical therapy at baseline, or was on dialysis.

Among the contributions of ISCHEMIA-CKD and its 5-year extension study, Dr. Bangalore told this news organization, is that the relative safety of revascularization they showed may help to counter “renalism,” that is, the aversion to invasive intervention in patients with advanced CKD in clinical practice.

For example, if a patient with advanced CKD presents with an acute myocardial infarction, “people are hesitant to take them to the cath lab,” Dr. Bangalore said. But “if you follow protocols, if you follow strategies to minimize the risk, you can safely go ahead and do it.”

But in patients with stable CAD, as the ISCHEMIA-CKD studies show, “routinely revascularizing them may not have significant benefits.”

ISCHEMIC-CKD and its extension study were funded by the National Heart, Lung, and Blood Institute. Dr. Bangalore discloses receiving research grants from NHLBI and serving as a consultant for Abbott Vascular, Biotronik, Boston Scientific, Amgen, Pfizer, Merck, and Reata. Dr. Bhatt has disclosed grants and/or personal fees from many companies; personal fees from WebMD and other publications or organizations; and having other relationships with Medscape Cardiology and other publications or organizations.

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

A trip to the cath lab for possible revascularization after a positive stress test, compared with a wait-and-see approach backed by optimal medications, did not improve 5-year survival for patients with advanced chronic kidney disease (CKD) in the ISCHEMIA-CKD trial’s extension study, ISCHEMIA-CKD EXTEND.

The long-term results, from the same 777 patients followed for an average of 2.2 years in the main trial, are consistent with the overall findings of no survival advantage with an initially invasive strategy, compared with one that is initially conservative. The finding applies to patients like those in the trial who had moderate to severe ischemia at stress testing and whose CKD put them in an especially high-risk and little-studied coronary artery disease (CAD) category.

Indeed, in a reflection of that high-risk status, 5-year all-cause mortality reached about 40% and cardiovascular (CV) mortality approached 30%, with no significant differences between patients in the invasive- and conservative-strategy groups.

MDedge News/Mitchel L. Zoler

Those numbers arguably put CKD’s effect on CAD survival in about the same league as an ejection fraction (EF) of 35% or less. For context, all-cause mortality over 3-4 years was about 32% in the REVIVED-BCIS2 trial of such patients with ischemic reduced-EF cardiomyopathy, whether or not they were revascularized, observed Sripal Bangalore, MD, MHA.

Yet in ISCHEMIA-CKD EXTEND, “you’re seeing in a group of patients, with largely preserved EF but advanced CKD, a mortality rate close to 40% at 5 years,” said Dr. Bangalore of New York University.

Although the study doesn’t show benefit from the initially invasive approach in CKD patients with stable CAD, for those with acute coronary syndromes (ACS), it seems to suggest that “at least the invasive strategy is safe,” Dr. Bangalore said during a press conference preceding his presentation of the study Aug. 29 at the annual congress of the European Society of Cardiology, held in Barcelona.

REVIVED-BCIS2 was also presented at the ESC sessions on Aug. 27, as reported by this news organization.

ISCHEMIA-CKD EXTEND “is a large trial and a very well-done trial. The results are robust, and they should influence clinical practice,” Deepak L. Bhatt, MD, MPH, Brigham and Women’s Hospital Heart & Vascular Center, Boston, said as the invited discussant after Dr. Bangalore’s presentation.

“The main message here, really, is don’t just go looking for ischemia, at least with the modalities used in this trial, in your CKD patients as a routine practice, and then try to stomp out that ischemia with revascularization,” Dr. Bhatt said. “The right thing to do in these high-risk patients is to focus on lifestyle modification and intensive medical therapy.”

A caveat, he said, is that the trial’s results don’t apply to the types of patients excluded from it, including those with recent ACS and those who are highly symptomatic or have an EF of less than 35%.

“Those CKD patients likely benefit from an invasive strategy with anatomically appropriate revascularization,” whether percutaneous coronary intervention (PCI) or coronary bypass surgery, Dr. Bhatt said.

At a median follow-up of 5 years in the extension study, the rates of death from any cause were 40.6% for patients in the invasive-strategy group and 37.4% for those in the conservative-strategy group. That yielded a hazard ratio of 1.12 (95% confidence interval, 0.89-1.41; P = .32) after adjustment for age, sex, diabetes status, EF, dialysis status, and – for patients not on dialysis – baseline estimated glomerular filtration rate.

The rates of CV death were 29% for patients managed invasively and 27% for those initially managed conservatively, for a similarly adjusted HR of 1.04 (95% CI, 0.80-1.37; P = .75).

In subgroup analyses, Dr. Bangalore reported, there were no significant differences in all-cause or CV mortality by diabetes status, by severity of baseline ischemia, or by whether the patient had recently experienced new or more frequent angina at study entry, was on guideline-directed medical therapy at baseline, or was on dialysis.

Among the contributions of ISCHEMIA-CKD and its 5-year extension study, Dr. Bangalore told this news organization, is that the relative safety of revascularization they showed may help to counter “renalism,” that is, the aversion to invasive intervention in patients with advanced CKD in clinical practice.

For example, if a patient with advanced CKD presents with an acute myocardial infarction, “people are hesitant to take them to the cath lab,” Dr. Bangalore said. But “if you follow protocols, if you follow strategies to minimize the risk, you can safely go ahead and do it.”

But in patients with stable CAD, as the ISCHEMIA-CKD studies show, “routinely revascularizing them may not have significant benefits.”

ISCHEMIC-CKD and its extension study were funded by the National Heart, Lung, and Blood Institute. Dr. Bangalore discloses receiving research grants from NHLBI and serving as a consultant for Abbott Vascular, Biotronik, Boston Scientific, Amgen, Pfizer, Merck, and Reata. Dr. Bhatt has disclosed grants and/or personal fees from many companies; personal fees from WebMD and other publications or organizations; and having other relationships with Medscape Cardiology and other publications or organizations.

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

Health concerns about the consumption of artificial sweeteners could be strengthened with the publication of a new study linking their intake to increased risk of heart disease and stroke events.

In this latest large-scale, prospective study of French adults, total artificial sweetener intake from all sources was associated with increased risk overall of cardiovascular and cerebrovascular disease.

The study was published online in the BMJ.

The current study differs from those done previously in that it includes artificial sweetener intake from both food and drinks, whereas previous studies have focused mainly on artificial sweetener content of beverages alone.

“Here we have quantified for the first time the global exposure to artificial sweeteners. This is not just beverages but includes the use of tabletop sweeteners, and other foods that include artificial sweeteners such as yogurts and desserts. This is the first time this information has been correlated to risk of heart disease,” senior author Mathilde Touvier, MD, Sorbonne Paris Nord University, told this news organization.

Just over half of the artificial sweetener intake in the study came from drinks, with the rest coming from tabletop sweeteners and foods.

“We included hard cardio- and cerebrovascular clinical endpoints such as a heart attack or stroke, and our results suggest that the amount of artificial sweetener in less than one can of soda could increase the risk of such events,” Dr. Touvier noted.

“This is an important and statistically significant association which shows robustness in all models after adjusting for many other possible confounding factors,” she said.

“There is now mounting evidence correlating artificial sweeteners to weight gain and heart disease,” she concluded. “My advice would be that we all need to try to limit sugar intake, but we should not consider artificial sweeteners as safe alternatives. Rather, we need to try to reduce our need for a sugary taste in our diet.”

But another leading researcher in the field urges caution in interpreting these results.

John Sievenpiper, MD, departments of nutritional sciences and medicine, University of Toronto, commented: “This paper shows the same relationship seen by many other large prospective cohorts which model the intake of artificial sweeteners as baseline or prevalent exposures.

“These observations are well recognized to be at high risk of residual confounding from behavior clustering and reverse causality in which being at risk for cardiovascular disease causes people to consume artificial sweeteners as a strategy to mitigate this risk as opposed to the other way around.”
 

Risk increased by 9%

The current study included 103,388 French adults from the NutriNet-Sante cohort, of whom 37.1% reported consumption of artificial sweeteners. The sweeteners assessed were mainly aspartame (58% of sweetener intake), acesulfame potassium (29%), and sucralose (10%), with the other 3% made up of various other sweeteners including cyclamates and saccharin.

Results showed that over an average 9 years of follow-up, artificial sweetener intake was associated with a 9% increased risk of cardiovascular or cerebrovascular events, including myocardial infarction, acute coronary syndrome, angioplasty, angina, stroke, or transient ischemic attack, with a hazard ratio of 1.09 (95% confidence interval, 1.01-1.18; P = .03).

The average intake of artificial sweeteners among those who reported consuming them was 42.46 mg/day, which corresponds to approximately one individual packet of tabletop sweetener or 100 mL of diet soda.

“We don’t have enough evidence to work out an amount of artificial sweetener that is harmful, but we did show a dose-effect association, with a higher risk of cardiovascular events with higher consumption,” Dr. Touvier said.

“Higher consumption in this study was a mean of 77 mg/day artificial sweetener, which is about 200 mL of soda – just a bit less than one standard can of soda,” she added.

The absolute incidence rate of cardiovascular or cerebrovascular events in higher consumers was 346 per 100,000 person-years vs. 314 per 100,000 person-years in nonconsumers.

Further analysis suggested that aspartame intake was particularly associated with increased risk of cerebrovascular events, while acesulfame potassium and sucralose were associated with increased coronary heart disease risk.
 

Study strengths

Dr. Touvier acknowledged that dietary studies, which generally rely on individuals self-reporting food and drink intake, are always hard to interpret. But she said this study used a more reliable method of dietary assessment, with repeated 24-hour dietary records, which were validated by interviews with a trained dietitian and against blood and urinary biomarkers.

And whereas residual confounding cannot be totally excluded, she pointed out that models were adjusted for a wide range of potential sociodemographic, anthropometric, dietary, and lifestyle confounders.

Dr. Touvier also noted that cases of cardiovascular disease in the first 2 years of follow-up were excluded to minimize the bias caused by individuals who maybe have switched to artificial sweeteners because of a cardiovascular issue.

“While this study has many strengths, it cannot on its own prove a causal relationship between artificial sweetener and increased cardiovascular risk,” she added. “We need health agencies to examine all the literature in the field. This is however another important piece of evidence.”

Dr. Touvier says that although observational studies have their issues, they will form the basis of the evidence on the effects of artificial sweeteners on health.

“Randomized studies in this area can only really look at short-term outcomes such as weight gain or biomarker changes. So, we will have to use observational studies together with experimental research to build the evidence. This is what happened with cigarette smoking and lung cancer. That link was not established by randomized trials, but by the accumulation of observational and experimental data.”
 

Different artificial sweeteners may be better?

Commenting on the study, Kim Williams Sr., MD, University of Louisville (Ky.), pointed out that this study included artificial sweeteners that increase insulin or decrease insulin sensitivity, and that insulin spikes increase obesity, insulin resistance, hypertension, and atherosclerosis.

“There are some safer artificial sweeteners that do not increase insulin much or at all, such as erythritol, yacon root/yacon syrup, stevia root, but they weren’t included in the analysis,” Dr. Williams added.

Dr. Sievenpiper explained that most studies on artificial sweeteners look at their consumption in isolation without considering how they compare to the intake of the sugars that they are intended to replace.

“The comparator matters as no food is consumed in a vacuum,” he said.

To address this, Dr. Sievenpiper and colleagues have recently published a systematic review and meta-analysis of the prospective cohort study evidence that shows if exposure to artificially sweetened beverages is modeled in substitution for sugar-sweetened beverages, then they are associated with less coronary heart disease, cardiovascular mortality, and all-cause mortality.

On the other hand, if exposure to artificially sweetened beverages is compared with water, then no difference in these outcomes was seen.

“These observations are more biologically plausible, robust, and reproducible and agree with the evidence for the effect of artificial sweeteners on intermediate risk factors in randomized trials,” Dr. Sievenpiper notes.

His group has also recently published a review of randomized studies showing that when compared with sugar-sweetened beverages, intake of artificially sweetened beverages was associated with small improvements in body weight and cardiometabolic risk factors without evidence of harm.

“I think the context provided by these studies is important, and taken together, the totality of the evidence suggests that artificial sweeteners are likely to be a useful tool in sugar reduction strategies,” Dr. Sievenpiper concludes.

The current study was funded by the European Research Council under the European Union’s Horizon 2020 research and innovation program, French National Cancer Institute, French Ministry of Health, IdEx Université de Paris Cité, Bettencourt-Schueller Foundation Research Prize 2021. The authors have disclosed no relevant financial relationships.

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

Health concerns about the consumption of artificial sweeteners could be strengthened with the publication of a new study linking their intake to increased risk of heart disease and stroke events.

In this latest large-scale, prospective study of French adults, total artificial sweetener intake from all sources was associated with increased risk overall of cardiovascular and cerebrovascular disease.

The study was published online in the BMJ.

The current study differs from those done previously in that it includes artificial sweetener intake from both food and drinks, whereas previous studies have focused mainly on artificial sweetener content of beverages alone.

“Here we have quantified for the first time the global exposure to artificial sweeteners. This is not just beverages but includes the use of tabletop sweeteners, and other foods that include artificial sweeteners such as yogurts and desserts. This is the first time this information has been correlated to risk of heart disease,” senior author Mathilde Touvier, MD, Sorbonne Paris Nord University, told this news organization.

Just over half of the artificial sweetener intake in the study came from drinks, with the rest coming from tabletop sweeteners and foods.

“We included hard cardio- and cerebrovascular clinical endpoints such as a heart attack or stroke, and our results suggest that the amount of artificial sweetener in less than one can of soda could increase the risk of such events,” Dr. Touvier noted.

“This is an important and statistically significant association which shows robustness in all models after adjusting for many other possible confounding factors,” she said.

“There is now mounting evidence correlating artificial sweeteners to weight gain and heart disease,” she concluded. “My advice would be that we all need to try to limit sugar intake, but we should not consider artificial sweeteners as safe alternatives. Rather, we need to try to reduce our need for a sugary taste in our diet.”

But another leading researcher in the field urges caution in interpreting these results.

John Sievenpiper, MD, departments of nutritional sciences and medicine, University of Toronto, commented: “This paper shows the same relationship seen by many other large prospective cohorts which model the intake of artificial sweeteners as baseline or prevalent exposures.

“These observations are well recognized to be at high risk of residual confounding from behavior clustering and reverse causality in which being at risk for cardiovascular disease causes people to consume artificial sweeteners as a strategy to mitigate this risk as opposed to the other way around.”
 

Risk increased by 9%

The current study included 103,388 French adults from the NutriNet-Sante cohort, of whom 37.1% reported consumption of artificial sweeteners. The sweeteners assessed were mainly aspartame (58% of sweetener intake), acesulfame potassium (29%), and sucralose (10%), with the other 3% made up of various other sweeteners including cyclamates and saccharin.

Results showed that over an average 9 years of follow-up, artificial sweetener intake was associated with a 9% increased risk of cardiovascular or cerebrovascular events, including myocardial infarction, acute coronary syndrome, angioplasty, angina, stroke, or transient ischemic attack, with a hazard ratio of 1.09 (95% confidence interval, 1.01-1.18; P = .03).

The average intake of artificial sweeteners among those who reported consuming them was 42.46 mg/day, which corresponds to approximately one individual packet of tabletop sweetener or 100 mL of diet soda.

“We don’t have enough evidence to work out an amount of artificial sweetener that is harmful, but we did show a dose-effect association, with a higher risk of cardiovascular events with higher consumption,” Dr. Touvier said.

“Higher consumption in this study was a mean of 77 mg/day artificial sweetener, which is about 200 mL of soda – just a bit less than one standard can of soda,” she added.

The absolute incidence rate of cardiovascular or cerebrovascular events in higher consumers was 346 per 100,000 person-years vs. 314 per 100,000 person-years in nonconsumers.

Further analysis suggested that aspartame intake was particularly associated with increased risk of cerebrovascular events, while acesulfame potassium and sucralose were associated with increased coronary heart disease risk.
 

Study strengths

Dr. Touvier acknowledged that dietary studies, which generally rely on individuals self-reporting food and drink intake, are always hard to interpret. But she said this study used a more reliable method of dietary assessment, with repeated 24-hour dietary records, which were validated by interviews with a trained dietitian and against blood and urinary biomarkers.

And whereas residual confounding cannot be totally excluded, she pointed out that models were adjusted for a wide range of potential sociodemographic, anthropometric, dietary, and lifestyle confounders.

Dr. Touvier also noted that cases of cardiovascular disease in the first 2 years of follow-up were excluded to minimize the bias caused by individuals who maybe have switched to artificial sweeteners because of a cardiovascular issue.

“While this study has many strengths, it cannot on its own prove a causal relationship between artificial sweetener and increased cardiovascular risk,” she added. “We need health agencies to examine all the literature in the field. This is however another important piece of evidence.”

Dr. Touvier says that although observational studies have their issues, they will form the basis of the evidence on the effects of artificial sweeteners on health.

“Randomized studies in this area can only really look at short-term outcomes such as weight gain or biomarker changes. So, we will have to use observational studies together with experimental research to build the evidence. This is what happened with cigarette smoking and lung cancer. That link was not established by randomized trials, but by the accumulation of observational and experimental data.”
 

Different artificial sweeteners may be better?

Commenting on the study, Kim Williams Sr., MD, University of Louisville (Ky.), pointed out that this study included artificial sweeteners that increase insulin or decrease insulin sensitivity, and that insulin spikes increase obesity, insulin resistance, hypertension, and atherosclerosis.

“There are some safer artificial sweeteners that do not increase insulin much or at all, such as erythritol, yacon root/yacon syrup, stevia root, but they weren’t included in the analysis,” Dr. Williams added.

Dr. Sievenpiper explained that most studies on artificial sweeteners look at their consumption in isolation without considering how they compare to the intake of the sugars that they are intended to replace.

“The comparator matters as no food is consumed in a vacuum,” he said.

To address this, Dr. Sievenpiper and colleagues have recently published a systematic review and meta-analysis of the prospective cohort study evidence that shows if exposure to artificially sweetened beverages is modeled in substitution for sugar-sweetened beverages, then they are associated with less coronary heart disease, cardiovascular mortality, and all-cause mortality.

On the other hand, if exposure to artificially sweetened beverages is compared with water, then no difference in these outcomes was seen.

“These observations are more biologically plausible, robust, and reproducible and agree with the evidence for the effect of artificial sweeteners on intermediate risk factors in randomized trials,” Dr. Sievenpiper notes.

His group has also recently published a review of randomized studies showing that when compared with sugar-sweetened beverages, intake of artificially sweetened beverages was associated with small improvements in body weight and cardiometabolic risk factors without evidence of harm.

“I think the context provided by these studies is important, and taken together, the totality of the evidence suggests that artificial sweeteners are likely to be a useful tool in sugar reduction strategies,” Dr. Sievenpiper concludes.

The current study was funded by the European Research Council under the European Union’s Horizon 2020 research and innovation program, French National Cancer Institute, French Ministry of Health, IdEx Université de Paris Cité, Bettencourt-Schueller Foundation Research Prize 2021. The authors have disclosed no relevant financial relationships.

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

Health concerns about the consumption of artificial sweeteners could be strengthened with the publication of a new study linking their intake to increased risk of heart disease and stroke events.

In this latest large-scale, prospective study of French adults, total artificial sweetener intake from all sources was associated with increased risk overall of cardiovascular and cerebrovascular disease.

The study was published online in the BMJ.

The current study differs from those done previously in that it includes artificial sweetener intake from both food and drinks, whereas previous studies have focused mainly on artificial sweetener content of beverages alone.

“Here we have quantified for the first time the global exposure to artificial sweeteners. This is not just beverages but includes the use of tabletop sweeteners, and other foods that include artificial sweeteners such as yogurts and desserts. This is the first time this information has been correlated to risk of heart disease,” senior author Mathilde Touvier, MD, Sorbonne Paris Nord University, told this news organization.

Just over half of the artificial sweetener intake in the study came from drinks, with the rest coming from tabletop sweeteners and foods.

“We included hard cardio- and cerebrovascular clinical endpoints such as a heart attack or stroke, and our results suggest that the amount of artificial sweetener in less than one can of soda could increase the risk of such events,” Dr. Touvier noted.

“This is an important and statistically significant association which shows robustness in all models after adjusting for many other possible confounding factors,” she said.

“There is now mounting evidence correlating artificial sweeteners to weight gain and heart disease,” she concluded. “My advice would be that we all need to try to limit sugar intake, but we should not consider artificial sweeteners as safe alternatives. Rather, we need to try to reduce our need for a sugary taste in our diet.”

But another leading researcher in the field urges caution in interpreting these results.

John Sievenpiper, MD, departments of nutritional sciences and medicine, University of Toronto, commented: “This paper shows the same relationship seen by many other large prospective cohorts which model the intake of artificial sweeteners as baseline or prevalent exposures.

“These observations are well recognized to be at high risk of residual confounding from behavior clustering and reverse causality in which being at risk for cardiovascular disease causes people to consume artificial sweeteners as a strategy to mitigate this risk as opposed to the other way around.”
 

Risk increased by 9%

The current study included 103,388 French adults from the NutriNet-Sante cohort, of whom 37.1% reported consumption of artificial sweeteners. The sweeteners assessed were mainly aspartame (58% of sweetener intake), acesulfame potassium (29%), and sucralose (10%), with the other 3% made up of various other sweeteners including cyclamates and saccharin.

Results showed that over an average 9 years of follow-up, artificial sweetener intake was associated with a 9% increased risk of cardiovascular or cerebrovascular events, including myocardial infarction, acute coronary syndrome, angioplasty, angina, stroke, or transient ischemic attack, with a hazard ratio of 1.09 (95% confidence interval, 1.01-1.18; P = .03).

The average intake of artificial sweeteners among those who reported consuming them was 42.46 mg/day, which corresponds to approximately one individual packet of tabletop sweetener or 100 mL of diet soda.

“We don’t have enough evidence to work out an amount of artificial sweetener that is harmful, but we did show a dose-effect association, with a higher risk of cardiovascular events with higher consumption,” Dr. Touvier said.

“Higher consumption in this study was a mean of 77 mg/day artificial sweetener, which is about 200 mL of soda – just a bit less than one standard can of soda,” she added.

The absolute incidence rate of cardiovascular or cerebrovascular events in higher consumers was 346 per 100,000 person-years vs. 314 per 100,000 person-years in nonconsumers.

Further analysis suggested that aspartame intake was particularly associated with increased risk of cerebrovascular events, while acesulfame potassium and sucralose were associated with increased coronary heart disease risk.
 

Study strengths

Dr. Touvier acknowledged that dietary studies, which generally rely on individuals self-reporting food and drink intake, are always hard to interpret. But she said this study used a more reliable method of dietary assessment, with repeated 24-hour dietary records, which were validated by interviews with a trained dietitian and against blood and urinary biomarkers.

And whereas residual confounding cannot be totally excluded, she pointed out that models were adjusted for a wide range of potential sociodemographic, anthropometric, dietary, and lifestyle confounders.

Dr. Touvier also noted that cases of cardiovascular disease in the first 2 years of follow-up were excluded to minimize the bias caused by individuals who maybe have switched to artificial sweeteners because of a cardiovascular issue.

“While this study has many strengths, it cannot on its own prove a causal relationship between artificial sweetener and increased cardiovascular risk,” she added. “We need health agencies to examine all the literature in the field. This is however another important piece of evidence.”

Dr. Touvier says that although observational studies have their issues, they will form the basis of the evidence on the effects of artificial sweeteners on health.

“Randomized studies in this area can only really look at short-term outcomes such as weight gain or biomarker changes. So, we will have to use observational studies together with experimental research to build the evidence. This is what happened with cigarette smoking and lung cancer. That link was not established by randomized trials, but by the accumulation of observational and experimental data.”
 

Different artificial sweeteners may be better?

Commenting on the study, Kim Williams Sr., MD, University of Louisville (Ky.), pointed out that this study included artificial sweeteners that increase insulin or decrease insulin sensitivity, and that insulin spikes increase obesity, insulin resistance, hypertension, and atherosclerosis.

“There are some safer artificial sweeteners that do not increase insulin much or at all, such as erythritol, yacon root/yacon syrup, stevia root, but they weren’t included in the analysis,” Dr. Williams added.

Dr. Sievenpiper explained that most studies on artificial sweeteners look at their consumption in isolation without considering how they compare to the intake of the sugars that they are intended to replace.

“The comparator matters as no food is consumed in a vacuum,” he said.

To address this, Dr. Sievenpiper and colleagues have recently published a systematic review and meta-analysis of the prospective cohort study evidence that shows if exposure to artificially sweetened beverages is modeled in substitution for sugar-sweetened beverages, then they are associated with less coronary heart disease, cardiovascular mortality, and all-cause mortality.

On the other hand, if exposure to artificially sweetened beverages is compared with water, then no difference in these outcomes was seen.

“These observations are more biologically plausible, robust, and reproducible and agree with the evidence for the effect of artificial sweeteners on intermediate risk factors in randomized trials,” Dr. Sievenpiper notes.

His group has also recently published a review of randomized studies showing that when compared with sugar-sweetened beverages, intake of artificially sweetened beverages was associated with small improvements in body weight and cardiometabolic risk factors without evidence of harm.

“I think the context provided by these studies is important, and taken together, the totality of the evidence suggests that artificial sweeteners are likely to be a useful tool in sugar reduction strategies,” Dr. Sievenpiper concludes.

The current study was funded by the European Research Council under the European Union’s Horizon 2020 research and innovation program, French National Cancer Institute, French Ministry of Health, IdEx Université de Paris Cité, Bettencourt-Schueller Foundation Research Prize 2021. The authors have disclosed no relevant financial relationships.

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

Imagine that instead of a patient visiting their doctor for blood tests, they could rely on a noninvasive at-home test to predict their risk of diabetes, a disease that affects nearly 15% of U.S. adults (23% of whom are undiagnosed), according to the U.S. Centers for Disease Control and Prevention.

This technology could become a reality thanks to a research team that developed a machine learning algorithm to predict whether people had type 2 diabetes, prediabetes, or no diabetes. In an article published in BMJ Innovations, the researchers describe how their algorithm sorted people into these three categories with 97% accuracy on the basis of measurements of the heart’s electrical activity, determined from an electrocardiogram.

To develop and train their machine learning model – a type of artificial intelligence (AI) that keeps getting smarter over time – researchers used ECG measurements from 1,262 people in Central India. The study participants were part of the Sindhi population, an ethnic group that has been shown in past studies to be at elevated risk for type 2 diabetes.

Why ECG data? Because “cardiovascular abnormalities and diabetes, they go hand in hand,” says study author Manju Mamtani, MD, general manager of M&H Research, San Antonio, and treasurer of the Lata Medical Research Foundation. Subtle cardiovascular changes can occur even early in the development of diabetes.

“ECG has the power to detect these fluctuations, at least in theory, but those fluctuations are so tiny that many times we as humans looking at that might miss it,” says study author Hemant Kulkarni, MD, chief executive officer of M&H Research and president of the Lata Medical Research Foundation. “But the AI, which is powered to detect such specific fluctuations or subtle features, we hypothesized for the study that the AI algorithm might be able to pick those things up. And it did.”

Although this isn’t the first AI algorithm developed to predict diabetes risk, it outperforms previous models, the researchers say.

The team hopes to test and validate the algorithm in a variety of populations so that it can eventually be developed into an accessible, user-friendly technology. They envision that someday their algorithm could be used in smartwatches or other smart devices and could be integrated into telehealth so that people could be screened for diabetes even if they weren’t able to travel to a health care facility for blood testing.

The team is also studying other noninvasive methods of early disease detection and predictive models for adverse outcomes using AI.

“The fact that these algorithms are able to pick up the things of interest and learn on their own and keep learning in the future also adds excitement to their use in these settings,” says Dr. Kulkarni.

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

Imagine that instead of a patient visiting their doctor for blood tests, they could rely on a noninvasive at-home test to predict their risk of diabetes, a disease that affects nearly 15% of U.S. adults (23% of whom are undiagnosed), according to the U.S. Centers for Disease Control and Prevention.

This technology could become a reality thanks to a research team that developed a machine learning algorithm to predict whether people had type 2 diabetes, prediabetes, or no diabetes. In an article published in BMJ Innovations, the researchers describe how their algorithm sorted people into these three categories with 97% accuracy on the basis of measurements of the heart’s electrical activity, determined from an electrocardiogram.

To develop and train their machine learning model – a type of artificial intelligence (AI) that keeps getting smarter over time – researchers used ECG measurements from 1,262 people in Central India. The study participants were part of the Sindhi population, an ethnic group that has been shown in past studies to be at elevated risk for type 2 diabetes.

Why ECG data? Because “cardiovascular abnormalities and diabetes, they go hand in hand,” says study author Manju Mamtani, MD, general manager of M&H Research, San Antonio, and treasurer of the Lata Medical Research Foundation. Subtle cardiovascular changes can occur even early in the development of diabetes.

“ECG has the power to detect these fluctuations, at least in theory, but those fluctuations are so tiny that many times we as humans looking at that might miss it,” says study author Hemant Kulkarni, MD, chief executive officer of M&H Research and president of the Lata Medical Research Foundation. “But the AI, which is powered to detect such specific fluctuations or subtle features, we hypothesized for the study that the AI algorithm might be able to pick those things up. And it did.”

Although this isn’t the first AI algorithm developed to predict diabetes risk, it outperforms previous models, the researchers say.

The team hopes to test and validate the algorithm in a variety of populations so that it can eventually be developed into an accessible, user-friendly technology. They envision that someday their algorithm could be used in smartwatches or other smart devices and could be integrated into telehealth so that people could be screened for diabetes even if they weren’t able to travel to a health care facility for blood testing.

The team is also studying other noninvasive methods of early disease detection and predictive models for adverse outcomes using AI.

“The fact that these algorithms are able to pick up the things of interest and learn on their own and keep learning in the future also adds excitement to their use in these settings,” says Dr. Kulkarni.

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

Imagine that instead of a patient visiting their doctor for blood tests, they could rely on a noninvasive at-home test to predict their risk of diabetes, a disease that affects nearly 15% of U.S. adults (23% of whom are undiagnosed), according to the U.S. Centers for Disease Control and Prevention.

This technology could become a reality thanks to a research team that developed a machine learning algorithm to predict whether people had type 2 diabetes, prediabetes, or no diabetes. In an article published in BMJ Innovations, the researchers describe how their algorithm sorted people into these three categories with 97% accuracy on the basis of measurements of the heart’s electrical activity, determined from an electrocardiogram.

To develop and train their machine learning model – a type of artificial intelligence (AI) that keeps getting smarter over time – researchers used ECG measurements from 1,262 people in Central India. The study participants were part of the Sindhi population, an ethnic group that has been shown in past studies to be at elevated risk for type 2 diabetes.

Why ECG data? Because “cardiovascular abnormalities and diabetes, they go hand in hand,” says study author Manju Mamtani, MD, general manager of M&H Research, San Antonio, and treasurer of the Lata Medical Research Foundation. Subtle cardiovascular changes can occur even early in the development of diabetes.

“ECG has the power to detect these fluctuations, at least in theory, but those fluctuations are so tiny that many times we as humans looking at that might miss it,” says study author Hemant Kulkarni, MD, chief executive officer of M&H Research and president of the Lata Medical Research Foundation. “But the AI, which is powered to detect such specific fluctuations or subtle features, we hypothesized for the study that the AI algorithm might be able to pick those things up. And it did.”

Although this isn’t the first AI algorithm developed to predict diabetes risk, it outperforms previous models, the researchers say.

The team hopes to test and validate the algorithm in a variety of populations so that it can eventually be developed into an accessible, user-friendly technology. They envision that someday their algorithm could be used in smartwatches or other smart devices and could be integrated into telehealth so that people could be screened for diabetes even if they weren’t able to travel to a health care facility for blood testing.

The team is also studying other noninvasive methods of early disease detection and predictive models for adverse outcomes using AI.

“The fact that these algorithms are able to pick up the things of interest and learn on their own and keep learning in the future also adds excitement to their use in these settings,” says Dr. Kulkarni.

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

Certain ultraprocessed foods – especially candy, prepackaged pastries, and frozen desserts – could be “gateway foods” for adolescents, leading them to increase their intake of other unhealthy foods, a new study suggests.

“For teens, gateway ultraprocessed foods (candy, store pastries, frozen desserts) should be prioritized for preventive dietary interventions as they increase intake across all other UPFs,” lead researcher Maria Balhara said in an interview.

“The good news,” said Ms. Balhara, is that even small changes, such as reducing how often gateway foods are consumed, may reduce overall intake of unhealthy foods and have a “big impact” on overall health.

Ms. Balhara has a unique perspective on adolescent eating habits: She’s 16 years old, from Florida, and conducted the study while dual-enrolled at Broward College and Cooper City High School.

Her study was released Sept. 7 ahead of presentation at the American Heart Association Hypertension Scientific Sessions 2022 in San Diego.
 

Blame the pandemic?

Over the past 30 years, there’s been a steady increase in consumption of UPFs worldwide, coupled with mounting evidence that diets rich in UPFs raise the risk for several chronic diseases, including weight gain, hypertension, and increased risk for heart disease and premature death.

For her research, Ms. Balhara asked 315 teenagers (42% male) from 12 high schools in South Florida how often they consumed UPFs over two time periods – before COVID in 2019 and after COVID restrictions were eased in 2022 – using a survey that she developed called the Processed Intake Evaluation (PIE).

More than 2 in 5 teens (43%) increased their consumption of UPFs between 2019 and 2022.

During this time, increased consumption of frozen desserts was associated with an 11% increase in consumption of all other UPFs, whereas increased consumption of prepackaged pastries and candy was associated with a 12% and 31%, respectively, increase in consumption of all other UPFs, Ms. Balhara found.

Encouragingly, 57% of teens decreased their consumption of UPFs between 2019 and 2022.

During this time, decreased consumption of processed meats was associated with an 8% decrease in consumption of all other UPFs, whereas decreased consumption of white bread and biscuits was associated with a 9% and 10%, respectively, decrease in consumption of all other UPFs.

The results provide initial evidence for a new “gateway food model,” Ms. Balhara told this news organization, in which certain UPFs, when increased, drive overall consumption of all UPFs among teens.

Limitations of the study include the self-reported dietary data and the fact that the PIE survey has not been validated.
 

Not all UPFs are bad

“I commend Ms. Balhara for her project, which highlights the importance of establishing good dietary patterns early in life,” Donna K. Arnett, PhD, past president of the AHA, said in a news release.

“The relationship between poor dietary quality and cardiovascular risk factors is well-established. While this is a small, preliminary study, it’s an important topic to continue to investigate and help us understand ways we can influence dietary behaviors to promote optimal cardiovascular health for all ages,” said Dr. Arnett, executive vice president for academic affairs and provost at the University of South Carolina, Columbia.

Offering perspective on the study, Taylor C. Wallace, PhD, with the department of nutrition and food studies, George Mason University, Fairfax, Va., made the point that “food processing and ultraprocessed foods aren’t the problem. The problem is the types of ultraprocessed foods on the market that people consume.”

“Remember, non-fat, vitamin D fortified yogurt is also ‘ultra-processed,’ and it’s very healthy,” he told this news organization.

Dr. Wallace said that it’s no surprise that teens increased their intake of UPFs during the pandemic.

“Of course, people increased processed food intake during the pandemic. Processed foods are shelf stable at a time when grocery stores were running out of things and supply chains weren’t able to keep up. Also, many were depressed and use food to indulge,” he noted.

The study had no funding. Ms. Balhara has no relevant disclosures. Dr. Wallace is principal and CEO of Think Healthy Group; chief food and nutrition scientist with Produce for Better Health Foundation; editor, Journal of Dietary Supplements; deputy editor, Journal of the American College of Nutrition; nutrition section editor, Annals of Medicine; and an advisory board member with Forbes Health.

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

Certain ultraprocessed foods – especially candy, prepackaged pastries, and frozen desserts – could be “gateway foods” for adolescents, leading them to increase their intake of other unhealthy foods, a new study suggests.

“For teens, gateway ultraprocessed foods (candy, store pastries, frozen desserts) should be prioritized for preventive dietary interventions as they increase intake across all other UPFs,” lead researcher Maria Balhara said in an interview.

“The good news,” said Ms. Balhara, is that even small changes, such as reducing how often gateway foods are consumed, may reduce overall intake of unhealthy foods and have a “big impact” on overall health.

Ms. Balhara has a unique perspective on adolescent eating habits: She’s 16 years old, from Florida, and conducted the study while dual-enrolled at Broward College and Cooper City High School.

Her study was released Sept. 7 ahead of presentation at the American Heart Association Hypertension Scientific Sessions 2022 in San Diego.
 

Blame the pandemic?

Over the past 30 years, there’s been a steady increase in consumption of UPFs worldwide, coupled with mounting evidence that diets rich in UPFs raise the risk for several chronic diseases, including weight gain, hypertension, and increased risk for heart disease and premature death.

For her research, Ms. Balhara asked 315 teenagers (42% male) from 12 high schools in South Florida how often they consumed UPFs over two time periods – before COVID in 2019 and after COVID restrictions were eased in 2022 – using a survey that she developed called the Processed Intake Evaluation (PIE).

More than 2 in 5 teens (43%) increased their consumption of UPFs between 2019 and 2022.

During this time, increased consumption of frozen desserts was associated with an 11% increase in consumption of all other UPFs, whereas increased consumption of prepackaged pastries and candy was associated with a 12% and 31%, respectively, increase in consumption of all other UPFs, Ms. Balhara found.

Encouragingly, 57% of teens decreased their consumption of UPFs between 2019 and 2022.

During this time, decreased consumption of processed meats was associated with an 8% decrease in consumption of all other UPFs, whereas decreased consumption of white bread and biscuits was associated with a 9% and 10%, respectively, decrease in consumption of all other UPFs.

The results provide initial evidence for a new “gateway food model,” Ms. Balhara told this news organization, in which certain UPFs, when increased, drive overall consumption of all UPFs among teens.

Limitations of the study include the self-reported dietary data and the fact that the PIE survey has not been validated.
 

Not all UPFs are bad

“I commend Ms. Balhara for her project, which highlights the importance of establishing good dietary patterns early in life,” Donna K. Arnett, PhD, past president of the AHA, said in a news release.

“The relationship between poor dietary quality and cardiovascular risk factors is well-established. While this is a small, preliminary study, it’s an important topic to continue to investigate and help us understand ways we can influence dietary behaviors to promote optimal cardiovascular health for all ages,” said Dr. Arnett, executive vice president for academic affairs and provost at the University of South Carolina, Columbia.

Offering perspective on the study, Taylor C. Wallace, PhD, with the department of nutrition and food studies, George Mason University, Fairfax, Va., made the point that “food processing and ultraprocessed foods aren’t the problem. The problem is the types of ultraprocessed foods on the market that people consume.”

“Remember, non-fat, vitamin D fortified yogurt is also ‘ultra-processed,’ and it’s very healthy,” he told this news organization.

Dr. Wallace said that it’s no surprise that teens increased their intake of UPFs during the pandemic.

“Of course, people increased processed food intake during the pandemic. Processed foods are shelf stable at a time when grocery stores were running out of things and supply chains weren’t able to keep up. Also, many were depressed and use food to indulge,” he noted.

The study had no funding. Ms. Balhara has no relevant disclosures. Dr. Wallace is principal and CEO of Think Healthy Group; chief food and nutrition scientist with Produce for Better Health Foundation; editor, Journal of Dietary Supplements; deputy editor, Journal of the American College of Nutrition; nutrition section editor, Annals of Medicine; and an advisory board member with Forbes Health.

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

Certain ultraprocessed foods – especially candy, prepackaged pastries, and frozen desserts – could be “gateway foods” for adolescents, leading them to increase their intake of other unhealthy foods, a new study suggests.

“For teens, gateway ultraprocessed foods (candy, store pastries, frozen desserts) should be prioritized for preventive dietary interventions as they increase intake across all other UPFs,” lead researcher Maria Balhara said in an interview.

“The good news,” said Ms. Balhara, is that even small changes, such as reducing how often gateway foods are consumed, may reduce overall intake of unhealthy foods and have a “big impact” on overall health.

Ms. Balhara has a unique perspective on adolescent eating habits: She’s 16 years old, from Florida, and conducted the study while dual-enrolled at Broward College and Cooper City High School.

Her study was released Sept. 7 ahead of presentation at the American Heart Association Hypertension Scientific Sessions 2022 in San Diego.
 

Blame the pandemic?

Over the past 30 years, there’s been a steady increase in consumption of UPFs worldwide, coupled with mounting evidence that diets rich in UPFs raise the risk for several chronic diseases, including weight gain, hypertension, and increased risk for heart disease and premature death.

For her research, Ms. Balhara asked 315 teenagers (42% male) from 12 high schools in South Florida how often they consumed UPFs over two time periods – before COVID in 2019 and after COVID restrictions were eased in 2022 – using a survey that she developed called the Processed Intake Evaluation (PIE).

More than 2 in 5 teens (43%) increased their consumption of UPFs between 2019 and 2022.

During this time, increased consumption of frozen desserts was associated with an 11% increase in consumption of all other UPFs, whereas increased consumption of prepackaged pastries and candy was associated with a 12% and 31%, respectively, increase in consumption of all other UPFs, Ms. Balhara found.

Encouragingly, 57% of teens decreased their consumption of UPFs between 2019 and 2022.

During this time, decreased consumption of processed meats was associated with an 8% decrease in consumption of all other UPFs, whereas decreased consumption of white bread and biscuits was associated with a 9% and 10%, respectively, decrease in consumption of all other UPFs.

The results provide initial evidence for a new “gateway food model,” Ms. Balhara told this news organization, in which certain UPFs, when increased, drive overall consumption of all UPFs among teens.

Limitations of the study include the self-reported dietary data and the fact that the PIE survey has not been validated.
 

Not all UPFs are bad

“I commend Ms. Balhara for her project, which highlights the importance of establishing good dietary patterns early in life,” Donna K. Arnett, PhD, past president of the AHA, said in a news release.

“The relationship between poor dietary quality and cardiovascular risk factors is well-established. While this is a small, preliminary study, it’s an important topic to continue to investigate and help us understand ways we can influence dietary behaviors to promote optimal cardiovascular health for all ages,” said Dr. Arnett, executive vice president for academic affairs and provost at the University of South Carolina, Columbia.

Offering perspective on the study, Taylor C. Wallace, PhD, with the department of nutrition and food studies, George Mason University, Fairfax, Va., made the point that “food processing and ultraprocessed foods aren’t the problem. The problem is the types of ultraprocessed foods on the market that people consume.”

“Remember, non-fat, vitamin D fortified yogurt is also ‘ultra-processed,’ and it’s very healthy,” he told this news organization.

Dr. Wallace said that it’s no surprise that teens increased their intake of UPFs during the pandemic.

“Of course, people increased processed food intake during the pandemic. Processed foods are shelf stable at a time when grocery stores were running out of things and supply chains weren’t able to keep up. Also, many were depressed and use food to indulge,” he noted.

The study had no funding. Ms. Balhara has no relevant disclosures. Dr. Wallace is principal and CEO of Think Healthy Group; chief food and nutrition scientist with Produce for Better Health Foundation; editor, Journal of Dietary Supplements; deputy editor, Journal of the American College of Nutrition; nutrition section editor, Annals of Medicine; and an advisory board member with Forbes Health.

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

Two large studies out of the United Kingdom and Norway show vitamin D supplementation has no benefit – as low dose, high dose, or in the form of cod liver oil supplementation – in preventing COVID-19 or acute respiratory tract infections, regardless of whether individuals are deficient or not.

copyright Joss/Fotolia.com

The studies, published in the BMJ, underscore that “vaccination is still the most effective way to protect people from COVID-19, and vitamin D and cod liver oil supplementation should not be offered to healthy people with normal vitamin D levels,” writes Peter Bergman, MD, of the Karolinska Institute, Stockholm, in an editorial published alongside the studies.

Suboptimal levels of vitamin D are known to be associated with an increased risk of acute respiratory infections, and some observational studies have linked low 25-hydroxyvitamin D (25[OH]D) with more severe COVID-19; however, data on a possible protective effect of vitamin D supplementation in preventing infection have been inconsistent.
 

U.K. study compares doses

To further investigate the relationship with infections, including COVID-19, in a large cohort, the authors of the first of the two BMJ studies, a phase 3 open-label trial, enrolled 6,200 people in the United Kingdom aged 16 and older between December 2020 and June 2021 who were not taking vitamin D supplements at baseline.

Half of participants were offered a finger-prick blood test, and of the 2,674 who accepted, 86.3% were found to have low concentrations of 25(OH)D (< 75 nmol/L). These participants were provided with vitamin D supplementation at a lower (800 IU/day; n = 1328) or higher dose (3,200 IU/day; n = 1,346) for 6 months. The other half of the group received no tests or supplements.

The results showed minimal differences between groups in terms of rates of developing at least one acute respiratory infection, which occurred in 5% of those in the lower-dose group, 5.7% in the higher-dose group, and 4.6% of participants not offered supplementation.

Similarly, there were no significant differences in the development of real-time PCR-confirmed COVID-19, with rates of 3.6% in the lower-dose group, 3.0% in the higher-dose group, and 2.6% in the group not offered supplementation.

The study is “the first phase 3 randomized controlled trial to evaluate the effectiveness of a test-and-treat approach for correction of suboptimal vitamin D status to prevent acute respiratory tract infections,” report the authors, led by Adrian R. Martineau, MD, PhD, of Barts and The London School of Medicine and Dentistry, Queen Mary University of London.

While uptake and supplementation in the study were favorable, “no statistically significant effect of either dose was seen on the primary outcome of swab test, doctor-confirmed acute respiratory tract infection, or on the major secondary outcome of swab test-confirmed COVID-19,” they conclude.
 

Traditional use of cod liver oil of benefit?

In the second study, researchers in Norway, led by Arne Soraas, MD, PhD, of the department of microbiology, Oslo University Hospital, evaluated whether that country’s long-held tradition of consuming cod liver oil during the winter to prevent vitamin D deficiency could affect the development of COVID-19 or outcomes.

For the Cod Liver Oil for COVID-19 Prevention Study (CLOC), a large cohort of 34,601 adults with a mean age of 44.9 years who were not taking daily vitamin D supplements were randomized to receive 5 mL/day of cod liver oil, representing a surrogate dose of 400 IU/day of vitamin D (n = 17,278), or placebo (n = 17,323) for up to 6 months.

In contrast with the first study, the vast majority of patients in the CLOC study (86%) had adequate vitamin D levels, defined as greater than 50 nmol/L, at baseline.

Again, however, the results showed no association between increased vitamin D supplementation with cod liver oil and PCR-confirmed COVID-19 or acute respiratory infections, with approximately 1.3% in each group testing positive for COVID-19 over a median of 164 days.

Supplementation with cod liver oil was also not associated with a reduced risk of any of the coprimary endpoints, including other acute respiratory infections.

“Daily supplementation with cod liver oil, a low-dose vitamin D, eicosapentaenoic acid, and docosahexaenoic acid supplement, for 6 months during the SARS-CoV-2pandemic among Norwegian adults did not reduce the incidence of SARS-CoV-2 infection, serious COVID-19, or other acute respiratory infections,” the authors report.
 

Key study limitations

In his editorial, Dr. Bergman underscores the limitations of two studies – also acknowledged by the authors – including the key confounding role of vaccines that emerged during the studies.

“The null findings of the studies should be interpreted in the context of a highly effective vaccine rolled out during both studies,” Dr. Bergman writes.

In the U.K. study, for instance, whereas only 1.2% of participants were vaccinated at baseline, the rate soared to 89.1% having received at least one dose by study end, potentially masking any effect of vitamin D, he says.

Additionally, for the Norway study, Dr. Bergman notes that cod liver oil also contains a substantial amount of vitamin A, which can be a potent immunomodulator.

“Excessive intake of vitamin A can cause adverse effects and may also interfere with vitamin D-mediated effects on the immune system,” he writes.

With two recent large meta-analyses showing benefits of vitamin D supplementation to be specifically among people who are vitamin D deficient, “a pragmatic approach for the clinician could be to focus on risk groups” for supplementation, Dr. Bergman writes.

“[These include] those who could be tested before supplementation, including people with dark skin, or skin that is rarely exposed to the sun, pregnant women, and elderly people with chronic diseases.”

The U.K. trial was supported by Barts Charity, Pharma Nord, the Fischer Family Foundation, DSM Nutritional Products, the Exilarch’s Foundation, the Karl R. Pfleger Foundation, the AIM Foundation, Synergy Biologics, Cytoplan, the Clinical Research Network of the U.K. National Institute for Health and Care Research, the HDR UK BREATHE Hub, the U.K. Research and Innovation Industrial Strategy Challenge Fund, Thornton & Ross, Warburtons, Hyphens Pharma, and philanthropist Matthew Isaacs.

The CLOC trial was funded by Orkla Health, the manufacturer of the cod liver oil used in the trial. Dr. Bergman has reported no relevant financial relationships.

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

Two large studies out of the United Kingdom and Norway show vitamin D supplementation has no benefit – as low dose, high dose, or in the form of cod liver oil supplementation – in preventing COVID-19 or acute respiratory tract infections, regardless of whether individuals are deficient or not.

copyright Joss/Fotolia.com

The studies, published in the BMJ, underscore that “vaccination is still the most effective way to protect people from COVID-19, and vitamin D and cod liver oil supplementation should not be offered to healthy people with normal vitamin D levels,” writes Peter Bergman, MD, of the Karolinska Institute, Stockholm, in an editorial published alongside the studies.

Suboptimal levels of vitamin D are known to be associated with an increased risk of acute respiratory infections, and some observational studies have linked low 25-hydroxyvitamin D (25[OH]D) with more severe COVID-19; however, data on a possible protective effect of vitamin D supplementation in preventing infection have been inconsistent.
 

U.K. study compares doses

To further investigate the relationship with infections, including COVID-19, in a large cohort, the authors of the first of the two BMJ studies, a phase 3 open-label trial, enrolled 6,200 people in the United Kingdom aged 16 and older between December 2020 and June 2021 who were not taking vitamin D supplements at baseline.

Half of participants were offered a finger-prick blood test, and of the 2,674 who accepted, 86.3% were found to have low concentrations of 25(OH)D (< 75 nmol/L). These participants were provided with vitamin D supplementation at a lower (800 IU/day; n = 1328) or higher dose (3,200 IU/day; n = 1,346) for 6 months. The other half of the group received no tests or supplements.

The results showed minimal differences between groups in terms of rates of developing at least one acute respiratory infection, which occurred in 5% of those in the lower-dose group, 5.7% in the higher-dose group, and 4.6% of participants not offered supplementation.

Similarly, there were no significant differences in the development of real-time PCR-confirmed COVID-19, with rates of 3.6% in the lower-dose group, 3.0% in the higher-dose group, and 2.6% in the group not offered supplementation.

The study is “the first phase 3 randomized controlled trial to evaluate the effectiveness of a test-and-treat approach for correction of suboptimal vitamin D status to prevent acute respiratory tract infections,” report the authors, led by Adrian R. Martineau, MD, PhD, of Barts and The London School of Medicine and Dentistry, Queen Mary University of London.

While uptake and supplementation in the study were favorable, “no statistically significant effect of either dose was seen on the primary outcome of swab test, doctor-confirmed acute respiratory tract infection, or on the major secondary outcome of swab test-confirmed COVID-19,” they conclude.
 

Traditional use of cod liver oil of benefit?

In the second study, researchers in Norway, led by Arne Soraas, MD, PhD, of the department of microbiology, Oslo University Hospital, evaluated whether that country’s long-held tradition of consuming cod liver oil during the winter to prevent vitamin D deficiency could affect the development of COVID-19 or outcomes.

For the Cod Liver Oil for COVID-19 Prevention Study (CLOC), a large cohort of 34,601 adults with a mean age of 44.9 years who were not taking daily vitamin D supplements were randomized to receive 5 mL/day of cod liver oil, representing a surrogate dose of 400 IU/day of vitamin D (n = 17,278), or placebo (n = 17,323) for up to 6 months.

In contrast with the first study, the vast majority of patients in the CLOC study (86%) had adequate vitamin D levels, defined as greater than 50 nmol/L, at baseline.

Again, however, the results showed no association between increased vitamin D supplementation with cod liver oil and PCR-confirmed COVID-19 or acute respiratory infections, with approximately 1.3% in each group testing positive for COVID-19 over a median of 164 days.

Supplementation with cod liver oil was also not associated with a reduced risk of any of the coprimary endpoints, including other acute respiratory infections.

“Daily supplementation with cod liver oil, a low-dose vitamin D, eicosapentaenoic acid, and docosahexaenoic acid supplement, for 6 months during the SARS-CoV-2pandemic among Norwegian adults did not reduce the incidence of SARS-CoV-2 infection, serious COVID-19, or other acute respiratory infections,” the authors report.
 

Key study limitations

In his editorial, Dr. Bergman underscores the limitations of two studies – also acknowledged by the authors – including the key confounding role of vaccines that emerged during the studies.

“The null findings of the studies should be interpreted in the context of a highly effective vaccine rolled out during both studies,” Dr. Bergman writes.

In the U.K. study, for instance, whereas only 1.2% of participants were vaccinated at baseline, the rate soared to 89.1% having received at least one dose by study end, potentially masking any effect of vitamin D, he says.

Additionally, for the Norway study, Dr. Bergman notes that cod liver oil also contains a substantial amount of vitamin A, which can be a potent immunomodulator.

“Excessive intake of vitamin A can cause adverse effects and may also interfere with vitamin D-mediated effects on the immune system,” he writes.

With two recent large meta-analyses showing benefits of vitamin D supplementation to be specifically among people who are vitamin D deficient, “a pragmatic approach for the clinician could be to focus on risk groups” for supplementation, Dr. Bergman writes.

“[These include] those who could be tested before supplementation, including people with dark skin, or skin that is rarely exposed to the sun, pregnant women, and elderly people with chronic diseases.”

The U.K. trial was supported by Barts Charity, Pharma Nord, the Fischer Family Foundation, DSM Nutritional Products, the Exilarch’s Foundation, the Karl R. Pfleger Foundation, the AIM Foundation, Synergy Biologics, Cytoplan, the Clinical Research Network of the U.K. National Institute for Health and Care Research, the HDR UK BREATHE Hub, the U.K. Research and Innovation Industrial Strategy Challenge Fund, Thornton & Ross, Warburtons, Hyphens Pharma, and philanthropist Matthew Isaacs.

The CLOC trial was funded by Orkla Health, the manufacturer of the cod liver oil used in the trial. Dr. Bergman has reported no relevant financial relationships.

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

Two large studies out of the United Kingdom and Norway show vitamin D supplementation has no benefit – as low dose, high dose, or in the form of cod liver oil supplementation – in preventing COVID-19 or acute respiratory tract infections, regardless of whether individuals are deficient or not.

copyright Joss/Fotolia.com

The studies, published in the BMJ, underscore that “vaccination is still the most effective way to protect people from COVID-19, and vitamin D and cod liver oil supplementation should not be offered to healthy people with normal vitamin D levels,” writes Peter Bergman, MD, of the Karolinska Institute, Stockholm, in an editorial published alongside the studies.

Suboptimal levels of vitamin D are known to be associated with an increased risk of acute respiratory infections, and some observational studies have linked low 25-hydroxyvitamin D (25[OH]D) with more severe COVID-19; however, data on a possible protective effect of vitamin D supplementation in preventing infection have been inconsistent.
 

U.K. study compares doses

To further investigate the relationship with infections, including COVID-19, in a large cohort, the authors of the first of the two BMJ studies, a phase 3 open-label trial, enrolled 6,200 people in the United Kingdom aged 16 and older between December 2020 and June 2021 who were not taking vitamin D supplements at baseline.

Half of participants were offered a finger-prick blood test, and of the 2,674 who accepted, 86.3% were found to have low concentrations of 25(OH)D (< 75 nmol/L). These participants were provided with vitamin D supplementation at a lower (800 IU/day; n = 1328) or higher dose (3,200 IU/day; n = 1,346) for 6 months. The other half of the group received no tests or supplements.

The results showed minimal differences between groups in terms of rates of developing at least one acute respiratory infection, which occurred in 5% of those in the lower-dose group, 5.7% in the higher-dose group, and 4.6% of participants not offered supplementation.

Similarly, there were no significant differences in the development of real-time PCR-confirmed COVID-19, with rates of 3.6% in the lower-dose group, 3.0% in the higher-dose group, and 2.6% in the group not offered supplementation.

The study is “the first phase 3 randomized controlled trial to evaluate the effectiveness of a test-and-treat approach for correction of suboptimal vitamin D status to prevent acute respiratory tract infections,” report the authors, led by Adrian R. Martineau, MD, PhD, of Barts and The London School of Medicine and Dentistry, Queen Mary University of London.

While uptake and supplementation in the study were favorable, “no statistically significant effect of either dose was seen on the primary outcome of swab test, doctor-confirmed acute respiratory tract infection, or on the major secondary outcome of swab test-confirmed COVID-19,” they conclude.
 

Traditional use of cod liver oil of benefit?

In the second study, researchers in Norway, led by Arne Soraas, MD, PhD, of the department of microbiology, Oslo University Hospital, evaluated whether that country’s long-held tradition of consuming cod liver oil during the winter to prevent vitamin D deficiency could affect the development of COVID-19 or outcomes.

For the Cod Liver Oil for COVID-19 Prevention Study (CLOC), a large cohort of 34,601 adults with a mean age of 44.9 years who were not taking daily vitamin D supplements were randomized to receive 5 mL/day of cod liver oil, representing a surrogate dose of 400 IU/day of vitamin D (n = 17,278), or placebo (n = 17,323) for up to 6 months.

In contrast with the first study, the vast majority of patients in the CLOC study (86%) had adequate vitamin D levels, defined as greater than 50 nmol/L, at baseline.

Again, however, the results showed no association between increased vitamin D supplementation with cod liver oil and PCR-confirmed COVID-19 or acute respiratory infections, with approximately 1.3% in each group testing positive for COVID-19 over a median of 164 days.

Supplementation with cod liver oil was also not associated with a reduced risk of any of the coprimary endpoints, including other acute respiratory infections.

“Daily supplementation with cod liver oil, a low-dose vitamin D, eicosapentaenoic acid, and docosahexaenoic acid supplement, for 6 months during the SARS-CoV-2pandemic among Norwegian adults did not reduce the incidence of SARS-CoV-2 infection, serious COVID-19, or other acute respiratory infections,” the authors report.
 

Key study limitations

In his editorial, Dr. Bergman underscores the limitations of two studies – also acknowledged by the authors – including the key confounding role of vaccines that emerged during the studies.

“The null findings of the studies should be interpreted in the context of a highly effective vaccine rolled out during both studies,” Dr. Bergman writes.

In the U.K. study, for instance, whereas only 1.2% of participants were vaccinated at baseline, the rate soared to 89.1% having received at least one dose by study end, potentially masking any effect of vitamin D, he says.

Additionally, for the Norway study, Dr. Bergman notes that cod liver oil also contains a substantial amount of vitamin A, which can be a potent immunomodulator.

“Excessive intake of vitamin A can cause adverse effects and may also interfere with vitamin D-mediated effects on the immune system,” he writes.

With two recent large meta-analyses showing benefits of vitamin D supplementation to be specifically among people who are vitamin D deficient, “a pragmatic approach for the clinician could be to focus on risk groups” for supplementation, Dr. Bergman writes.

“[These include] those who could be tested before supplementation, including people with dark skin, or skin that is rarely exposed to the sun, pregnant women, and elderly people with chronic diseases.”

The U.K. trial was supported by Barts Charity, Pharma Nord, the Fischer Family Foundation, DSM Nutritional Products, the Exilarch’s Foundation, the Karl R. Pfleger Foundation, the AIM Foundation, Synergy Biologics, Cytoplan, the Clinical Research Network of the U.K. National Institute for Health and Care Research, the HDR UK BREATHE Hub, the U.K. Research and Innovation Industrial Strategy Challenge Fund, Thornton & Ross, Warburtons, Hyphens Pharma, and philanthropist Matthew Isaacs.

The CLOC trial was funded by Orkla Health, the manufacturer of the cod liver oil used in the trial. Dr. Bergman has reported no relevant financial relationships.

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

Among men who have not been vaccinated against COVID-19, having low levels of testosterone may increase the risk of hospitalization from the disease – but hormone therapy appears to reduce the likelihood of severe COVID, researchers have found.

Low testosterone has long been linked to multiple chronic conditions, including obesity, heart disease, and type 2 diabetes, as well as acute conditions, such as heart attack and stroke. A study published earlier in the pandemic suggested that suppressing the sex hormone might protect against COVID-19. The new study, published in JAMA Network Open, is among the first to suggest a link between low testosterone and the risk for severe COVID.

Researchers at Washington University in St. Louis evaluated data from 723 unvaccinated men who had been infected with SARS-CoV-2. Of those, 116 had been diagnosed with hypogonadism, and 180 were receiving testosterone supplementation.

The study found that men whose testosterone levels were less than 200 ng/dL were 2.4 times more likely to experience a severe case of COVID-19 that required hospitalization than were those with normal levels of the hormone. The study accounted for the fact that participants with low testosterone were also more likely to have comorbidities such as diabetes and obesity.

Paresh Dandona, MD, PhD, distinguished professor of medicine and endocrinology at the State University of New York at Buffalo, called the findings “very exciting” and “fundamental.”

“In the world of hypogonadism, this is the first to show that low testosterone makes you vulnerable” to COVID, added Dr. Dandona, who was not involved with the research.

Men who were receiving hormone replacement therapy were at lower risk of hospitalization, compared with those who were not receiving treatment, the study found.

“Testosterone therapy seemed to negate the harmful effects of COVID,” said Sandeep Dhindsa, MD, an endocrinologist at Saint Louis University and lead author of the study.

Approximately 50% more men have died from confirmed COVID-19 than women since the start of the pandemic, according to the Sex, Gender and COVID-19 Project. Previous findings suggesting that sex may be a risk factor for death from COVID prompted researchers to consider whether hormones may play a role in the increased risk among men and whether treatments that suppress androgen levels could cut hospitalizations, but researchers consistently found that androgen suppression was not effective.

“There are other reasons women might be doing better – they may have followed public health guidelines a lot better,” according to Abhinav Diwan, MD, professor of medicine at Washington University in St. Louis, who helped conduct the new study. “It may be chromosomal and not necessarily just hormonal. The differences between men and women go beyond one factor.”

According to the researchers, the findings do not suggest that hormone therapy be used as a preventive measure against COVID.

“We don’t want patients to get excited and start to ask their doctors for testosterone,” Dr. Dhindsa said.

However, viewing low testosterone as a risk factor for COVID could be considered a shift in thinking for some clinicians, according to Dr. Dandana.

“All obese and all [men with] type 2 diabetes should be tested for testosterone, which is the practice in my clinic right now, even if they have no symptoms,” Dr. Dandana said. “Certainly, those with symptoms [of low testosterone] but no diagnosis, they should be tested, too.”

Participants in the study were infected with SARS-CoV-2 early in 2020, before vaccines were available. The researchers did not assess whether the rate of hospitalizations among participants with low testosterone would be different had they been vaccinated.

“Whatever benefits we saw with testosterone might be minor compared to getting the vaccine,” Dr. Dhindsa said.

Dr. Diwan agreed. “COVID hospitalization continues to be a problem, the strains are evolving, and new vaccines are coming in,” he said. “The bottom line is to get vaccinated.”

Dr. Dhindsa has received personal fees from Bayer and Acerus Pharmaceuticals and grants from Clarus Therapeutics outside the submitted work. Dr. Diwan has served as a consultant for the interpretation of echocardiograms for clinical trials for Clario (previously ERT) and has received nonfinancial support from Dewpoint Therapeutics outside the submitted work. Dr. Dandana has disclosed no relevant financial relationships.

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

Among men who have not been vaccinated against COVID-19, having low levels of testosterone may increase the risk of hospitalization from the disease – but hormone therapy appears to reduce the likelihood of severe COVID, researchers have found.

Low testosterone has long been linked to multiple chronic conditions, including obesity, heart disease, and type 2 diabetes, as well as acute conditions, such as heart attack and stroke. A study published earlier in the pandemic suggested that suppressing the sex hormone might protect against COVID-19. The new study, published in JAMA Network Open, is among the first to suggest a link between low testosterone and the risk for severe COVID.

Researchers at Washington University in St. Louis evaluated data from 723 unvaccinated men who had been infected with SARS-CoV-2. Of those, 116 had been diagnosed with hypogonadism, and 180 were receiving testosterone supplementation.

The study found that men whose testosterone levels were less than 200 ng/dL were 2.4 times more likely to experience a severe case of COVID-19 that required hospitalization than were those with normal levels of the hormone. The study accounted for the fact that participants with low testosterone were also more likely to have comorbidities such as diabetes and obesity.

Paresh Dandona, MD, PhD, distinguished professor of medicine and endocrinology at the State University of New York at Buffalo, called the findings “very exciting” and “fundamental.”

“In the world of hypogonadism, this is the first to show that low testosterone makes you vulnerable” to COVID, added Dr. Dandona, who was not involved with the research.

Men who were receiving hormone replacement therapy were at lower risk of hospitalization, compared with those who were not receiving treatment, the study found.

“Testosterone therapy seemed to negate the harmful effects of COVID,” said Sandeep Dhindsa, MD, an endocrinologist at Saint Louis University and lead author of the study.

Approximately 50% more men have died from confirmed COVID-19 than women since the start of the pandemic, according to the Sex, Gender and COVID-19 Project. Previous findings suggesting that sex may be a risk factor for death from COVID prompted researchers to consider whether hormones may play a role in the increased risk among men and whether treatments that suppress androgen levels could cut hospitalizations, but researchers consistently found that androgen suppression was not effective.

“There are other reasons women might be doing better – they may have followed public health guidelines a lot better,” according to Abhinav Diwan, MD, professor of medicine at Washington University in St. Louis, who helped conduct the new study. “It may be chromosomal and not necessarily just hormonal. The differences between men and women go beyond one factor.”

According to the researchers, the findings do not suggest that hormone therapy be used as a preventive measure against COVID.

“We don’t want patients to get excited and start to ask their doctors for testosterone,” Dr. Dhindsa said.

However, viewing low testosterone as a risk factor for COVID could be considered a shift in thinking for some clinicians, according to Dr. Dandana.

“All obese and all [men with] type 2 diabetes should be tested for testosterone, which is the practice in my clinic right now, even if they have no symptoms,” Dr. Dandana said. “Certainly, those with symptoms [of low testosterone] but no diagnosis, they should be tested, too.”

Participants in the study were infected with SARS-CoV-2 early in 2020, before vaccines were available. The researchers did not assess whether the rate of hospitalizations among participants with low testosterone would be different had they been vaccinated.

“Whatever benefits we saw with testosterone might be minor compared to getting the vaccine,” Dr. Dhindsa said.

Dr. Diwan agreed. “COVID hospitalization continues to be a problem, the strains are evolving, and new vaccines are coming in,” he said. “The bottom line is to get vaccinated.”

Dr. Dhindsa has received personal fees from Bayer and Acerus Pharmaceuticals and grants from Clarus Therapeutics outside the submitted work. Dr. Diwan has served as a consultant for the interpretation of echocardiograms for clinical trials for Clario (previously ERT) and has received nonfinancial support from Dewpoint Therapeutics outside the submitted work. Dr. Dandana has disclosed no relevant financial relationships.

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

Among men who have not been vaccinated against COVID-19, having low levels of testosterone may increase the risk of hospitalization from the disease – but hormone therapy appears to reduce the likelihood of severe COVID, researchers have found.

Low testosterone has long been linked to multiple chronic conditions, including obesity, heart disease, and type 2 diabetes, as well as acute conditions, such as heart attack and stroke. A study published earlier in the pandemic suggested that suppressing the sex hormone might protect against COVID-19. The new study, published in JAMA Network Open, is among the first to suggest a link between low testosterone and the risk for severe COVID.

Researchers at Washington University in St. Louis evaluated data from 723 unvaccinated men who had been infected with SARS-CoV-2. Of those, 116 had been diagnosed with hypogonadism, and 180 were receiving testosterone supplementation.

The study found that men whose testosterone levels were less than 200 ng/dL were 2.4 times more likely to experience a severe case of COVID-19 that required hospitalization than were those with normal levels of the hormone. The study accounted for the fact that participants with low testosterone were also more likely to have comorbidities such as diabetes and obesity.

Paresh Dandona, MD, PhD, distinguished professor of medicine and endocrinology at the State University of New York at Buffalo, called the findings “very exciting” and “fundamental.”

“In the world of hypogonadism, this is the first to show that low testosterone makes you vulnerable” to COVID, added Dr. Dandona, who was not involved with the research.

Men who were receiving hormone replacement therapy were at lower risk of hospitalization, compared with those who were not receiving treatment, the study found.

“Testosterone therapy seemed to negate the harmful effects of COVID,” said Sandeep Dhindsa, MD, an endocrinologist at Saint Louis University and lead author of the study.

Approximately 50% more men have died from confirmed COVID-19 than women since the start of the pandemic, according to the Sex, Gender and COVID-19 Project. Previous findings suggesting that sex may be a risk factor for death from COVID prompted researchers to consider whether hormones may play a role in the increased risk among men and whether treatments that suppress androgen levels could cut hospitalizations, but researchers consistently found that androgen suppression was not effective.

“There are other reasons women might be doing better – they may have followed public health guidelines a lot better,” according to Abhinav Diwan, MD, professor of medicine at Washington University in St. Louis, who helped conduct the new study. “It may be chromosomal and not necessarily just hormonal. The differences between men and women go beyond one factor.”

According to the researchers, the findings do not suggest that hormone therapy be used as a preventive measure against COVID.

“We don’t want patients to get excited and start to ask their doctors for testosterone,” Dr. Dhindsa said.

However, viewing low testosterone as a risk factor for COVID could be considered a shift in thinking for some clinicians, according to Dr. Dandana.

“All obese and all [men with] type 2 diabetes should be tested for testosterone, which is the practice in my clinic right now, even if they have no symptoms,” Dr. Dandana said. “Certainly, those with symptoms [of low testosterone] but no diagnosis, they should be tested, too.”

Participants in the study were infected with SARS-CoV-2 early in 2020, before vaccines were available. The researchers did not assess whether the rate of hospitalizations among participants with low testosterone would be different had they been vaccinated.

“Whatever benefits we saw with testosterone might be minor compared to getting the vaccine,” Dr. Dhindsa said.

Dr. Diwan agreed. “COVID hospitalization continues to be a problem, the strains are evolving, and new vaccines are coming in,” he said. “The bottom line is to get vaccinated.”

Dr. Dhindsa has received personal fees from Bayer and Acerus Pharmaceuticals and grants from Clarus Therapeutics outside the submitted work. Dr. Diwan has served as a consultant for the interpretation of echocardiograms for clinical trials for Clario (previously ERT) and has received nonfinancial support from Dewpoint Therapeutics outside the submitted work. Dr. Dandana has disclosed no relevant financial relationships.

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