Joann E. Manson, MD, DrPH

I’d like to talk with you about ultraprocessed foods (UPFs) and risk for cardiovascular disease (CVD) and try to separate some of the facts from the myths. I’d like to discuss a recent report in The Lancet Regional Health that looks at this topic comprehensively and in detail.

This report includes three large-scale prospective cohort studies of US female and male health professionals, more than 200,000 participants in total. It also includes a meta-analysis of 22 international cohorts with about 1.2 million participants. I’d like to acknowledge that I’m a co-author of this study.

What are UPFs, and why are they important? Why do we care, and what are the knowledge gaps? UPFs are generally packaged foods that contain ingredients to extend shelf life and improve taste and palatability. It’s important because 60%-70% of the US diet, if not more, is made up of UPFs. So, the relationship between UPFs and CVD and other health outcomes is actually very important. 

And the research to date on this subject has been quite limited. 

Often, UPFs will include additives, such as preservatives, flavor enhancers, colorants, emulsifiers, and sweeteners, and they tend to have an excess amount of calories, added sugars, added salt, sodium, and saturated fat. The packaging can be high in bisphenols, which have also been linked to some health outcomes.

In other studies, these UPFs have been linked to weight gain and dyslipidemia; some tissue glycation has been found, and some changes in the microbiome. Some studies have linked higher UPF intake with type 2 diabetes. A few have looked at certain selected UPF foods and found a higher risk for CVD, but a really comprehensive look at this question hasn’t been done. 

So, that’s what we did in this paper and in the meta-analysis with the 22 cohorts, and we saw a very clear and distinct significant increase in coronary heart disease by 23%, total CVD by 17%, and stroke by 9% when comparing the highest vs the lowest category [of UPF intake]. When we drilled down deeply into the types of UPFs in the US health professional cohorts, we saw that there were some major differences in the relationship with CVD depending on the type of UPF.

In comparing the highest quintile vs the lowest quintile [of total UPF intake], we saw that some of the UPFs were associated with significant elevations in risk for CVD. These included sugar-sweetened beverages and processed meats. But some UPFs were linked with a lower risk for CVD. These included breakfast cereals, yogurt, some dairy desserts, and whole grains.

Overall, it seemed that UPFs are actually quite diverse in their association with health. It’s not one size fits all. They’re not all created equal, and some of these differences matter. Although overall we would recommend that our diets be focused on whole foods, primarily plant based, lots of fruits and vegetables, whole grains, fish, and other whole foods, it seems from this report and the meta-analysis that certain types of UPFs can be incorporated into a healthy diet and don’t need to be avoided entirely. 

Dr. Manson is Professor of Medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, and Chief of the Division of Preventive Medicine, Brigham and Women’s Hospital, both in Boston, Massachusetts. She reported receiving donations and infrastructure support from Mars Symbioscience.

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

I’d like to talk with you about ultraprocessed foods (UPFs) and risk for cardiovascular disease (CVD) and try to separate some of the facts from the myths. I’d like to discuss a recent report in The Lancet Regional Health that looks at this topic comprehensively and in detail.

This report includes three large-scale prospective cohort studies of US female and male health professionals, more than 200,000 participants in total. It also includes a meta-analysis of 22 international cohorts with about 1.2 million participants. I’d like to acknowledge that I’m a co-author of this study.

What are UPFs, and why are they important? Why do we care, and what are the knowledge gaps? UPFs are generally packaged foods that contain ingredients to extend shelf life and improve taste and palatability. It’s important because 60%-70% of the US diet, if not more, is made up of UPFs. So, the relationship between UPFs and CVD and other health outcomes is actually very important. 

And the research to date on this subject has been quite limited. 

Often, UPFs will include additives, such as preservatives, flavor enhancers, colorants, emulsifiers, and sweeteners, and they tend to have an excess amount of calories, added sugars, added salt, sodium, and saturated fat. The packaging can be high in bisphenols, which have also been linked to some health outcomes.

In other studies, these UPFs have been linked to weight gain and dyslipidemia; some tissue glycation has been found, and some changes in the microbiome. Some studies have linked higher UPF intake with type 2 diabetes. A few have looked at certain selected UPF foods and found a higher risk for CVD, but a really comprehensive look at this question hasn’t been done. 

So, that’s what we did in this paper and in the meta-analysis with the 22 cohorts, and we saw a very clear and distinct significant increase in coronary heart disease by 23%, total CVD by 17%, and stroke by 9% when comparing the highest vs the lowest category [of UPF intake]. When we drilled down deeply into the types of UPFs in the US health professional cohorts, we saw that there were some major differences in the relationship with CVD depending on the type of UPF.

In comparing the highest quintile vs the lowest quintile [of total UPF intake], we saw that some of the UPFs were associated with significant elevations in risk for CVD. These included sugar-sweetened beverages and processed meats. But some UPFs were linked with a lower risk for CVD. These included breakfast cereals, yogurt, some dairy desserts, and whole grains.

Overall, it seemed that UPFs are actually quite diverse in their association with health. It’s not one size fits all. They’re not all created equal, and some of these differences matter. Although overall we would recommend that our diets be focused on whole foods, primarily plant based, lots of fruits and vegetables, whole grains, fish, and other whole foods, it seems from this report and the meta-analysis that certain types of UPFs can be incorporated into a healthy diet and don’t need to be avoided entirely. 

Dr. Manson is Professor of Medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, and Chief of the Division of Preventive Medicine, Brigham and Women’s Hospital, both in Boston, Massachusetts. She reported receiving donations and infrastructure support from Mars Symbioscience.

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

I’d like to talk with you about ultraprocessed foods (UPFs) and risk for cardiovascular disease (CVD) and try to separate some of the facts from the myths. I’d like to discuss a recent report in The Lancet Regional Health that looks at this topic comprehensively and in detail.

This report includes three large-scale prospective cohort studies of US female and male health professionals, more than 200,000 participants in total. It also includes a meta-analysis of 22 international cohorts with about 1.2 million participants. I’d like to acknowledge that I’m a co-author of this study.

What are UPFs, and why are they important? Why do we care, and what are the knowledge gaps? UPFs are generally packaged foods that contain ingredients to extend shelf life and improve taste and palatability. It’s important because 60%-70% of the US diet, if not more, is made up of UPFs. So, the relationship between UPFs and CVD and other health outcomes is actually very important. 

And the research to date on this subject has been quite limited. 

Often, UPFs will include additives, such as preservatives, flavor enhancers, colorants, emulsifiers, and sweeteners, and they tend to have an excess amount of calories, added sugars, added salt, sodium, and saturated fat. The packaging can be high in bisphenols, which have also been linked to some health outcomes.

In other studies, these UPFs have been linked to weight gain and dyslipidemia; some tissue glycation has been found, and some changes in the microbiome. Some studies have linked higher UPF intake with type 2 diabetes. A few have looked at certain selected UPF foods and found a higher risk for CVD, but a really comprehensive look at this question hasn’t been done. 

So, that’s what we did in this paper and in the meta-analysis with the 22 cohorts, and we saw a very clear and distinct significant increase in coronary heart disease by 23%, total CVD by 17%, and stroke by 9% when comparing the highest vs the lowest category [of UPF intake]. When we drilled down deeply into the types of UPFs in the US health professional cohorts, we saw that there were some major differences in the relationship with CVD depending on the type of UPF.

In comparing the highest quintile vs the lowest quintile [of total UPF intake], we saw that some of the UPFs were associated with significant elevations in risk for CVD. These included sugar-sweetened beverages and processed meats. But some UPFs were linked with a lower risk for CVD. These included breakfast cereals, yogurt, some dairy desserts, and whole grains.

Overall, it seemed that UPFs are actually quite diverse in their association with health. It’s not one size fits all. They’re not all created equal, and some of these differences matter. Although overall we would recommend that our diets be focused on whole foods, primarily plant based, lots of fruits and vegetables, whole grains, fish, and other whole foods, it seems from this report and the meta-analysis that certain types of UPFs can be incorporated into a healthy diet and don’t need to be avoided entirely. 

Dr. Manson is Professor of Medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, and Chief of the Division of Preventive Medicine, Brigham and Women’s Hospital, both in Boston, Massachusetts. She reported receiving donations and infrastructure support from Mars Symbioscience.

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

This transcript has been edited for clarity.

I’d like to talk about a recent report in the journal Menopause linking menopausal symptoms to increased risk for cognitive impairment. I’d also like to discuss some of the recent studies that have addressed whether hot flashes are linked to increased risk for heart disease and other forms of cardiovascular disease (CVD). 

Given that 75%-80% of perimenopausal and postmenopausal women have hot flashes and vasomotor symptoms, it’s undoubtedly a more complex relationship between hot flashes and these outcomes than a simple one-size-fits-all, yes-or-no question.

Increasing evidence shows that several additional factors are important, including the age at which the symptoms are occurring, the time since menopause, the severity of the symptoms, whether they co-occur with night sweats and sleep disruption, and the cardiovascular status of the woman.

Several studies suggest that women who have more severe hot flashes and vasomotor symptoms are more likely to have prevalent cardiovascular risk factors — hypertension, dyslipidemia, high body mass index, endothelial dysfunction — as measured by flow-mediated vasodilation and other measures.

It is quite plausible that hot flashes could be a marker for increased risk for cognitive impairment. But the question remains, are hot flashes associated with cognitive impairment independent of these other risk factors? It appears that the associations between hot flashes, vasomotor symptoms, and CVD, and other adverse outcomes, may be more likely when hot flashes persist after age 60 or are newly occurring in later menopause. In the Women’s Health Initiative observational study, the presence of hot flashes and vasomotor symptoms in early menopause was not linked to any increased risk for heart attack, stroke, total CVD, or all-cause mortality.

However, the onset of these symptoms, especially new onset of these symptoms after age 60 or in later menopause, was in fact linked to increased risk for CVD and all-cause mortality. With respect to cognitive impairment, if a woman is having hot flashes and night sweats with regular sleep disruption, performance on cognitive testing would not be as favorable as it would be in the absence of these symptoms.

This brings us to the new study in Menopause that included approximately 1300 Latino women in nine Latin American countries, with an average age of 55 years. Looking at the association between severe menopausal symptoms and cognitive impairment, researchers found that women with severe symptoms were more likely to have cognitive impairment.

Conversely, they found that the women who had a favorable CVD risk factor status (physically active, lower BMI, healthier) and were ever users of estrogen were less likely to have cognitive impairment.

Clearly, for estrogen therapy, we need randomized clinical trials of the presence or absence of vasomotor symptoms and cognitive and CVD outcomes. Such analyses are ongoing, and new randomized trials focused specifically on women in early menopause would be very beneficial.

At the present time, it’s important that we not alarm women about the associations seen in some of these studies because often they are not independent associations; they aren’t independent of other risk factors that are commonly linked to hot flashes and night sweats. There are many other complexities in the relationship between hot flashes and cognitive impairment.

We need to appreciate that women who have moderate to severe hot flashes (especially when associated with disrupted sleep) do have impaired quality of life. It’s important to treat these symptoms, especially in early menopause, and very effective hormonal and nonhormonal treatments are available.

For women with symptoms that persist into later menopause or who have new onset of symptoms in later menopause, it’s important to prioritize cardiovascular health. For example, be more vigilant about behavioral lifestyle counseling to lower risk, and be even more aggressive in treating dyslipidemia and diabetes.

JoAnn E. Manson, Professor of Medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School; Chief, Division of Preventive Medicine, Brigham and Women’s Hospital, Boston, Massachusetts; and Past President, North American Menopause Society, 2011-2012, has disclosed the following relevant financial relationships: Received study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).

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

This transcript has been edited for clarity.

I’d like to talk about a recent report in the journal Menopause linking menopausal symptoms to increased risk for cognitive impairment. I’d also like to discuss some of the recent studies that have addressed whether hot flashes are linked to increased risk for heart disease and other forms of cardiovascular disease (CVD). 

Given that 75%-80% of perimenopausal and postmenopausal women have hot flashes and vasomotor symptoms, it’s undoubtedly a more complex relationship between hot flashes and these outcomes than a simple one-size-fits-all, yes-or-no question.

Increasing evidence shows that several additional factors are important, including the age at which the symptoms are occurring, the time since menopause, the severity of the symptoms, whether they co-occur with night sweats and sleep disruption, and the cardiovascular status of the woman.

Several studies suggest that women who have more severe hot flashes and vasomotor symptoms are more likely to have prevalent cardiovascular risk factors — hypertension, dyslipidemia, high body mass index, endothelial dysfunction — as measured by flow-mediated vasodilation and other measures.

It is quite plausible that hot flashes could be a marker for increased risk for cognitive impairment. But the question remains, are hot flashes associated with cognitive impairment independent of these other risk factors? It appears that the associations between hot flashes, vasomotor symptoms, and CVD, and other adverse outcomes, may be more likely when hot flashes persist after age 60 or are newly occurring in later menopause. In the Women’s Health Initiative observational study, the presence of hot flashes and vasomotor symptoms in early menopause was not linked to any increased risk for heart attack, stroke, total CVD, or all-cause mortality.

However, the onset of these symptoms, especially new onset of these symptoms after age 60 or in later menopause, was in fact linked to increased risk for CVD and all-cause mortality. With respect to cognitive impairment, if a woman is having hot flashes and night sweats with regular sleep disruption, performance on cognitive testing would not be as favorable as it would be in the absence of these symptoms.

This brings us to the new study in Menopause that included approximately 1300 Latino women in nine Latin American countries, with an average age of 55 years. Looking at the association between severe menopausal symptoms and cognitive impairment, researchers found that women with severe symptoms were more likely to have cognitive impairment.

Conversely, they found that the women who had a favorable CVD risk factor status (physically active, lower BMI, healthier) and were ever users of estrogen were less likely to have cognitive impairment.

Clearly, for estrogen therapy, we need randomized clinical trials of the presence or absence of vasomotor symptoms and cognitive and CVD outcomes. Such analyses are ongoing, and new randomized trials focused specifically on women in early menopause would be very beneficial.

At the present time, it’s important that we not alarm women about the associations seen in some of these studies because often they are not independent associations; they aren’t independent of other risk factors that are commonly linked to hot flashes and night sweats. There are many other complexities in the relationship between hot flashes and cognitive impairment.

We need to appreciate that women who have moderate to severe hot flashes (especially when associated with disrupted sleep) do have impaired quality of life. It’s important to treat these symptoms, especially in early menopause, and very effective hormonal and nonhormonal treatments are available.

For women with symptoms that persist into later menopause or who have new onset of symptoms in later menopause, it’s important to prioritize cardiovascular health. For example, be more vigilant about behavioral lifestyle counseling to lower risk, and be even more aggressive in treating dyslipidemia and diabetes.

JoAnn E. Manson, Professor of Medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School; Chief, Division of Preventive Medicine, Brigham and Women’s Hospital, Boston, Massachusetts; and Past President, North American Menopause Society, 2011-2012, has disclosed the following relevant financial relationships: Received study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).

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

This transcript has been edited for clarity.

I’d like to talk about a recent report in the journal Menopause linking menopausal symptoms to increased risk for cognitive impairment. I’d also like to discuss some of the recent studies that have addressed whether hot flashes are linked to increased risk for heart disease and other forms of cardiovascular disease (CVD). 

Given that 75%-80% of perimenopausal and postmenopausal women have hot flashes and vasomotor symptoms, it’s undoubtedly a more complex relationship between hot flashes and these outcomes than a simple one-size-fits-all, yes-or-no question.

Increasing evidence shows that several additional factors are important, including the age at which the symptoms are occurring, the time since menopause, the severity of the symptoms, whether they co-occur with night sweats and sleep disruption, and the cardiovascular status of the woman.

Several studies suggest that women who have more severe hot flashes and vasomotor symptoms are more likely to have prevalent cardiovascular risk factors — hypertension, dyslipidemia, high body mass index, endothelial dysfunction — as measured by flow-mediated vasodilation and other measures.

It is quite plausible that hot flashes could be a marker for increased risk for cognitive impairment. But the question remains, are hot flashes associated with cognitive impairment independent of these other risk factors? It appears that the associations between hot flashes, vasomotor symptoms, and CVD, and other adverse outcomes, may be more likely when hot flashes persist after age 60 or are newly occurring in later menopause. In the Women’s Health Initiative observational study, the presence of hot flashes and vasomotor symptoms in early menopause was not linked to any increased risk for heart attack, stroke, total CVD, or all-cause mortality.

However, the onset of these symptoms, especially new onset of these symptoms after age 60 or in later menopause, was in fact linked to increased risk for CVD and all-cause mortality. With respect to cognitive impairment, if a woman is having hot flashes and night sweats with regular sleep disruption, performance on cognitive testing would not be as favorable as it would be in the absence of these symptoms.

This brings us to the new study in Menopause that included approximately 1300 Latino women in nine Latin American countries, with an average age of 55 years. Looking at the association between severe menopausal symptoms and cognitive impairment, researchers found that women with severe symptoms were more likely to have cognitive impairment.

Conversely, they found that the women who had a favorable CVD risk factor status (physically active, lower BMI, healthier) and were ever users of estrogen were less likely to have cognitive impairment.

Clearly, for estrogen therapy, we need randomized clinical trials of the presence or absence of vasomotor symptoms and cognitive and CVD outcomes. Such analyses are ongoing, and new randomized trials focused specifically on women in early menopause would be very beneficial.

At the present time, it’s important that we not alarm women about the associations seen in some of these studies because often they are not independent associations; they aren’t independent of other risk factors that are commonly linked to hot flashes and night sweats. There are many other complexities in the relationship between hot flashes and cognitive impairment.

We need to appreciate that women who have moderate to severe hot flashes (especially when associated with disrupted sleep) do have impaired quality of life. It’s important to treat these symptoms, especially in early menopause, and very effective hormonal and nonhormonal treatments are available.

For women with symptoms that persist into later menopause or who have new onset of symptoms in later menopause, it’s important to prioritize cardiovascular health. For example, be more vigilant about behavioral lifestyle counseling to lower risk, and be even more aggressive in treating dyslipidemia and diabetes.

JoAnn E. Manson, Professor of Medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School; Chief, Division of Preventive Medicine, Brigham and Women’s Hospital, Boston, Massachusetts; and Past President, North American Menopause Society, 2011-2012, has disclosed the following relevant financial relationships: Received study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).

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

A new report on the preventability of dementia is both exciting and paradigm-shifting. The new study, published in The Lancet by the Lancet Commission on Dementia, estimates that close to 50% of cases of dementia worldwide can be prevented or delayed by improving 14 modifiable risk factors. 

This is paradigm-shifting because dementia is often perceived as an inevitable consequence of the aging process, with a major genetic component. But this study suggests that modifying these risk factors can benefit everyone, irrespective of genetic risk, and that it’s important to have a life-course approach. It’s never too early or too late to start to modify these factors. 

We’ve known for a long time that many chronic diseases are highly preventable and modifiable. Some that come to mind are type 2 diabetes, coronary heart disease, and even certain forms of cancer. Modifiable risk factors include cigarette smoking, diet, physical activity, and maintaining a healthy weight. This study suggests that many of the same risk factors and more are relevant to reducing risk for dementia. 

Let’s go through the risk factors, many of which are behavioral. These risk factors include lifestyle factors such as lack of physical activity, cigarette smoking, excessive alcohol consumption, and obesity. The cardiovascular or vascular-specific risk factors include not only those behavioral factors but also hypertension, high LDL cholesterol, and diabetes. Cognitive engagement–specific risk factors include social isolation, which is a major risk factor for dementia, as well as untreated hearing or vision loss, which can exacerbate social isolation and depression, and low educational attainment, which can be related to less cognitive engagement.

They also mention traumatic brain injury from an accident or contact sports without head protection as a risk factor, and the environmental risk factor of air pollution or poor air quality. 

Two of these risk factors are new since the previous report in 2020: elevated LDL cholesterol and untreated vision loss, both of which are quite treatable. Overall, these findings suggest that a lot can be done to lower dementia risk, but it requires individual behavior modifications as well as a comprehensive approach with involvement of the healthcare system for improved screening, access, and public policy to reduce air pollution.

Some of these risk factors are more relevant to women, especially the social isolation that is so common later in life in women. In the United States, close to two out of three patients with dementia are women.

So, informing our patients about these risk factors and what can be done in terms of behavior modification, increased screening, and treatment for these conditions can go a long way in helping our patients reduce their risk for dementia.
 

Dr. Manson is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, chief, Division of Preventive Medicine, Brigham and Women’s Hospital, Boston, and past president, North American Menopause Society, 2011-2012. She disclosed receiving study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).

A version of this article appeared on Medscape.com.

A new report on the preventability of dementia is both exciting and paradigm-shifting. The new study, published in The Lancet by the Lancet Commission on Dementia, estimates that close to 50% of cases of dementia worldwide can be prevented or delayed by improving 14 modifiable risk factors. 

This is paradigm-shifting because dementia is often perceived as an inevitable consequence of the aging process, with a major genetic component. But this study suggests that modifying these risk factors can benefit everyone, irrespective of genetic risk, and that it’s important to have a life-course approach. It’s never too early or too late to start to modify these factors. 

We’ve known for a long time that many chronic diseases are highly preventable and modifiable. Some that come to mind are type 2 diabetes, coronary heart disease, and even certain forms of cancer. Modifiable risk factors include cigarette smoking, diet, physical activity, and maintaining a healthy weight. This study suggests that many of the same risk factors and more are relevant to reducing risk for dementia. 

Let’s go through the risk factors, many of which are behavioral. These risk factors include lifestyle factors such as lack of physical activity, cigarette smoking, excessive alcohol consumption, and obesity. The cardiovascular or vascular-specific risk factors include not only those behavioral factors but also hypertension, high LDL cholesterol, and diabetes. Cognitive engagement–specific risk factors include social isolation, which is a major risk factor for dementia, as well as untreated hearing or vision loss, which can exacerbate social isolation and depression, and low educational attainment, which can be related to less cognitive engagement.

They also mention traumatic brain injury from an accident or contact sports without head protection as a risk factor, and the environmental risk factor of air pollution or poor air quality. 

Two of these risk factors are new since the previous report in 2020: elevated LDL cholesterol and untreated vision loss, both of which are quite treatable. Overall, these findings suggest that a lot can be done to lower dementia risk, but it requires individual behavior modifications as well as a comprehensive approach with involvement of the healthcare system for improved screening, access, and public policy to reduce air pollution.

Some of these risk factors are more relevant to women, especially the social isolation that is so common later in life in women. In the United States, close to two out of three patients with dementia are women.

So, informing our patients about these risk factors and what can be done in terms of behavior modification, increased screening, and treatment for these conditions can go a long way in helping our patients reduce their risk for dementia.
 

Dr. Manson is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, chief, Division of Preventive Medicine, Brigham and Women’s Hospital, Boston, and past president, North American Menopause Society, 2011-2012. She disclosed receiving study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).

A version of this article appeared on Medscape.com.

A new report on the preventability of dementia is both exciting and paradigm-shifting. The new study, published in The Lancet by the Lancet Commission on Dementia, estimates that close to 50% of cases of dementia worldwide can be prevented or delayed by improving 14 modifiable risk factors. 

This is paradigm-shifting because dementia is often perceived as an inevitable consequence of the aging process, with a major genetic component. But this study suggests that modifying these risk factors can benefit everyone, irrespective of genetic risk, and that it’s important to have a life-course approach. It’s never too early or too late to start to modify these factors. 

We’ve known for a long time that many chronic diseases are highly preventable and modifiable. Some that come to mind are type 2 diabetes, coronary heart disease, and even certain forms of cancer. Modifiable risk factors include cigarette smoking, diet, physical activity, and maintaining a healthy weight. This study suggests that many of the same risk factors and more are relevant to reducing risk for dementia. 

Let’s go through the risk factors, many of which are behavioral. These risk factors include lifestyle factors such as lack of physical activity, cigarette smoking, excessive alcohol consumption, and obesity. The cardiovascular or vascular-specific risk factors include not only those behavioral factors but also hypertension, high LDL cholesterol, and diabetes. Cognitive engagement–specific risk factors include social isolation, which is a major risk factor for dementia, as well as untreated hearing or vision loss, which can exacerbate social isolation and depression, and low educational attainment, which can be related to less cognitive engagement.

They also mention traumatic brain injury from an accident or contact sports without head protection as a risk factor, and the environmental risk factor of air pollution or poor air quality. 

Two of these risk factors are new since the previous report in 2020: elevated LDL cholesterol and untreated vision loss, both of which are quite treatable. Overall, these findings suggest that a lot can be done to lower dementia risk, but it requires individual behavior modifications as well as a comprehensive approach with involvement of the healthcare system for improved screening, access, and public policy to reduce air pollution.

Some of these risk factors are more relevant to women, especially the social isolation that is so common later in life in women. In the United States, close to two out of three patients with dementia are women.

So, informing our patients about these risk factors and what can be done in terms of behavior modification, increased screening, and treatment for these conditions can go a long way in helping our patients reduce their risk for dementia.
 

Dr. Manson is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, chief, Division of Preventive Medicine, Brigham and Women’s Hospital, Boston, and past president, North American Menopause Society, 2011-2012. She disclosed receiving study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

This is Dr JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk with you about a recent report in JAMA Network Open on the subject of whether statin therapy may be able to offset some of the excess risk for venous thromboembolism (VTE) among women taking menopausal hormone therapy.

It’s an important issue because we know that menopausal hormone therapy, especially oral therapy, is linked to an excess risk for VTE, approximately doubling of risk in the randomized clinical trials. There is also emerging evidence from some randomized trials, such as the Jupiter trial, that step therapy may be linked to a reduction in risk. This may be related to anti-inflammatory or antithrombotic effects of statin therapy.

The authors made use of a very large administrative claims database, Optum Health, to look at more than 15 million annual members. They were able to identify 2000 women with a diagnostic code for VTE treatment. The women were between ages 50 and 64 years, and they were compared with 200,000 controls without VTE, matched in 10-to-1 fashion.

About 50% of the women were taking oral hormone therapy, and about 50% took non-oral transdermal or other non-oral formulations of hormone therapy. The odds ratio for VTE was 1.53 among the women who did not also have prescription records for statin therapy. They were able to look at prescribed prescriptions for both the hormone therapy and the statins. Among the women prescribed hormone therapy and also low- to intermediate-dose statins, the odds ratio was 1.29. So that was quite a mitigation of the elevated risk. Among the women taking high-intensity statins, the odds ratio was 1.06, and there was no significant elevation.

We do need more data and more research on this question. One approach would be a meta-analysis of all of the existing randomized trials of hormone therapy in recent years wherein there was increased uptake of statin therapy to look at this question not only for VTE but also for coronary heart disease, stroke, and other CVD outcomes to see whether statin therapy is associated with some attenuation of the excess risk. We also need a targeted randomized trial of statins vs placebo among women who have clear indications for hormone therapy but may be at some increased risk for VTE. That type of trial would be extremely helpful.

In the interim, there are ways to minimize risk for VTE among women who are clear candidates for menopausal hormone therapy, especially among women at increased risk for VTE. These include choosing a transdermal rather than an oral formulation of hormone therapy and using lower doses of hormone therapy. Also, women who are clear candidates for hormone therapy and also for statins, it’s obvious that statins could be co-prescribed. Even among women who are clear candidates for hormone therapy but only intermediate borderline candidates for statin therapy, the prescription of statins might be considered in that clinical scenario to try to mitigate that excess risk for VTE.

JoAnn E. Manson, MD, DrPH, has disclosed the following relevant financial relationships: Received study pill donation and infrastructure support from: Mars Symbioscience (for the COSMOS trial).

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

This is Dr JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk with you about a recent report in JAMA Network Open on the subject of whether statin therapy may be able to offset some of the excess risk for venous thromboembolism (VTE) among women taking menopausal hormone therapy.

It’s an important issue because we know that menopausal hormone therapy, especially oral therapy, is linked to an excess risk for VTE, approximately doubling of risk in the randomized clinical trials. There is also emerging evidence from some randomized trials, such as the Jupiter trial, that step therapy may be linked to a reduction in risk. This may be related to anti-inflammatory or antithrombotic effects of statin therapy.

The authors made use of a very large administrative claims database, Optum Health, to look at more than 15 million annual members. They were able to identify 2000 women with a diagnostic code for VTE treatment. The women were between ages 50 and 64 years, and they were compared with 200,000 controls without VTE, matched in 10-to-1 fashion.

About 50% of the women were taking oral hormone therapy, and about 50% took non-oral transdermal or other non-oral formulations of hormone therapy. The odds ratio for VTE was 1.53 among the women who did not also have prescription records for statin therapy. They were able to look at prescribed prescriptions for both the hormone therapy and the statins. Among the women prescribed hormone therapy and also low- to intermediate-dose statins, the odds ratio was 1.29. So that was quite a mitigation of the elevated risk. Among the women taking high-intensity statins, the odds ratio was 1.06, and there was no significant elevation.

We do need more data and more research on this question. One approach would be a meta-analysis of all of the existing randomized trials of hormone therapy in recent years wherein there was increased uptake of statin therapy to look at this question not only for VTE but also for coronary heart disease, stroke, and other CVD outcomes to see whether statin therapy is associated with some attenuation of the excess risk. We also need a targeted randomized trial of statins vs placebo among women who have clear indications for hormone therapy but may be at some increased risk for VTE. That type of trial would be extremely helpful.

In the interim, there are ways to minimize risk for VTE among women who are clear candidates for menopausal hormone therapy, especially among women at increased risk for VTE. These include choosing a transdermal rather than an oral formulation of hormone therapy and using lower doses of hormone therapy. Also, women who are clear candidates for hormone therapy and also for statins, it’s obvious that statins could be co-prescribed. Even among women who are clear candidates for hormone therapy but only intermediate borderline candidates for statin therapy, the prescription of statins might be considered in that clinical scenario to try to mitigate that excess risk for VTE.

JoAnn E. Manson, MD, DrPH, has disclosed the following relevant financial relationships: Received study pill donation and infrastructure support from: Mars Symbioscience (for the COSMOS trial).

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

This is Dr JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk with you about a recent report in JAMA Network Open on the subject of whether statin therapy may be able to offset some of the excess risk for venous thromboembolism (VTE) among women taking menopausal hormone therapy.

It’s an important issue because we know that menopausal hormone therapy, especially oral therapy, is linked to an excess risk for VTE, approximately doubling of risk in the randomized clinical trials. There is also emerging evidence from some randomized trials, such as the Jupiter trial, that step therapy may be linked to a reduction in risk. This may be related to anti-inflammatory or antithrombotic effects of statin therapy.

The authors made use of a very large administrative claims database, Optum Health, to look at more than 15 million annual members. They were able to identify 2000 women with a diagnostic code for VTE treatment. The women were between ages 50 and 64 years, and they were compared with 200,000 controls without VTE, matched in 10-to-1 fashion.

About 50% of the women were taking oral hormone therapy, and about 50% took non-oral transdermal or other non-oral formulations of hormone therapy. The odds ratio for VTE was 1.53 among the women who did not also have prescription records for statin therapy. They were able to look at prescribed prescriptions for both the hormone therapy and the statins. Among the women prescribed hormone therapy and also low- to intermediate-dose statins, the odds ratio was 1.29. So that was quite a mitigation of the elevated risk. Among the women taking high-intensity statins, the odds ratio was 1.06, and there was no significant elevation.

We do need more data and more research on this question. One approach would be a meta-analysis of all of the existing randomized trials of hormone therapy in recent years wherein there was increased uptake of statin therapy to look at this question not only for VTE but also for coronary heart disease, stroke, and other CVD outcomes to see whether statin therapy is associated with some attenuation of the excess risk. We also need a targeted randomized trial of statins vs placebo among women who have clear indications for hormone therapy but may be at some increased risk for VTE. That type of trial would be extremely helpful.

In the interim, there are ways to minimize risk for VTE among women who are clear candidates for menopausal hormone therapy, especially among women at increased risk for VTE. These include choosing a transdermal rather than an oral formulation of hormone therapy and using lower doses of hormone therapy. Also, women who are clear candidates for hormone therapy and also for statins, it’s obvious that statins could be co-prescribed. Even among women who are clear candidates for hormone therapy but only intermediate borderline candidates for statin therapy, the prescription of statins might be considered in that clinical scenario to try to mitigate that excess risk for VTE.

JoAnn E. Manson, MD, DrPH, has disclosed the following relevant financial relationships: Received study pill donation and infrastructure support from: Mars Symbioscience (for the COSMOS trial).

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

This is Dr. JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk about a recent report in the journal Hypertension that raises questions about whether blood pressure (BP) guidelines should be revisited and whether sex-specific thresholds and targets should be considered. Current BP guidelines are sex-agnostic.

This study was done in the large-scale nationally representative NHANES cohort. It included more than 53,000 US men and women. The average age was about 45 years, with an average duration of follow-up of 9.5 years. During that time, about 2400 cardiovascular (CVD) deaths were documented at baseline. The BP was measured three times, and the results were averaged. About 20% of the cohort were taking antihypertensive medications, and 80% were not.

Sex differences were observed in the association between BP and CVD mortality. The systolic BP associated with the lowest risk for CVD death was 110-119 mm Hg in men and 100-109 mm Hg in women. In men, however, compared with a reference category of systolic BP of 100-109 mm Hg, the risk for CVD death began to increase significantly at a systolic BP ≥ 160 mm Hg, at which point, the hazard ratio was 1.76, or 76% higher risk.

In women, the risk for CVD death began to increase significantly at a lower threshold. Compared with a reference category of systolic BP of 100-109 mm Hg, women whose systolic BP was 130-139 mm Hg had a significant 61% increase in CVD death, and among those with a systolic BP of 140-159 mm Hg, the risk was increased by 75%. With a systolic BP ≥ 160 mm Hg, CVD deaths among women were more than doubled, with a hazard ratio of 2.13.

Overall, these findings suggest sex differences, with women having an increased risk for CVD death beginning at a lower elevation of their systolic BP. For diastolic BP, both men and women showed the typical U-shaped curve and the diastolic BP associated with the lowest risk for CVD death was 70-80 mm Hg.

If these findings can be replicated with additional research and other large-scale cohort studies, and randomized trials show differences in lowering BP, then sex-specific BP guidelines could have advantages and should be seriously considered. Furthermore, some of the CVD risk scores and risk modeling should perhaps use sex-specific blood pressure thresholds.Dr. Manson received study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

This is Dr. JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk about a recent report in the journal Hypertension that raises questions about whether blood pressure (BP) guidelines should be revisited and whether sex-specific thresholds and targets should be considered. Current BP guidelines are sex-agnostic.

This study was done in the large-scale nationally representative NHANES cohort. It included more than 53,000 US men and women. The average age was about 45 years, with an average duration of follow-up of 9.5 years. During that time, about 2400 cardiovascular (CVD) deaths were documented at baseline. The BP was measured three times, and the results were averaged. About 20% of the cohort were taking antihypertensive medications, and 80% were not.

Sex differences were observed in the association between BP and CVD mortality. The systolic BP associated with the lowest risk for CVD death was 110-119 mm Hg in men and 100-109 mm Hg in women. In men, however, compared with a reference category of systolic BP of 100-109 mm Hg, the risk for CVD death began to increase significantly at a systolic BP ≥ 160 mm Hg, at which point, the hazard ratio was 1.76, or 76% higher risk.

In women, the risk for CVD death began to increase significantly at a lower threshold. Compared with a reference category of systolic BP of 100-109 mm Hg, women whose systolic BP was 130-139 mm Hg had a significant 61% increase in CVD death, and among those with a systolic BP of 140-159 mm Hg, the risk was increased by 75%. With a systolic BP ≥ 160 mm Hg, CVD deaths among women were more than doubled, with a hazard ratio of 2.13.

Overall, these findings suggest sex differences, with women having an increased risk for CVD death beginning at a lower elevation of their systolic BP. For diastolic BP, both men and women showed the typical U-shaped curve and the diastolic BP associated with the lowest risk for CVD death was 70-80 mm Hg.

If these findings can be replicated with additional research and other large-scale cohort studies, and randomized trials show differences in lowering BP, then sex-specific BP guidelines could have advantages and should be seriously considered. Furthermore, some of the CVD risk scores and risk modeling should perhaps use sex-specific blood pressure thresholds.Dr. Manson received study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

This is Dr. JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk about a recent report in the journal Hypertension that raises questions about whether blood pressure (BP) guidelines should be revisited and whether sex-specific thresholds and targets should be considered. Current BP guidelines are sex-agnostic.

This study was done in the large-scale nationally representative NHANES cohort. It included more than 53,000 US men and women. The average age was about 45 years, with an average duration of follow-up of 9.5 years. During that time, about 2400 cardiovascular (CVD) deaths were documented at baseline. The BP was measured three times, and the results were averaged. About 20% of the cohort were taking antihypertensive medications, and 80% were not.

Sex differences were observed in the association between BP and CVD mortality. The systolic BP associated with the lowest risk for CVD death was 110-119 mm Hg in men and 100-109 mm Hg in women. In men, however, compared with a reference category of systolic BP of 100-109 mm Hg, the risk for CVD death began to increase significantly at a systolic BP ≥ 160 mm Hg, at which point, the hazard ratio was 1.76, or 76% higher risk.

In women, the risk for CVD death began to increase significantly at a lower threshold. Compared with a reference category of systolic BP of 100-109 mm Hg, women whose systolic BP was 130-139 mm Hg had a significant 61% increase in CVD death, and among those with a systolic BP of 140-159 mm Hg, the risk was increased by 75%. With a systolic BP ≥ 160 mm Hg, CVD deaths among women were more than doubled, with a hazard ratio of 2.13.

Overall, these findings suggest sex differences, with women having an increased risk for CVD death beginning at a lower elevation of their systolic BP. For diastolic BP, both men and women showed the typical U-shaped curve and the diastolic BP associated with the lowest risk for CVD death was 70-80 mm Hg.

If these findings can be replicated with additional research and other large-scale cohort studies, and randomized trials show differences in lowering BP, then sex-specific BP guidelines could have advantages and should be seriously considered. Furthermore, some of the CVD risk scores and risk modeling should perhaps use sex-specific blood pressure thresholds.Dr. Manson received study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).

A version of this article appeared on Medscape.com.

I’d like to talk with you about a recent report from the large-scale Black Women’s Health Study, published in the new journal NEJM Evidence.

This study looked at the association between hypertensive disorders of pregnancy, including preeclampsia and gestational hypertension, and the risk for stroke over the next 20 (median, 22) years. Previous studies have linked hypertensive disorders of pregnancy with an increased risk for stroke. However, most of these studies have been done in White women of European ancestry, and evidence in Black women has been very limited, despite a disproportionately high risk of having a hypertensive disorder of pregnancy and also of stroke.

This study, in more than 40,000 U.S. women, found an increased risk for subsequent stroke among women with a prior history of hypertensive disorder of pregnancy – overall, a 66% increased risk, an 80% increased risk with gestational hypertension, and about a 50% increased risk with preeclampsia.

We know that pregnancy itself can lead to some remodeling of the vascular system, but we don’t know whether a direct causal relationship exists between preeclampsia or gestational hypertension and subsequent stroke. Another potential explanation is that these complications of pregnancy serve as a window into a woman’s future cardiometabolic health and a marker of her cardiovascular risk.

Regardless, the clinical implications are the same. First, we would want to prevent these complications of pregnancy whenever possible. Some women will be candidates for the use of aspirin if they are at high risk for preeclampsia, and certainly for monitoring blood pressure very closely during pregnancy. It will also be important to maintain blood pressure control in the postpartum period and during the subsequent years of adulthood to minimize risk for stroke, because hypertension is such a powerful risk factor for stroke.

It will also be tremendously important to intensify lifestyle modifications such as increasing physical activity and having a heart-healthy diet. These complications of pregnancy have also been linked in other studies to an increased risk for subsequent coronary heart disease events and heart failure.

This transcript has been edited for clarity.

Dr. Manson is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, and chief of the division of preventive medicine, Brigham and Women’s Hospital, both in Boston, and past president, North American Menopause Society, 2011-2012. She disclosed receiving study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).

A version of this article appeared on Medscape.com.

I’d like to talk with you about a recent report from the large-scale Black Women’s Health Study, published in the new journal NEJM Evidence.

This study looked at the association between hypertensive disorders of pregnancy, including preeclampsia and gestational hypertension, and the risk for stroke over the next 20 (median, 22) years. Previous studies have linked hypertensive disorders of pregnancy with an increased risk for stroke. However, most of these studies have been done in White women of European ancestry, and evidence in Black women has been very limited, despite a disproportionately high risk of having a hypertensive disorder of pregnancy and also of stroke.

This study, in more than 40,000 U.S. women, found an increased risk for subsequent stroke among women with a prior history of hypertensive disorder of pregnancy – overall, a 66% increased risk, an 80% increased risk with gestational hypertension, and about a 50% increased risk with preeclampsia.

We know that pregnancy itself can lead to some remodeling of the vascular system, but we don’t know whether a direct causal relationship exists between preeclampsia or gestational hypertension and subsequent stroke. Another potential explanation is that these complications of pregnancy serve as a window into a woman’s future cardiometabolic health and a marker of her cardiovascular risk.

Regardless, the clinical implications are the same. First, we would want to prevent these complications of pregnancy whenever possible. Some women will be candidates for the use of aspirin if they are at high risk for preeclampsia, and certainly for monitoring blood pressure very closely during pregnancy. It will also be important to maintain blood pressure control in the postpartum period and during the subsequent years of adulthood to minimize risk for stroke, because hypertension is such a powerful risk factor for stroke.

It will also be tremendously important to intensify lifestyle modifications such as increasing physical activity and having a heart-healthy diet. These complications of pregnancy have also been linked in other studies to an increased risk for subsequent coronary heart disease events and heart failure.

This transcript has been edited for clarity.

Dr. Manson is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, and chief of the division of preventive medicine, Brigham and Women’s Hospital, both in Boston, and past president, North American Menopause Society, 2011-2012. She disclosed receiving study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).

A version of this article appeared on Medscape.com.

I’d like to talk with you about a recent report from the large-scale Black Women’s Health Study, published in the new journal NEJM Evidence.

This study looked at the association between hypertensive disorders of pregnancy, including preeclampsia and gestational hypertension, and the risk for stroke over the next 20 (median, 22) years. Previous studies have linked hypertensive disorders of pregnancy with an increased risk for stroke. However, most of these studies have been done in White women of European ancestry, and evidence in Black women has been very limited, despite a disproportionately high risk of having a hypertensive disorder of pregnancy and also of stroke.

This study, in more than 40,000 U.S. women, found an increased risk for subsequent stroke among women with a prior history of hypertensive disorder of pregnancy – overall, a 66% increased risk, an 80% increased risk with gestational hypertension, and about a 50% increased risk with preeclampsia.

We know that pregnancy itself can lead to some remodeling of the vascular system, but we don’t know whether a direct causal relationship exists between preeclampsia or gestational hypertension and subsequent stroke. Another potential explanation is that these complications of pregnancy serve as a window into a woman’s future cardiometabolic health and a marker of her cardiovascular risk.

Regardless, the clinical implications are the same. First, we would want to prevent these complications of pregnancy whenever possible. Some women will be candidates for the use of aspirin if they are at high risk for preeclampsia, and certainly for monitoring blood pressure very closely during pregnancy. It will also be important to maintain blood pressure control in the postpartum period and during the subsequent years of adulthood to minimize risk for stroke, because hypertension is such a powerful risk factor for stroke.

It will also be tremendously important to intensify lifestyle modifications such as increasing physical activity and having a heart-healthy diet. These complications of pregnancy have also been linked in other studies to an increased risk for subsequent coronary heart disease events and heart failure.

This transcript has been edited for clarity.

Dr. Manson is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, and chief of the division of preventive medicine, Brigham and Women’s Hospital, both in Boston, and past president, North American Menopause Society, 2011-2012. She disclosed receiving study pill donation and infrastructure support from Mars Symbioscience (for the COSMOS trial).

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

This is Dr. JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk with you about a recent report on the American Heart Association Life’s Essential 8 metric and its association with both life expectancy and health span or life expectancy free of chronic diseases such as cardiovascular disease (CVD), cancer, diabetes, and dementia.

This study leveraged the UK Biobank and included more than 135,000 U.K. adults with a mean age of 55. The AHA metric was defined as including the following lifestyle behavioral factors:

• Not smoking.
• Regular physical activity.
• Healthy weight.
• Healthy diet.
• Healthy sleep (defined as an average of 7-9 hours nightly).
• Blood pressure in a healthy range.
• Blood glucose in a healthy range.
• Non-HDL cholesterol in a healthy range.

This study was just published in JAMA Internal Medicine. I’d like to acknowledge that I’m a coauthor of this study, along with my colleagues at Tulane.

We divided the study population into three groups: those with low, moderate, and high scores on the Life’s Essential 8 metric – low, moderate, and high cardiovascular health. Overall, the average life expectancy free of chronic disease was estimated to be age 50, with 25 additional years in men and 30 additional years in women.

We saw large differences across the Life’s Essential 8 metric group. Men with high cardiovascular health scores tended to have an additional 7 years of life expectancy free of chronic disease, compared with those who had poorer scores. In women, the difference was about 9.5 years between high scores and lower scores. Also, the number of years lived with chronic disease was compressed in those with high cardiovascular health scores. They tended to have fewer years living with those chronic diseases but more years living free of chronic diseases.

We were interested in how these results might differ by socioeconomic status, educational level, and income level, as well as the Townsend deprivation index. We were intrigued by the finding that the gain in life expectancy free of chronic disease was very similar across all socioeconomic strata – those with lower education and lower income gained as much in terms of chronic disease–free life expectancy as those who were in the higher socioeconomic strata.

Overall, the findings make a compelling case for the importance of lifestyle factors in extending health span and years free of chronic disease. It can be motivating to tell our patients that a healthy lifestyle not only extends life expectancy but also extends years of health free of chronic disease.

Nonetheless, we do have many disparities in life expectancy and health span. So it will be very important to population health to narrow those health disparities through education about the importance of lifestyle factors, more research on implementation of lifestyle factors and behaviors, and public policy to make a healthy lifestyle both affordable and accessible to all people across all of these socioeconomic groups.

Thank you so much for your attention.

JoAnn E. Manson, MD, DrPH, is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, Boston.

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

This transcript has been edited for clarity.

This is Dr. JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk with you about a recent report on the American Heart Association Life’s Essential 8 metric and its association with both life expectancy and health span or life expectancy free of chronic diseases such as cardiovascular disease (CVD), cancer, diabetes, and dementia.

This study leveraged the UK Biobank and included more than 135,000 U.K. adults with a mean age of 55. The AHA metric was defined as including the following lifestyle behavioral factors:

• Not smoking.
• Regular physical activity.
• Healthy weight.
• Healthy diet.
• Healthy sleep (defined as an average of 7-9 hours nightly).
• Blood pressure in a healthy range.
• Blood glucose in a healthy range.
• Non-HDL cholesterol in a healthy range.

This study was just published in JAMA Internal Medicine. I’d like to acknowledge that I’m a coauthor of this study, along with my colleagues at Tulane.

We divided the study population into three groups: those with low, moderate, and high scores on the Life’s Essential 8 metric – low, moderate, and high cardiovascular health. Overall, the average life expectancy free of chronic disease was estimated to be age 50, with 25 additional years in men and 30 additional years in women.

We saw large differences across the Life’s Essential 8 metric group. Men with high cardiovascular health scores tended to have an additional 7 years of life expectancy free of chronic disease, compared with those who had poorer scores. In women, the difference was about 9.5 years between high scores and lower scores. Also, the number of years lived with chronic disease was compressed in those with high cardiovascular health scores. They tended to have fewer years living with those chronic diseases but more years living free of chronic diseases.

We were interested in how these results might differ by socioeconomic status, educational level, and income level, as well as the Townsend deprivation index. We were intrigued by the finding that the gain in life expectancy free of chronic disease was very similar across all socioeconomic strata – those with lower education and lower income gained as much in terms of chronic disease–free life expectancy as those who were in the higher socioeconomic strata.

Overall, the findings make a compelling case for the importance of lifestyle factors in extending health span and years free of chronic disease. It can be motivating to tell our patients that a healthy lifestyle not only extends life expectancy but also extends years of health free of chronic disease.

Nonetheless, we do have many disparities in life expectancy and health span. So it will be very important to population health to narrow those health disparities through education about the importance of lifestyle factors, more research on implementation of lifestyle factors and behaviors, and public policy to make a healthy lifestyle both affordable and accessible to all people across all of these socioeconomic groups.

Thank you so much for your attention.

JoAnn E. Manson, MD, DrPH, is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, Boston.

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

This transcript has been edited for clarity.

This is Dr. JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk with you about a recent report on the American Heart Association Life’s Essential 8 metric and its association with both life expectancy and health span or life expectancy free of chronic diseases such as cardiovascular disease (CVD), cancer, diabetes, and dementia.

This study leveraged the UK Biobank and included more than 135,000 U.K. adults with a mean age of 55. The AHA metric was defined as including the following lifestyle behavioral factors:

• Not smoking.
• Regular physical activity.
• Healthy weight.
• Healthy diet.
• Healthy sleep (defined as an average of 7-9 hours nightly).
• Blood pressure in a healthy range.
• Blood glucose in a healthy range.
• Non-HDL cholesterol in a healthy range.

This study was just published in JAMA Internal Medicine. I’d like to acknowledge that I’m a coauthor of this study, along with my colleagues at Tulane.

We divided the study population into three groups: those with low, moderate, and high scores on the Life’s Essential 8 metric – low, moderate, and high cardiovascular health. Overall, the average life expectancy free of chronic disease was estimated to be age 50, with 25 additional years in men and 30 additional years in women.

We saw large differences across the Life’s Essential 8 metric group. Men with high cardiovascular health scores tended to have an additional 7 years of life expectancy free of chronic disease, compared with those who had poorer scores. In women, the difference was about 9.5 years between high scores and lower scores. Also, the number of years lived with chronic disease was compressed in those with high cardiovascular health scores. They tended to have fewer years living with those chronic diseases but more years living free of chronic diseases.

We were interested in how these results might differ by socioeconomic status, educational level, and income level, as well as the Townsend deprivation index. We were intrigued by the finding that the gain in life expectancy free of chronic disease was very similar across all socioeconomic strata – those with lower education and lower income gained as much in terms of chronic disease–free life expectancy as those who were in the higher socioeconomic strata.

Overall, the findings make a compelling case for the importance of lifestyle factors in extending health span and years free of chronic disease. It can be motivating to tell our patients that a healthy lifestyle not only extends life expectancy but also extends years of health free of chronic disease.

Nonetheless, we do have many disparities in life expectancy and health span. So it will be very important to population health to narrow those health disparities through education about the importance of lifestyle factors, more research on implementation of lifestyle factors and behaviors, and public policy to make a healthy lifestyle both affordable and accessible to all people across all of these socioeconomic groups.

Thank you so much for your attention.

JoAnn E. Manson, MD, DrPH, is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, Boston.

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

This transcript has been edited for clarity.

Hello. This is Dr. JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk with you about a recent report in JAMA Cardiology on atrial fibrillation (AF), sex differences, and modifiable risk factors.

We looked at these questions in our vitamin D and omega-3 trial VITAL in an ancillary study called VITAL Rhythm, led by Dr. Christine Albert at Cedars-Sinai. And this particular project was led by Dr. Hasan Siddiqi at Vanderbilt.

As you know, AF is the most common arrhythmia in the world, and it’s burgeoning in numbers, primarily because of the aging of the population. It’s also a major cause of stroke, heart failure, and cardiovascular mortality. Although women are known to have lower rates of AF than men, they’re also known to have a higher risk for cardiovascular complications and sequelae, such as higher risk for stroke and CVD mortality. Therefore, we thought that understanding sex differences in risk and modifiable risk factors for AF that could reduce the burden of disease would be important.

It’s known that greater height is a risk factor for AF, but the extent to which it explains the differences in AF risk between men and women isn’t really known. So we looked at these questions in the VITAL cohort. VITAL has more than 25,000 participants. It’s a large, diverse, nationwide cohort. About 51% are women, and all are aged 50 years or older, with a mean age of 67. All were free of known clinical cardiovascular disease at the start of the study.

AF reports were confirmed by medical records and also supplemented by Medicare CMS linkage for fuller ascertainment of outcomes. We had 900 incident cases of AF in the study, and we did see that women were less likely to be diagnosed with AF. They had a 32% lower risk – strongly statistically significant compared with men, with a P < .001. Women were also more likely to be symptomatic: About 77% of women vs. 63% of men had symptoms prior to or at diagnosis.

It was very interesting that adjustment for height eliminated the lower risk for AF in women compared with men. After accounting for height, there was not only no reduction in risk for AF among the women, there was actually a reversal of the association so that there was a slightly higher risk for AF in the women. Other risk factors for AF in the cohort included older age, higher body mass index, hypertension, and higher consumption of alcohol. We did not see an association between diabetes and higher risk for AF. We also saw no clear association with physical activity, although very strenuous physical activity has been linked to AF in some other studies.

We looked at the interventions of vitamin D (2,000 IU/day) and omega-3 fatty acids (460 mg/day of EPA and 380 mg/day of DHA) and found no association with AF, although some other studies have seen increased risk for AF with higher doses of the marine omega-3s > 1 g/day and certainly at doses of 4 g/day. So overall, the findings highlight the fact that many of the risk factors for AF do seem to be modifiable, and it is really important to identify and try to reduce these risk factors in order to reduce the burden of AF. This may be particularly important in women because women are more likely to have stroke and cardiovascular mortality in these adverse cardiovascular outcomes.

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

This transcript has been edited for clarity.

Hello. This is Dr. JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk with you about a recent report in JAMA Cardiology on atrial fibrillation (AF), sex differences, and modifiable risk factors.

We looked at these questions in our vitamin D and omega-3 trial VITAL in an ancillary study called VITAL Rhythm, led by Dr. Christine Albert at Cedars-Sinai. And this particular project was led by Dr. Hasan Siddiqi at Vanderbilt.

As you know, AF is the most common arrhythmia in the world, and it’s burgeoning in numbers, primarily because of the aging of the population. It’s also a major cause of stroke, heart failure, and cardiovascular mortality. Although women are known to have lower rates of AF than men, they’re also known to have a higher risk for cardiovascular complications and sequelae, such as higher risk for stroke and CVD mortality. Therefore, we thought that understanding sex differences in risk and modifiable risk factors for AF that could reduce the burden of disease would be important.

It’s known that greater height is a risk factor for AF, but the extent to which it explains the differences in AF risk between men and women isn’t really known. So we looked at these questions in the VITAL cohort. VITAL has more than 25,000 participants. It’s a large, diverse, nationwide cohort. About 51% are women, and all are aged 50 years or older, with a mean age of 67. All were free of known clinical cardiovascular disease at the start of the study.

AF reports were confirmed by medical records and also supplemented by Medicare CMS linkage for fuller ascertainment of outcomes. We had 900 incident cases of AF in the study, and we did see that women were less likely to be diagnosed with AF. They had a 32% lower risk – strongly statistically significant compared with men, with a P < .001. Women were also more likely to be symptomatic: About 77% of women vs. 63% of men had symptoms prior to or at diagnosis.

It was very interesting that adjustment for height eliminated the lower risk for AF in women compared with men. After accounting for height, there was not only no reduction in risk for AF among the women, there was actually a reversal of the association so that there was a slightly higher risk for AF in the women. Other risk factors for AF in the cohort included older age, higher body mass index, hypertension, and higher consumption of alcohol. We did not see an association between diabetes and higher risk for AF. We also saw no clear association with physical activity, although very strenuous physical activity has been linked to AF in some other studies.

We looked at the interventions of vitamin D (2,000 IU/day) and omega-3 fatty acids (460 mg/day of EPA and 380 mg/day of DHA) and found no association with AF, although some other studies have seen increased risk for AF with higher doses of the marine omega-3s > 1 g/day and certainly at doses of 4 g/day. So overall, the findings highlight the fact that many of the risk factors for AF do seem to be modifiable, and it is really important to identify and try to reduce these risk factors in order to reduce the burden of AF. This may be particularly important in women because women are more likely to have stroke and cardiovascular mortality in these adverse cardiovascular outcomes.

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

This transcript has been edited for clarity.

Hello. This is Dr. JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk with you about a recent report in JAMA Cardiology on atrial fibrillation (AF), sex differences, and modifiable risk factors.

We looked at these questions in our vitamin D and omega-3 trial VITAL in an ancillary study called VITAL Rhythm, led by Dr. Christine Albert at Cedars-Sinai. And this particular project was led by Dr. Hasan Siddiqi at Vanderbilt.

As you know, AF is the most common arrhythmia in the world, and it’s burgeoning in numbers, primarily because of the aging of the population. It’s also a major cause of stroke, heart failure, and cardiovascular mortality. Although women are known to have lower rates of AF than men, they’re also known to have a higher risk for cardiovascular complications and sequelae, such as higher risk for stroke and CVD mortality. Therefore, we thought that understanding sex differences in risk and modifiable risk factors for AF that could reduce the burden of disease would be important.

It’s known that greater height is a risk factor for AF, but the extent to which it explains the differences in AF risk between men and women isn’t really known. So we looked at these questions in the VITAL cohort. VITAL has more than 25,000 participants. It’s a large, diverse, nationwide cohort. About 51% are women, and all are aged 50 years or older, with a mean age of 67. All were free of known clinical cardiovascular disease at the start of the study.

AF reports were confirmed by medical records and also supplemented by Medicare CMS linkage for fuller ascertainment of outcomes. We had 900 incident cases of AF in the study, and we did see that women were less likely to be diagnosed with AF. They had a 32% lower risk – strongly statistically significant compared with men, with a P < .001. Women were also more likely to be symptomatic: About 77% of women vs. 63% of men had symptoms prior to or at diagnosis.

It was very interesting that adjustment for height eliminated the lower risk for AF in women compared with men. After accounting for height, there was not only no reduction in risk for AF among the women, there was actually a reversal of the association so that there was a slightly higher risk for AF in the women. Other risk factors for AF in the cohort included older age, higher body mass index, hypertension, and higher consumption of alcohol. We did not see an association between diabetes and higher risk for AF. We also saw no clear association with physical activity, although very strenuous physical activity has been linked to AF in some other studies.

We looked at the interventions of vitamin D (2,000 IU/day) and omega-3 fatty acids (460 mg/day of EPA and 380 mg/day of DHA) and found no association with AF, although some other studies have seen increased risk for AF with higher doses of the marine omega-3s > 1 g/day and certainly at doses of 4 g/day. So overall, the findings highlight the fact that many of the risk factors for AF do seem to be modifiable, and it is really important to identify and try to reduce these risk factors in order to reduce the burden of AF. This may be particularly important in women because women are more likely to have stroke and cardiovascular mortality in these adverse cardiovascular outcomes.

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

This transcript has been edited for clarity.

Hello. This is Dr JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk with you about the recent research (particularly randomized clinical trials) of vitamin D supplementation and the implications for clinical practice. As a director of the Vitamin D and Omega-3 trial (VITAL), the largest randomized clinical trial in the world, I’m often asked, “How much vitamin D do we need, and should I take a vitamin D supplement?” I want to review the findings from recent randomized clinical trials and the implications for practice.

For a long time, vitamin D has been perceived as a magic bullet, a panacea, and a cure-all for many chronic health conditions such as cancer, cardiovascular disease, diabetes, bone fractures, cognitive decline, and depression. Many of the findings, though, have been from observational studies where a higher blood level of 25-hydroxy vitamin D has been linked to a lower risk for these health conditions.

We know in epidemiology that correlation doesn’t prove causation. Other factors could be involved; for example, people who have higher blood levels of vitamin D may have healthier diets, or they may be spending more time outdoors, being physically active and exposed to the sun. Some of these other factors could be lowering their risk.

When the randomized trials began to emerge, in many of these large-scale trials, the findings were generally neutral or null for cardiovascular disease, total cancer, diabetes, cognitive decline, depression, and many other health outcomes, including fracture. So, the question was asked, does this mean that vitamin D is not important to health?

To the contrary, these findings suggest that vitamin D is so essential to health that we need only small to moderate amounts of vitamin D. Vitamin D is very tightly regulated in the body – the metabolism and function of vitamin D. Even small to moderate amounts will meet the requirements for vitamin D and bone health and many other outcomes.

This is what the National Academy of Medicine, U.S. Preventive Services Task Force, and many other professional organizations have advised, that widespread screening for vitamin D deficiency and blanket universal supplementation with vitamin D would not be indicated.

The randomized trials of vitamin D, including the VITAL study, have generally not shown reductions in the major health outcomes. We found two exceptions in VITAL. We saw promising signals, including a 22% reduction in autoimmune conditions (rheumatoid arthritis and psoriasis) and a 17% reduction in advanced (metastatic or fatal) cancers. In meta-analyses of other large-scale randomized trials, the findings were a signal for a reduction in advanced cancers, even with very small doses of vitamin D (400-800 IUs daily). We tested 2,000 IUs daily in VITAL.

Overall, it’s recommended that small to moderate amounts of vitamin D are adequate, and among the healthy population, most people do not need screening or supplements.

The reduction in autoimmune diseases suggests that vitamin D may play a role in tamping down inflammation. The question has been raised about whether vitamin D is beneficial in reducing the severity of COVID illness, the need for hospitalization, and long COVID. We are looking at this question in a separate trial called VIVID (Vitamin D for COVID Trial) which tests a higher dose (> 3,000 IUs daily) of vitamin D. Those results will be available at the end of this year or early next year.

In other randomized trials of COVID and vitamin D, the results have been mixed and inconsistent, with no clear answer. During the COVID pandemic, I have generally advised that it’s reasonable to take 1,000-2,000 IUs of vitamin D daily as a form of insurance. This dose is known to be very safe. Over 5.3 years in the VITAL trial we saw that a dose of 2,000 IUs was very safe.

But it’s not essential to take a supplement. And overall, aside from some high-risk groups, most people do not need a supplement. The high-risk groups include patients in nursing homes who may have restricted diets and limited time out of doors. For people with malabsorption conditions such as Crohn’s disease, celiac disease, post–gastric bypass surgery, and those with osteoporosis who are on medications for osteoporosis, it’s still quite reasonable to prescribe calcium and vitamin D.

Recommendations for vitamin D in the generally healthy population really should focus on a healthy diet. The United States has a fortified food supply. Vitamin D is added to many foods, dairy products, and cereals, as well as beverages. Natural sources of vitamin D include fatty fish and wild mushrooms.

We should be looking at food labels (which now include vitamin D content) and try to get adequate vitamin D from our diet, and also do our best to spend time outdoors, being physically active, because it is of great benefit to our health. The general principle is that a dietary supplement will never be a substitute for a healthy diet or healthy lifestyle. And those other behaviors really should be the focus at this time.

Dr. Manson is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, and chief of the division of preventive medicine at Brigham and Women’s Hospital, both in Boston. She has received infrastructure support from Mars Symbioscience for the COSMOS trial.

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

This transcript has been edited for clarity.

Hello. This is Dr JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk with you about the recent research (particularly randomized clinical trials) of vitamin D supplementation and the implications for clinical practice. As a director of the Vitamin D and Omega-3 trial (VITAL), the largest randomized clinical trial in the world, I’m often asked, “How much vitamin D do we need, and should I take a vitamin D supplement?” I want to review the findings from recent randomized clinical trials and the implications for practice.

For a long time, vitamin D has been perceived as a magic bullet, a panacea, and a cure-all for many chronic health conditions such as cancer, cardiovascular disease, diabetes, bone fractures, cognitive decline, and depression. Many of the findings, though, have been from observational studies where a higher blood level of 25-hydroxy vitamin D has been linked to a lower risk for these health conditions.

We know in epidemiology that correlation doesn’t prove causation. Other factors could be involved; for example, people who have higher blood levels of vitamin D may have healthier diets, or they may be spending more time outdoors, being physically active and exposed to the sun. Some of these other factors could be lowering their risk.

When the randomized trials began to emerge, in many of these large-scale trials, the findings were generally neutral or null for cardiovascular disease, total cancer, diabetes, cognitive decline, depression, and many other health outcomes, including fracture. So, the question was asked, does this mean that vitamin D is not important to health?

To the contrary, these findings suggest that vitamin D is so essential to health that we need only small to moderate amounts of vitamin D. Vitamin D is very tightly regulated in the body – the metabolism and function of vitamin D. Even small to moderate amounts will meet the requirements for vitamin D and bone health and many other outcomes.

This is what the National Academy of Medicine, U.S. Preventive Services Task Force, and many other professional organizations have advised, that widespread screening for vitamin D deficiency and blanket universal supplementation with vitamin D would not be indicated.

The randomized trials of vitamin D, including the VITAL study, have generally not shown reductions in the major health outcomes. We found two exceptions in VITAL. We saw promising signals, including a 22% reduction in autoimmune conditions (rheumatoid arthritis and psoriasis) and a 17% reduction in advanced (metastatic or fatal) cancers. In meta-analyses of other large-scale randomized trials, the findings were a signal for a reduction in advanced cancers, even with very small doses of vitamin D (400-800 IUs daily). We tested 2,000 IUs daily in VITAL.

Overall, it’s recommended that small to moderate amounts of vitamin D are adequate, and among the healthy population, most people do not need screening or supplements.

The reduction in autoimmune diseases suggests that vitamin D may play a role in tamping down inflammation. The question has been raised about whether vitamin D is beneficial in reducing the severity of COVID illness, the need for hospitalization, and long COVID. We are looking at this question in a separate trial called VIVID (Vitamin D for COVID Trial) which tests a higher dose (> 3,000 IUs daily) of vitamin D. Those results will be available at the end of this year or early next year.

In other randomized trials of COVID and vitamin D, the results have been mixed and inconsistent, with no clear answer. During the COVID pandemic, I have generally advised that it’s reasonable to take 1,000-2,000 IUs of vitamin D daily as a form of insurance. This dose is known to be very safe. Over 5.3 years in the VITAL trial we saw that a dose of 2,000 IUs was very safe.

But it’s not essential to take a supplement. And overall, aside from some high-risk groups, most people do not need a supplement. The high-risk groups include patients in nursing homes who may have restricted diets and limited time out of doors. For people with malabsorption conditions such as Crohn’s disease, celiac disease, post–gastric bypass surgery, and those with osteoporosis who are on medications for osteoporosis, it’s still quite reasonable to prescribe calcium and vitamin D.

Recommendations for vitamin D in the generally healthy population really should focus on a healthy diet. The United States has a fortified food supply. Vitamin D is added to many foods, dairy products, and cereals, as well as beverages. Natural sources of vitamin D include fatty fish and wild mushrooms.

We should be looking at food labels (which now include vitamin D content) and try to get adequate vitamin D from our diet, and also do our best to spend time outdoors, being physically active, because it is of great benefit to our health. The general principle is that a dietary supplement will never be a substitute for a healthy diet or healthy lifestyle. And those other behaviors really should be the focus at this time.

Dr. Manson is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, and chief of the division of preventive medicine at Brigham and Women’s Hospital, both in Boston. She has received infrastructure support from Mars Symbioscience for the COSMOS trial.

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

This transcript has been edited for clarity.

Hello. This is Dr JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk with you about the recent research (particularly randomized clinical trials) of vitamin D supplementation and the implications for clinical practice. As a director of the Vitamin D and Omega-3 trial (VITAL), the largest randomized clinical trial in the world, I’m often asked, “How much vitamin D do we need, and should I take a vitamin D supplement?” I want to review the findings from recent randomized clinical trials and the implications for practice.

For a long time, vitamin D has been perceived as a magic bullet, a panacea, and a cure-all for many chronic health conditions such as cancer, cardiovascular disease, diabetes, bone fractures, cognitive decline, and depression. Many of the findings, though, have been from observational studies where a higher blood level of 25-hydroxy vitamin D has been linked to a lower risk for these health conditions.

We know in epidemiology that correlation doesn’t prove causation. Other factors could be involved; for example, people who have higher blood levels of vitamin D may have healthier diets, or they may be spending more time outdoors, being physically active and exposed to the sun. Some of these other factors could be lowering their risk.

When the randomized trials began to emerge, in many of these large-scale trials, the findings were generally neutral or null for cardiovascular disease, total cancer, diabetes, cognitive decline, depression, and many other health outcomes, including fracture. So, the question was asked, does this mean that vitamin D is not important to health?

To the contrary, these findings suggest that vitamin D is so essential to health that we need only small to moderate amounts of vitamin D. Vitamin D is very tightly regulated in the body – the metabolism and function of vitamin D. Even small to moderate amounts will meet the requirements for vitamin D and bone health and many other outcomes.

This is what the National Academy of Medicine, U.S. Preventive Services Task Force, and many other professional organizations have advised, that widespread screening for vitamin D deficiency and blanket universal supplementation with vitamin D would not be indicated.

The randomized trials of vitamin D, including the VITAL study, have generally not shown reductions in the major health outcomes. We found two exceptions in VITAL. We saw promising signals, including a 22% reduction in autoimmune conditions (rheumatoid arthritis and psoriasis) and a 17% reduction in advanced (metastatic or fatal) cancers. In meta-analyses of other large-scale randomized trials, the findings were a signal for a reduction in advanced cancers, even with very small doses of vitamin D (400-800 IUs daily). We tested 2,000 IUs daily in VITAL.

Overall, it’s recommended that small to moderate amounts of vitamin D are adequate, and among the healthy population, most people do not need screening or supplements.

The reduction in autoimmune diseases suggests that vitamin D may play a role in tamping down inflammation. The question has been raised about whether vitamin D is beneficial in reducing the severity of COVID illness, the need for hospitalization, and long COVID. We are looking at this question in a separate trial called VIVID (Vitamin D for COVID Trial) which tests a higher dose (> 3,000 IUs daily) of vitamin D. Those results will be available at the end of this year or early next year.

In other randomized trials of COVID and vitamin D, the results have been mixed and inconsistent, with no clear answer. During the COVID pandemic, I have generally advised that it’s reasonable to take 1,000-2,000 IUs of vitamin D daily as a form of insurance. This dose is known to be very safe. Over 5.3 years in the VITAL trial we saw that a dose of 2,000 IUs was very safe.

But it’s not essential to take a supplement. And overall, aside from some high-risk groups, most people do not need a supplement. The high-risk groups include patients in nursing homes who may have restricted diets and limited time out of doors. For people with malabsorption conditions such as Crohn’s disease, celiac disease, post–gastric bypass surgery, and those with osteoporosis who are on medications for osteoporosis, it’s still quite reasonable to prescribe calcium and vitamin D.

Recommendations for vitamin D in the generally healthy population really should focus on a healthy diet. The United States has a fortified food supply. Vitamin D is added to many foods, dairy products, and cereals, as well as beverages. Natural sources of vitamin D include fatty fish and wild mushrooms.

We should be looking at food labels (which now include vitamin D content) and try to get adequate vitamin D from our diet, and also do our best to spend time outdoors, being physically active, because it is of great benefit to our health. The general principle is that a dietary supplement will never be a substitute for a healthy diet or healthy lifestyle. And those other behaviors really should be the focus at this time.

Dr. Manson is professor of medicine and the Michael and Lee Bell Professor of Women’s Health, Harvard Medical School, and chief of the division of preventive medicine at Brigham and Women’s Hospital, both in Boston. She has received infrastructure support from Mars Symbioscience for the COSMOS trial.

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

This recently published study from Finland generated headlines when its authors concluded that stopping HT elevates the risk of mortality from cardiovascular disease (CVD), including cardiac and cerebrovascular events. Using nationwide data, investigators compared the CVD mortality rate among women who discontinued HT during the years 1994 through 2009 (n = 332,202) with expected (not actual) CVD mortality rates in the background population.
Within the first year after HT discontinuation, elevations in death rates from cardiac events and stroke were noted (standardized mortality ratio, 1.26 and 1.63, respectively), while in the subsequent year, reductions in such mortality were observed (P<.05 for all comparisons).
The absolute increased risk of death from cardiac events reported within the first year after discontinuation of HT was 4 deaths per 10,000 woman-years of exposure. The absolute risk of death from stroke was 5 additional events per 10,000 woman-years. This level of risk is considered to be rare.

How these data compare to those of other studiesIn contrast with these Finnish data, findings from the Women’s Health Initiative—the largest randomized trial of menopausal HT—do not indicate an increase in mortality or an increase in coronary heart or stroke events among women stopping HT.^1,2
It seems likely that limitations associated with the Finnish observational data account for this discordance. For example, Mikkola and colleagues did not know why women discontinued HT, raising the possibility that women with symptoms suggestive of CVD or development of new risk factors preferentially stopped HT, potentially introducing important bias into the Finnish analysis.

What this evidence means for practiceWomen and their clinicians should make decisions regarding whether to continue, reduce the dose, or discontinue HT through shared decision making, focusing on individual patient quality of life parameters as well as changing risk concerns related to such entities as cancer, CVD, and osteoporosis.³ Dramatic as they are, findings from this Finnish report should not impact how we counsel women regarding use or discontinuation of HT.
—Andrew M. Kaunitz, MD; JoAnn E. Manson, MD, DrPH; and Cynthia A. Stuenkel, MD

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

This recently published study from Finland generated headlines when its authors concluded that stopping HT elevates the risk of mortality from cardiovascular disease (CVD), including cardiac and cerebrovascular events. Using nationwide data, investigators compared the CVD mortality rate among women who discontinued HT during the years 1994 through 2009 (n = 332,202) with expected (not actual) CVD mortality rates in the background population.
Within the first year after HT discontinuation, elevations in death rates from cardiac events and stroke were noted (standardized mortality ratio, 1.26 and 1.63, respectively), while in the subsequent year, reductions in such mortality were observed (P<.05 for all comparisons).
The absolute increased risk of death from cardiac events reported within the first year after discontinuation of HT was 4 deaths per 10,000 woman-years of exposure. The absolute risk of death from stroke was 5 additional events per 10,000 woman-years. This level of risk is considered to be rare.

How these data compare to those of other studiesIn contrast with these Finnish data, findings from the Women’s Health Initiative—the largest randomized trial of menopausal HT—do not indicate an increase in mortality or an increase in coronary heart or stroke events among women stopping HT.^1,2
It seems likely that limitations associated with the Finnish observational data account for this discordance. For example, Mikkola and colleagues did not know why women discontinued HT, raising the possibility that women with symptoms suggestive of CVD or development of new risk factors preferentially stopped HT, potentially introducing important bias into the Finnish analysis.

What this evidence means for practiceWomen and their clinicians should make decisions regarding whether to continue, reduce the dose, or discontinue HT through shared decision making, focusing on individual patient quality of life parameters as well as changing risk concerns related to such entities as cancer, CVD, and osteoporosis.³ Dramatic as they are, findings from this Finnish report should not impact how we counsel women regarding use or discontinuation of HT.
—Andrew M. Kaunitz, MD; JoAnn E. Manson, MD, DrPH; and Cynthia A. Stuenkel, MD

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

This recently published study from Finland generated headlines when its authors concluded that stopping HT elevates the risk of mortality from cardiovascular disease (CVD), including cardiac and cerebrovascular events. Using nationwide data, investigators compared the CVD mortality rate among women who discontinued HT during the years 1994 through 2009 (n = 332,202) with expected (not actual) CVD mortality rates in the background population.
Within the first year after HT discontinuation, elevations in death rates from cardiac events and stroke were noted (standardized mortality ratio, 1.26 and 1.63, respectively), while in the subsequent year, reductions in such mortality were observed (P<.05 for all comparisons).
The absolute increased risk of death from cardiac events reported within the first year after discontinuation of HT was 4 deaths per 10,000 woman-years of exposure. The absolute risk of death from stroke was 5 additional events per 10,000 woman-years. This level of risk is considered to be rare.

How these data compare to those of other studiesIn contrast with these Finnish data, findings from the Women’s Health Initiative—the largest randomized trial of menopausal HT—do not indicate an increase in mortality or an increase in coronary heart or stroke events among women stopping HT.^1,2
It seems likely that limitations associated with the Finnish observational data account for this discordance. For example, Mikkola and colleagues did not know why women discontinued HT, raising the possibility that women with symptoms suggestive of CVD or development of new risk factors preferentially stopped HT, potentially introducing important bias into the Finnish analysis.

What this evidence means for practiceWomen and their clinicians should make decisions regarding whether to continue, reduce the dose, or discontinue HT through shared decision making, focusing on individual patient quality of life parameters as well as changing risk concerns related to such entities as cancer, CVD, and osteoporosis.³ Dramatic as they are, findings from this Finnish report should not impact how we counsel women regarding use or discontinuation of HT.
—Andrew M. Kaunitz, MD; JoAnn E. Manson, MD, DrPH; and Cynthia A. Stuenkel, MD

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.