Jon O. Ebbert, MD

The only thing certain in life is change. This is certainly true of medicine in general and dietary information in particular. Salt restriction recommendations for heart failure, once considered a core foundational practice tantamount to diuretics for fluid overload, are now being questioned.

European and North American heart failure management guidelines recommend sodium restriction for patients with systolic and diastolic heart failure with preserved ejection fraction. Available data now suggest that sodium restriction may actually increase mortality among patients with systolic heart failure. As a generalist, perhaps I was not aware of this raging debate among the subspecialists, but now would be a great time to pay attention and try to understand what is being said.

Pharmacist James J DiNicolantonio of Wegmans Pharmacy, Ithaca, NY, and colleagues recently published a systematic review evaluating the impact of a restricted sodium diet in patients with systolic heart failure. The authors included randomized controlled clinical trials enrolling adults with systolic heart failure (ejection fraction < 40%) evaluating studies restricting salt through a dietary intervention or recommending reduced salt intake.

Six studies with 2,747 subjects were included in the analysis. Studies reported that all subjects consumed the same diet, except for the level of sodium, which ranged from low (< 1.8 g/day) to normal (2.8 g/day). Trials measured 24-hour urinary sodium levels.

Compared with a normal sodium diet, a low sodium diet increased the risk for mortality (RR 1.95; 1.66 to 2.29), sudden cardiac death (RR 1.72; 1.21 to 2.44), heart failure (RR 2.23; 1.77 to 2.81), and heart failure readmissions (RR 2.10; 1.67 to 2.64) (Heart doi:10.1136/heartjnl-2012-302337).

The trials showed that a normal sodium intake improved ejection fraction, renal function, hydration status, aldosterone/renin activity, heart rate, BNP, TNF-alpha, IL-6 and prevented hyponatremia. These data may suggest that harm is caused at lower levels of sodium intake due to the counter-regulatory mechanisms addressing hypovolemia. Indeed, hyponatremia is an independent risk predictor of mortality.

This article is likely to generate more discussion. Many of us will likely “wait and see” how large organizations such as the American Heart Association are going to respond to or challenge this information. Let’s hope they can convince us with open minds and thoughtful analysis rather than reflexive defense of traditional paradigms.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflict of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

The only thing certain in life is change. This is certainly true of medicine in general and dietary information in particular. Salt restriction recommendations for heart failure, once considered a core foundational practice tantamount to diuretics for fluid overload, are now being questioned.

European and North American heart failure management guidelines recommend sodium restriction for patients with systolic and diastolic heart failure with preserved ejection fraction. Available data now suggest that sodium restriction may actually increase mortality among patients with systolic heart failure. As a generalist, perhaps I was not aware of this raging debate among the subspecialists, but now would be a great time to pay attention and try to understand what is being said.

Pharmacist James J DiNicolantonio of Wegmans Pharmacy, Ithaca, NY, and colleagues recently published a systematic review evaluating the impact of a restricted sodium diet in patients with systolic heart failure. The authors included randomized controlled clinical trials enrolling adults with systolic heart failure (ejection fraction < 40%) evaluating studies restricting salt through a dietary intervention or recommending reduced salt intake.

Six studies with 2,747 subjects were included in the analysis. Studies reported that all subjects consumed the same diet, except for the level of sodium, which ranged from low (< 1.8 g/day) to normal (2.8 g/day). Trials measured 24-hour urinary sodium levels.

Compared with a normal sodium diet, a low sodium diet increased the risk for mortality (RR 1.95; 1.66 to 2.29), sudden cardiac death (RR 1.72; 1.21 to 2.44), heart failure (RR 2.23; 1.77 to 2.81), and heart failure readmissions (RR 2.10; 1.67 to 2.64) (Heart doi:10.1136/heartjnl-2012-302337).

The trials showed that a normal sodium intake improved ejection fraction, renal function, hydration status, aldosterone/renin activity, heart rate, BNP, TNF-alpha, IL-6 and prevented hyponatremia. These data may suggest that harm is caused at lower levels of sodium intake due to the counter-regulatory mechanisms addressing hypovolemia. Indeed, hyponatremia is an independent risk predictor of mortality.

This article is likely to generate more discussion. Many of us will likely “wait and see” how large organizations such as the American Heart Association are going to respond to or challenge this information. Let’s hope they can convince us with open minds and thoughtful analysis rather than reflexive defense of traditional paradigms.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflict of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

The only thing certain in life is change. This is certainly true of medicine in general and dietary information in particular. Salt restriction recommendations for heart failure, once considered a core foundational practice tantamount to diuretics for fluid overload, are now being questioned.

European and North American heart failure management guidelines recommend sodium restriction for patients with systolic and diastolic heart failure with preserved ejection fraction. Available data now suggest that sodium restriction may actually increase mortality among patients with systolic heart failure. As a generalist, perhaps I was not aware of this raging debate among the subspecialists, but now would be a great time to pay attention and try to understand what is being said.

Pharmacist James J DiNicolantonio of Wegmans Pharmacy, Ithaca, NY, and colleagues recently published a systematic review evaluating the impact of a restricted sodium diet in patients with systolic heart failure. The authors included randomized controlled clinical trials enrolling adults with systolic heart failure (ejection fraction < 40%) evaluating studies restricting salt through a dietary intervention or recommending reduced salt intake.

Six studies with 2,747 subjects were included in the analysis. Studies reported that all subjects consumed the same diet, except for the level of sodium, which ranged from low (< 1.8 g/day) to normal (2.8 g/day). Trials measured 24-hour urinary sodium levels.

Compared with a normal sodium diet, a low sodium diet increased the risk for mortality (RR 1.95; 1.66 to 2.29), sudden cardiac death (RR 1.72; 1.21 to 2.44), heart failure (RR 2.23; 1.77 to 2.81), and heart failure readmissions (RR 2.10; 1.67 to 2.64) (Heart doi:10.1136/heartjnl-2012-302337).

The trials showed that a normal sodium intake improved ejection fraction, renal function, hydration status, aldosterone/renin activity, heart rate, BNP, TNF-alpha, IL-6 and prevented hyponatremia. These data may suggest that harm is caused at lower levels of sodium intake due to the counter-regulatory mechanisms addressing hypovolemia. Indeed, hyponatremia is an independent risk predictor of mortality.

This article is likely to generate more discussion. Many of us will likely “wait and see” how large organizations such as the American Heart Association are going to respond to or challenge this information. Let’s hope they can convince us with open minds and thoughtful analysis rather than reflexive defense of traditional paradigms.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflict of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

Few presenting complaints are as disconcerting to patients as vertigo. Patient anxiety levels correlate highly with the degree of functional impairment. A diagnosis of benign paroxysmal positional vertigo (BPPV), the most common cause of benign vertigo, is supported by historical elements linking it with head movement and a positive Dix-Hallpike maneuver.

BPPV most commonly affects the posterior semicircular canals. The prevailing theory is that “canalolithiasis” occurs with particles moving through the canal influenced by gravity and head movement. Symptoms occur as a result of the hydrodynamic pull of endolymphatic fluid caused by stone precipitates. Symptoms tend to spontaneously resolve after an average of 39 days.

A clear diagnosis of BPPV allows us to roll into reassurance mode and provide patients with self-management techniques. Patients self-treat BPPV with the Epley maneuver. Another commonly employed technique is the Semont maneuver. 

More evidence exists regarding the efficacy of the Epley than the Semont maneuver. Dr. Ying Chen and colleagues at Changzheng Hospital in Shanghai, China, published the results of a trial evaluating the efficacy of the Semont maneuver (Otol. Neurotol. 2012;33:1127-30).

In this study, 128 patients with unilateral posterior canal benign paroxysmal positional vertigo (PC-BPPV) were randomly assigned to treatment with the Semont maneuver or sham procedure. PC-BPPV is diagnosed by observing torsion towards the lower-most ear and upbeating nystagmus. Cycles of Dix-Hallpike testing and a Semont maneuver were repeated during the treatment session until no more nystagmus or vertigo could be elicited or until 4 cycles had been completed. The sham procedure was the Semont maneuver for the unaffected side. No medications or postprocedural instructions were provided. Patients returned after four days for re-evaluation. Successful treatment was defined as absence of vertigo and a negative Dix-Hallpike test.

On the fourth day, 55 of 65 patients (85%) in the Semont maneuver group were free of vertigo and nystagmus as determined by Dix-Hallpike testing compared with 9 of 63 (14%) patients in the sham group. Forty-three percent of patients were free of vertigo after a single Semont procedure.

This study provides us with useful clinical information for patients who have unilateral BPPV with symptoms localizing to posterior semicircular canal disease. How the procedure compares to the Epley maneuver was not evaluated. The Semont procedure is easy to perform and patients can quickly be quickly trained on how to performance it. For tech-savvy patients, providing them with links to internet videos demonstrating the maneuver may be helpful.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He declares having no conflicts of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

Few presenting complaints are as disconcerting to patients as vertigo. Patient anxiety levels correlate highly with the degree of functional impairment. A diagnosis of benign paroxysmal positional vertigo (BPPV), the most common cause of benign vertigo, is supported by historical elements linking it with head movement and a positive Dix-Hallpike maneuver.

BPPV most commonly affects the posterior semicircular canals. The prevailing theory is that “canalolithiasis” occurs with particles moving through the canal influenced by gravity and head movement. Symptoms occur as a result of the hydrodynamic pull of endolymphatic fluid caused by stone precipitates. Symptoms tend to spontaneously resolve after an average of 39 days.

A clear diagnosis of BPPV allows us to roll into reassurance mode and provide patients with self-management techniques. Patients self-treat BPPV with the Epley maneuver. Another commonly employed technique is the Semont maneuver. 

More evidence exists regarding the efficacy of the Epley than the Semont maneuver. Dr. Ying Chen and colleagues at Changzheng Hospital in Shanghai, China, published the results of a trial evaluating the efficacy of the Semont maneuver (Otol. Neurotol. 2012;33:1127-30).

In this study, 128 patients with unilateral posterior canal benign paroxysmal positional vertigo (PC-BPPV) were randomly assigned to treatment with the Semont maneuver or sham procedure. PC-BPPV is diagnosed by observing torsion towards the lower-most ear and upbeating nystagmus. Cycles of Dix-Hallpike testing and a Semont maneuver were repeated during the treatment session until no more nystagmus or vertigo could be elicited or until 4 cycles had been completed. The sham procedure was the Semont maneuver for the unaffected side. No medications or postprocedural instructions were provided. Patients returned after four days for re-evaluation. Successful treatment was defined as absence of vertigo and a negative Dix-Hallpike test.

On the fourth day, 55 of 65 patients (85%) in the Semont maneuver group were free of vertigo and nystagmus as determined by Dix-Hallpike testing compared with 9 of 63 (14%) patients in the sham group. Forty-three percent of patients were free of vertigo after a single Semont procedure.

This study provides us with useful clinical information for patients who have unilateral BPPV with symptoms localizing to posterior semicircular canal disease. How the procedure compares to the Epley maneuver was not evaluated. The Semont procedure is easy to perform and patients can quickly be quickly trained on how to performance it. For tech-savvy patients, providing them with links to internet videos demonstrating the maneuver may be helpful.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He declares having no conflicts of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

Few presenting complaints are as disconcerting to patients as vertigo. Patient anxiety levels correlate highly with the degree of functional impairment. A diagnosis of benign paroxysmal positional vertigo (BPPV), the most common cause of benign vertigo, is supported by historical elements linking it with head movement and a positive Dix-Hallpike maneuver.

BPPV most commonly affects the posterior semicircular canals. The prevailing theory is that “canalolithiasis” occurs with particles moving through the canal influenced by gravity and head movement. Symptoms occur as a result of the hydrodynamic pull of endolymphatic fluid caused by stone precipitates. Symptoms tend to spontaneously resolve after an average of 39 days.

A clear diagnosis of BPPV allows us to roll into reassurance mode and provide patients with self-management techniques. Patients self-treat BPPV with the Epley maneuver. Another commonly employed technique is the Semont maneuver. 

More evidence exists regarding the efficacy of the Epley than the Semont maneuver. Dr. Ying Chen and colleagues at Changzheng Hospital in Shanghai, China, published the results of a trial evaluating the efficacy of the Semont maneuver (Otol. Neurotol. 2012;33:1127-30).

In this study, 128 patients with unilateral posterior canal benign paroxysmal positional vertigo (PC-BPPV) were randomly assigned to treatment with the Semont maneuver or sham procedure. PC-BPPV is diagnosed by observing torsion towards the lower-most ear and upbeating nystagmus. Cycles of Dix-Hallpike testing and a Semont maneuver were repeated during the treatment session until no more nystagmus or vertigo could be elicited or until 4 cycles had been completed. The sham procedure was the Semont maneuver for the unaffected side. No medications or postprocedural instructions were provided. Patients returned after four days for re-evaluation. Successful treatment was defined as absence of vertigo and a negative Dix-Hallpike test.

On the fourth day, 55 of 65 patients (85%) in the Semont maneuver group were free of vertigo and nystagmus as determined by Dix-Hallpike testing compared with 9 of 63 (14%) patients in the sham group. Forty-three percent of patients were free of vertigo after a single Semont procedure.

This study provides us with useful clinical information for patients who have unilateral BPPV with symptoms localizing to posterior semicircular canal disease. How the procedure compares to the Epley maneuver was not evaluated. The Semont procedure is easy to perform and patients can quickly be quickly trained on how to performance it. For tech-savvy patients, providing them with links to internet videos demonstrating the maneuver may be helpful.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He declares having no conflicts of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

Musculoskeletal complaints are one of the most common reasons for office visits. According to the 2010 National Health Interview Survey, 29% of U.S. individuals over the age of 18 years have chronic joint symptoms defined as having pain, aching or stiffness in and around a joint in the past 30 days.

No day on the “front lines” is complete without being asked to triage knee pain in a patient who is simultaneously battling excessive body weight. I’ve heard it said that every extra pound over ideal body weight puts an extra four pounds of stress across the knee. Is it any wonder that we perform over 600,000 knee replacements in the U.S. annually? To be fair, obesity is not the only culprit accounting for knee osteoarthritis requiring surgical intervention, but it’s the elephant in the room on this issue.

How many times have we half-heartedly told our patients to lose weight in order to decrease knee symptoms, while feeling certain that they won’t adhere to this advice since their exercise ability is compromised? Some physicians also may question the evidence behind this clinical wisdom.

The fact is that weight loss is indeed a first-line treatment for knee osteoarthritis (OA). Evidence shows that OA symptoms tend to worsen in obese patients, and that weight loss prevents the development of OA. A direct relationship exists between weight loss and the degree of symptomatic improvement among obese patients with OA. But what about patients whose X-rays show significant degeneration? Is it too late for their OA to improve by losing weight?

A recent study from the Parker Institute at Copenhagen University Hospital provides evidence that the degree of baseline structural damage does not predict changes in pain and function with weight loss among obese patients with OA. In this study, knee OA patients with an age greater than 50 years and a body mass index of at least 30 received 16 weeks of a weight loss intervention. Baseline MRI and radiographs were obtained on the most symptomatic knee. More than 10% of patients achieved significant weight loss and almost two-thirds achieved significant symptomatic improvement (Osteoarthritis Cartilage 2012;20:495-502).

The results indicate that for obese patients with OA, weight loss will reduce pain and improve function regardless of the degree of structural damage. This information should help clinicians feel more confident in making their usual recommendations. For patients who suggest that they cannot lose weight because they cannot exercise, it is helpful to remind them that significant weight loss can occur with modifications to total calorie intake and types of calories consumed in the absence of significant increases in activity.

Jon O. Ebbert, M.D, is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He declares having no conflict of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

Musculoskeletal complaints are one of the most common reasons for office visits. According to the 2010 National Health Interview Survey, 29% of U.S. individuals over the age of 18 years have chronic joint symptoms defined as having pain, aching or stiffness in and around a joint in the past 30 days.

No day on the “front lines” is complete without being asked to triage knee pain in a patient who is simultaneously battling excessive body weight. I’ve heard it said that every extra pound over ideal body weight puts an extra four pounds of stress across the knee. Is it any wonder that we perform over 600,000 knee replacements in the U.S. annually? To be fair, obesity is not the only culprit accounting for knee osteoarthritis requiring surgical intervention, but it’s the elephant in the room on this issue.

How many times have we half-heartedly told our patients to lose weight in order to decrease knee symptoms, while feeling certain that they won’t adhere to this advice since their exercise ability is compromised? Some physicians also may question the evidence behind this clinical wisdom.

The fact is that weight loss is indeed a first-line treatment for knee osteoarthritis (OA). Evidence shows that OA symptoms tend to worsen in obese patients, and that weight loss prevents the development of OA. A direct relationship exists between weight loss and the degree of symptomatic improvement among obese patients with OA. But what about patients whose X-rays show significant degeneration? Is it too late for their OA to improve by losing weight?

A recent study from the Parker Institute at Copenhagen University Hospital provides evidence that the degree of baseline structural damage does not predict changes in pain and function with weight loss among obese patients with OA. In this study, knee OA patients with an age greater than 50 years and a body mass index of at least 30 received 16 weeks of a weight loss intervention. Baseline MRI and radiographs were obtained on the most symptomatic knee. More than 10% of patients achieved significant weight loss and almost two-thirds achieved significant symptomatic improvement (Osteoarthritis Cartilage 2012;20:495-502).

The results indicate that for obese patients with OA, weight loss will reduce pain and improve function regardless of the degree of structural damage. This information should help clinicians feel more confident in making their usual recommendations. For patients who suggest that they cannot lose weight because they cannot exercise, it is helpful to remind them that significant weight loss can occur with modifications to total calorie intake and types of calories consumed in the absence of significant increases in activity.

Jon O. Ebbert, M.D, is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He declares having no conflict of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

Musculoskeletal complaints are one of the most common reasons for office visits. According to the 2010 National Health Interview Survey, 29% of U.S. individuals over the age of 18 years have chronic joint symptoms defined as having pain, aching or stiffness in and around a joint in the past 30 days.

No day on the “front lines” is complete without being asked to triage knee pain in a patient who is simultaneously battling excessive body weight. I’ve heard it said that every extra pound over ideal body weight puts an extra four pounds of stress across the knee. Is it any wonder that we perform over 600,000 knee replacements in the U.S. annually? To be fair, obesity is not the only culprit accounting for knee osteoarthritis requiring surgical intervention, but it’s the elephant in the room on this issue.

How many times have we half-heartedly told our patients to lose weight in order to decrease knee symptoms, while feeling certain that they won’t adhere to this advice since their exercise ability is compromised? Some physicians also may question the evidence behind this clinical wisdom.

The fact is that weight loss is indeed a first-line treatment for knee osteoarthritis (OA). Evidence shows that OA symptoms tend to worsen in obese patients, and that weight loss prevents the development of OA. A direct relationship exists between weight loss and the degree of symptomatic improvement among obese patients with OA. But what about patients whose X-rays show significant degeneration? Is it too late for their OA to improve by losing weight?

A recent study from the Parker Institute at Copenhagen University Hospital provides evidence that the degree of baseline structural damage does not predict changes in pain and function with weight loss among obese patients with OA. In this study, knee OA patients with an age greater than 50 years and a body mass index of at least 30 received 16 weeks of a weight loss intervention. Baseline MRI and radiographs were obtained on the most symptomatic knee. More than 10% of patients achieved significant weight loss and almost two-thirds achieved significant symptomatic improvement (Osteoarthritis Cartilage 2012;20:495-502).

The results indicate that for obese patients with OA, weight loss will reduce pain and improve function regardless of the degree of structural damage. This information should help clinicians feel more confident in making their usual recommendations. For patients who suggest that they cannot lose weight because they cannot exercise, it is helpful to remind them that significant weight loss can occur with modifications to total calorie intake and types of calories consumed in the absence of significant increases in activity.

Jon O. Ebbert, M.D, is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He declares having no conflict of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

We all appreciate the importance of physical activity for the maintenance of health and the prevention of adverse health outcomes. I frequently struggle with how to motivate patients to physically exert themselves in a meaningful, consistent, and self-sustaining way.

Technology, in the form of video game systems, has been bandied about as a way to get patients moving. The Nintendo Wii console has become popular in hospitals, residential care facilities, and rehabilitation programs as a means to engage patients in physical activity.

As a consumer of modern technology, I frequently, and likely erroneously, assume that my patients love gadgets as much as I do. When I tell my older patients to consider a video game system as a component of a physical activity program, are my words falling on deaf ears? Recently published data suggest that I need to curb my enthusiasm, at least for now, among my older patients.

Kate Laver of Flinders University, Adelaide, Australia, and colleagues conducted a discrete choice analysis (DCE) among 21 participants prior to and following several sessions of the Wii Fit in physiotherapy. DCEs are based on the assumptions that health care interventions or services can be described by their characteristics (or attributes) and that the consumer’s evaluation of the intervention or service is based on the levels of these attributes. In this study, participants were selected from a geriatric rehabilitation unit in South Australia. A physiotherapist prescribed Wii Fit activities and supervised patients during therapy sessions. Patients had a mean age of 85 years and most were female (86%). After participating in an average of six sessions, many expressed an aversion to the Wii as a therapeutic intervention and preferred traditional therapy programs (BMC Geriatrics 2011;11:64 [doi:10.1186/1471-2318-11-64]).

The study highlights the importance of carefully considering the likely preferences of different patient cohorts. Indeed, game consoles require comfort with a video interface, and this fact may pose challenges to people who are not comfortable with menu navigation and remote control. Middle-age patients (that is, my generation) will be significantly more likely to embrace this technology and new applications of it should be continue to be sought. I typically do not encourage my octogenarians to invest in a Wii, but what about people younger than that? The "iPhone generation" will not only prefer, but might likely expect this option when it becomes necessary for others to motivate us to engage in physical activity.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflicts of interest. The opinions expressed are solely those of the author.

We all appreciate the importance of physical activity for the maintenance of health and the prevention of adverse health outcomes. I frequently struggle with how to motivate patients to physically exert themselves in a meaningful, consistent, and self-sustaining way.

Technology, in the form of video game systems, has been bandied about as a way to get patients moving. The Nintendo Wii console has become popular in hospitals, residential care facilities, and rehabilitation programs as a means to engage patients in physical activity.

As a consumer of modern technology, I frequently, and likely erroneously, assume that my patients love gadgets as much as I do. When I tell my older patients to consider a video game system as a component of a physical activity program, are my words falling on deaf ears? Recently published data suggest that I need to curb my enthusiasm, at least for now, among my older patients.

Kate Laver of Flinders University, Adelaide, Australia, and colleagues conducted a discrete choice analysis (DCE) among 21 participants prior to and following several sessions of the Wii Fit in physiotherapy. DCEs are based on the assumptions that health care interventions or services can be described by their characteristics (or attributes) and that the consumer’s evaluation of the intervention or service is based on the levels of these attributes. In this study, participants were selected from a geriatric rehabilitation unit in South Australia. A physiotherapist prescribed Wii Fit activities and supervised patients during therapy sessions. Patients had a mean age of 85 years and most were female (86%). After participating in an average of six sessions, many expressed an aversion to the Wii as a therapeutic intervention and preferred traditional therapy programs (BMC Geriatrics 2011;11:64 [doi:10.1186/1471-2318-11-64]).

The study highlights the importance of carefully considering the likely preferences of different patient cohorts. Indeed, game consoles require comfort with a video interface, and this fact may pose challenges to people who are not comfortable with menu navigation and remote control. Middle-age patients (that is, my generation) will be significantly more likely to embrace this technology and new applications of it should be continue to be sought. I typically do not encourage my octogenarians to invest in a Wii, but what about people younger than that? The "iPhone generation" will not only prefer, but might likely expect this option when it becomes necessary for others to motivate us to engage in physical activity.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflicts of interest. The opinions expressed are solely those of the author.

We all appreciate the importance of physical activity for the maintenance of health and the prevention of adverse health outcomes. I frequently struggle with how to motivate patients to physically exert themselves in a meaningful, consistent, and self-sustaining way.

Technology, in the form of video game systems, has been bandied about as a way to get patients moving. The Nintendo Wii console has become popular in hospitals, residential care facilities, and rehabilitation programs as a means to engage patients in physical activity.

As a consumer of modern technology, I frequently, and likely erroneously, assume that my patients love gadgets as much as I do. When I tell my older patients to consider a video game system as a component of a physical activity program, are my words falling on deaf ears? Recently published data suggest that I need to curb my enthusiasm, at least for now, among my older patients.

Kate Laver of Flinders University, Adelaide, Australia, and colleagues conducted a discrete choice analysis (DCE) among 21 participants prior to and following several sessions of the Wii Fit in physiotherapy. DCEs are based on the assumptions that health care interventions or services can be described by their characteristics (or attributes) and that the consumer’s evaluation of the intervention or service is based on the levels of these attributes. In this study, participants were selected from a geriatric rehabilitation unit in South Australia. A physiotherapist prescribed Wii Fit activities and supervised patients during therapy sessions. Patients had a mean age of 85 years and most were female (86%). After participating in an average of six sessions, many expressed an aversion to the Wii as a therapeutic intervention and preferred traditional therapy programs (BMC Geriatrics 2011;11:64 [doi:10.1186/1471-2318-11-64]).

The study highlights the importance of carefully considering the likely preferences of different patient cohorts. Indeed, game consoles require comfort with a video interface, and this fact may pose challenges to people who are not comfortable with menu navigation and remote control. Middle-age patients (that is, my generation) will be significantly more likely to embrace this technology and new applications of it should be continue to be sought. I typically do not encourage my octogenarians to invest in a Wii, but what about people younger than that? The "iPhone generation" will not only prefer, but might likely expect this option when it becomes necessary for others to motivate us to engage in physical activity.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflicts of interest. The opinions expressed are solely those of the author.

We all appreciate the importance of physical activity for the maintenance of health and the prevention of adverse health outcomes. I frequently struggle with how to motivate patients to physically exert themselves in a meaningful, consistent, and self-sustaining way.

Technology, in the form of video game systems, has been bandied about as a way to get patients moving. The Nintendo Wii console has become popular in hospitals, residential care facilities, and rehabilitation programs as a means to engage patients in physical activity.

As a consumer of modern technology, I frequently, and likely erroneously, assume that my patients love gadgets as much as I do. When I tell my older patients to consider a video game system as a component of a physical activity program, are my words falling on deaf ears? Recently published data suggest that I need to curb my enthusiasm, at least for now, among my older patients.

Kate Laver of Flinders University, Adelaide, Australia, and colleagues, conducted a discrete choice analysis (DCE) among 21 participants prior to and following several sessions of the Wii Fit in physiotherapy. Participants were selected from a geriatric rehabilitation unit in South Australia. A physiotherapist prescribed Wii Fit activities and supervised patients during therapy sessions. Patients had a mean age of 85 years and most were female (86%). After an average of 6 sessions, participants expressed an aversion to the Wii as a therapeutic intervention and preferred traditional therapy programs (BMC Geriatrics 2011,11:64 doi:10.1186/1471-2318-11-64).

The findings highlight the importance of carefully considering the likely preferences of different cohorts of patients. Indeed, game consoles require comfort with a video interface, and this fact may pose challenges to people who are not comfortable with menu navigation and remote control. Middle-aged patients (i.e, my generation) will be significantly more likely to embrace this technology and new applications of it should be continue to be sought. I typically do not encourage my octogenarians to invest in a Wii, but what about people younger than that? The “iPhone generation” will not only prefer, but might likely expect this option when it becomes necessary for others to motivate us to engage in physical activity.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflicts of interest. The opinions expressed are solely those of the author. 

We all appreciate the importance of physical activity for the maintenance of health and the prevention of adverse health outcomes. I frequently struggle with how to motivate patients to physically exert themselves in a meaningful, consistent, and self-sustaining way.

Technology, in the form of video game systems, has been bandied about as a way to get patients moving. The Nintendo Wii console has become popular in hospitals, residential care facilities, and rehabilitation programs as a means to engage patients in physical activity.

As a consumer of modern technology, I frequently, and likely erroneously, assume that my patients love gadgets as much as I do. When I tell my older patients to consider a video game system as a component of a physical activity program, are my words falling on deaf ears? Recently published data suggest that I need to curb my enthusiasm, at least for now, among my older patients.

Kate Laver of Flinders University, Adelaide, Australia, and colleagues, conducted a discrete choice analysis (DCE) among 21 participants prior to and following several sessions of the Wii Fit in physiotherapy. Participants were selected from a geriatric rehabilitation unit in South Australia. A physiotherapist prescribed Wii Fit activities and supervised patients during therapy sessions. Patients had a mean age of 85 years and most were female (86%). After an average of 6 sessions, participants expressed an aversion to the Wii as a therapeutic intervention and preferred traditional therapy programs (BMC Geriatrics 2011,11:64 doi:10.1186/1471-2318-11-64).

The findings highlight the importance of carefully considering the likely preferences of different cohorts of patients. Indeed, game consoles require comfort with a video interface, and this fact may pose challenges to people who are not comfortable with menu navigation and remote control. Middle-aged patients (i.e, my generation) will be significantly more likely to embrace this technology and new applications of it should be continue to be sought. I typically do not encourage my octogenarians to invest in a Wii, but what about people younger than that? The “iPhone generation” will not only prefer, but might likely expect this option when it becomes necessary for others to motivate us to engage in physical activity.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflicts of interest. The opinions expressed are solely those of the author. 

We all appreciate the importance of physical activity for the maintenance of health and the prevention of adverse health outcomes. I frequently struggle with how to motivate patients to physically exert themselves in a meaningful, consistent, and self-sustaining way.

Technology, in the form of video game systems, has been bandied about as a way to get patients moving. The Nintendo Wii console has become popular in hospitals, residential care facilities, and rehabilitation programs as a means to engage patients in physical activity.

As a consumer of modern technology, I frequently, and likely erroneously, assume that my patients love gadgets as much as I do. When I tell my older patients to consider a video game system as a component of a physical activity program, are my words falling on deaf ears? Recently published data suggest that I need to curb my enthusiasm, at least for now, among my older patients.

Kate Laver of Flinders University, Adelaide, Australia, and colleagues, conducted a discrete choice analysis (DCE) among 21 participants prior to and following several sessions of the Wii Fit in physiotherapy. Participants were selected from a geriatric rehabilitation unit in South Australia. A physiotherapist prescribed Wii Fit activities and supervised patients during therapy sessions. Patients had a mean age of 85 years and most were female (86%). After an average of 6 sessions, participants expressed an aversion to the Wii as a therapeutic intervention and preferred traditional therapy programs (BMC Geriatrics 2011,11:64 doi:10.1186/1471-2318-11-64).

The findings highlight the importance of carefully considering the likely preferences of different cohorts of patients. Indeed, game consoles require comfort with a video interface, and this fact may pose challenges to people who are not comfortable with menu navigation and remote control. Middle-aged patients (i.e, my generation) will be significantly more likely to embrace this technology and new applications of it should be continue to be sought. I typically do not encourage my octogenarians to invest in a Wii, but what about people younger than that? The “iPhone generation” will not only prefer, but might likely expect this option when it becomes necessary for others to motivate us to engage in physical activity.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He reports having no conflicts of interest. The opinions expressed are solely those of the author. 

Omega-3 fatty acids are “essential fatty acids” meaning they are vital for normal metabolism, but cannot be synthesized by the human body. Many omega-3 FAs are formed in the chloroplasts of green leaves and algae, which is where fish obtain them since fish do not manufacture them either. Interest in omega-3 FAs exploded in the 1970s after it was discovered that an Inuit tribe in Greenland consumed large amounts of fish and had no identifiable cardiovascular disease.

©Clayton Hansen/iStockphoto

While some continue to suggest that the cardiovascular benefits of omega-3 FAs are “controversial,” data continue to accumulate supporting their benefits.  
In a recently published systematic review, the effect of omega-3 FAs supplementation on endothelial function was measured by flow-mediated dilation and endothelium-independent vasodilation. A total of 16 eligible studies involving 901 participants were included.

All the studies evaluated eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) – the most well known omega-3 FAs – or alpha-linolenic acid (ALA) from walnuts. At a dose of 0.45 to 4.5 grams/day over a median of 56 days, omega-3 FAs significantly increased flow-mediated dilation by 2.30% (95% CI: 0.89–3.72%, P = 0.001). (Atherosclerosis 2012;221:536-43).

For clinicians, dosing recommendations of omega-3 FAs are important to keep in mind since many of our patients believe that “more is better.” While low doses may be anti-inflammatory, higher doses may be pro-inflammatory. Taken in excess of 3 grams per day, omega-3 FAs may increase bleeding, levels of low-density lipoproteins, and blood sugars in diabetics.

Perhaps the only thing “controversial” about fish oil for reducing cardiovascular risk is that we are not recommending it to our patients frequently enough.

Plant-based sources of omega-3 FAs include flaxseed, pecans, and hazelnuts. Fish oil tablets are an easy way for our patients to get omega-3 FAs from an animal source, but it may be important to select slightly more expensive brands that advertise the removal of mercury since cold-water oily fish sources may accumulate mercury and fat-soluble toxins. For patients who do not wish to take it because of “fish burps,” purchasing “burpless brands” or putting pills in the freezer before consumption may eliminate this effect. Worked for me.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He declares having no conflicts of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

Omega-3 fatty acids are “essential fatty acids” meaning they are vital for normal metabolism, but cannot be synthesized by the human body. Many omega-3 FAs are formed in the chloroplasts of green leaves and algae, which is where fish obtain them since fish do not manufacture them either. Interest in omega-3 FAs exploded in the 1970s after it was discovered that an Inuit tribe in Greenland consumed large amounts of fish and had no identifiable cardiovascular disease.

©Clayton Hansen/iStockphoto

While some continue to suggest that the cardiovascular benefits of omega-3 FAs are “controversial,” data continue to accumulate supporting their benefits.  
In a recently published systematic review, the effect of omega-3 FAs supplementation on endothelial function was measured by flow-mediated dilation and endothelium-independent vasodilation. A total of 16 eligible studies involving 901 participants were included.

All the studies evaluated eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) – the most well known omega-3 FAs – or alpha-linolenic acid (ALA) from walnuts. At a dose of 0.45 to 4.5 grams/day over a median of 56 days, omega-3 FAs significantly increased flow-mediated dilation by 2.30% (95% CI: 0.89–3.72%, P = 0.001). (Atherosclerosis 2012;221:536-43).

For clinicians, dosing recommendations of omega-3 FAs are important to keep in mind since many of our patients believe that “more is better.” While low doses may be anti-inflammatory, higher doses may be pro-inflammatory. Taken in excess of 3 grams per day, omega-3 FAs may increase bleeding, levels of low-density lipoproteins, and blood sugars in diabetics.

Perhaps the only thing “controversial” about fish oil for reducing cardiovascular risk is that we are not recommending it to our patients frequently enough.

Plant-based sources of omega-3 FAs include flaxseed, pecans, and hazelnuts. Fish oil tablets are an easy way for our patients to get omega-3 FAs from an animal source, but it may be important to select slightly more expensive brands that advertise the removal of mercury since cold-water oily fish sources may accumulate mercury and fat-soluble toxins. For patients who do not wish to take it because of “fish burps,” purchasing “burpless brands” or putting pills in the freezer before consumption may eliminate this effect. Worked for me.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He declares having no conflicts of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

Omega-3 fatty acids are “essential fatty acids” meaning they are vital for normal metabolism, but cannot be synthesized by the human body. Many omega-3 FAs are formed in the chloroplasts of green leaves and algae, which is where fish obtain them since fish do not manufacture them either. Interest in omega-3 FAs exploded in the 1970s after it was discovered that an Inuit tribe in Greenland consumed large amounts of fish and had no identifiable cardiovascular disease.

©Clayton Hansen/iStockphoto

While some continue to suggest that the cardiovascular benefits of omega-3 FAs are “controversial,” data continue to accumulate supporting their benefits.  
In a recently published systematic review, the effect of omega-3 FAs supplementation on endothelial function was measured by flow-mediated dilation and endothelium-independent vasodilation. A total of 16 eligible studies involving 901 participants were included.

All the studies evaluated eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) – the most well known omega-3 FAs – or alpha-linolenic acid (ALA) from walnuts. At a dose of 0.45 to 4.5 grams/day over a median of 56 days, omega-3 FAs significantly increased flow-mediated dilation by 2.30% (95% CI: 0.89–3.72%, P = 0.001). (Atherosclerosis 2012;221:536-43).

For clinicians, dosing recommendations of omega-3 FAs are important to keep in mind since many of our patients believe that “more is better.” While low doses may be anti-inflammatory, higher doses may be pro-inflammatory. Taken in excess of 3 grams per day, omega-3 FAs may increase bleeding, levels of low-density lipoproteins, and blood sugars in diabetics.

Perhaps the only thing “controversial” about fish oil for reducing cardiovascular risk is that we are not recommending it to our patients frequently enough.

Plant-based sources of omega-3 FAs include flaxseed, pecans, and hazelnuts. Fish oil tablets are an easy way for our patients to get omega-3 FAs from an animal source, but it may be important to select slightly more expensive brands that advertise the removal of mercury since cold-water oily fish sources may accumulate mercury and fat-soluble toxins. For patients who do not wish to take it because of “fish burps,” purchasing “burpless brands” or putting pills in the freezer before consumption may eliminate this effect. Worked for me.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He declares having no conflicts of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

With the droughts and record temperatures throughout the U.S., many of our patients are wisely staying in the air conditioned indoors. Yet invariably, we will find ourselves dispensing advice on the use of sunscreens to prevent the development of skin cancer. But before we do, it may be important to remind ourselves of the controversial link between solar ultraviolet (UV) exposure and melanoma, and the utility of sunscreen to protect against its development.

The evidence is overwhelming that UV radiation is a risk factor for melanoma. UV-B causes the most DNA damage and may be more closely associated with melanoma than UV-A. Sun protection factor (SPF) measures the protection against UVB. SPF refers to the ratio of the minimal dose of solar radiation producing perceptible erythema (minimal erythema dose, MED) on sunscreen-protected skin and the MED for unprotected skin. New FDA regulations slated to take effect last month allow sunscreens to be labeled “broad spectrum” if they protect against both UVA and UVB. Products may only be called a “sunscreen” if they decrease the risk of cancer and premature skin aging.

Courtesy of the Food and Drug Administration

The effectiveness of sunscreen for the prevention of melanoma has been controversial. The United States Preventive Services Task Force noted only limited evidence suggesting that sunscreen decreases melanoma incidence (Ann. Intern. Med. 2011;154:190-201).

However, a randomized trial involving more than 1,600 patients, aged 25 to 75 years, conducted in Queensland, Australia, suggested that sunscreen is very effective for reducing melanoma incidence. In this study, subjects were randomized to daily sunscreen (SPF 15+) use to head and arms over a 5-year period combined with 30 mg beta carotene or discretionary sunscreen application plus placebo supplements. After 10 years, 11 primary melanomas were diagnosed in the daily sunscreen group while 22 were diagnosed in the discretionary group (hazard ratio [HR], 0.50; 95% CI, 0.24 to 1.02; P = .051). A substantial reduction in invasive melanomas also was observed (3 active vs. 11 control; HR, 0.27; 95% CI, 0.08 to 0.97) (JCO 2011;29:257-63).

Only sun avoidance affords the best protection against melanoma. But for many of our patients this is not realistic. The best “skin tips” include: 1) use at least an SPF 15 (additional UVB protection above this rating is minimal); 2) apply at least a shot-glass full of sunscreen to cover exposed areas; and 3) re-apply sunscreen if out for several hours or if in contact with water.

Jon O. Ebbert, M.D. is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He declares having no conflict of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

With the droughts and record temperatures throughout the U.S., many of our patients are wisely staying in the air conditioned indoors. Yet invariably, we will find ourselves dispensing advice on the use of sunscreens to prevent the development of skin cancer. But before we do, it may be important to remind ourselves of the controversial link between solar ultraviolet (UV) exposure and melanoma, and the utility of sunscreen to protect against its development.

The evidence is overwhelming that UV radiation is a risk factor for melanoma. UV-B causes the most DNA damage and may be more closely associated with melanoma than UV-A. Sun protection factor (SPF) measures the protection against UVB. SPF refers to the ratio of the minimal dose of solar radiation producing perceptible erythema (minimal erythema dose, MED) on sunscreen-protected skin and the MED for unprotected skin. New FDA regulations slated to take effect last month allow sunscreens to be labeled “broad spectrum” if they protect against both UVA and UVB. Products may only be called a “sunscreen” if they decrease the risk of cancer and premature skin aging.

Courtesy of the Food and Drug Administration

The effectiveness of sunscreen for the prevention of melanoma has been controversial. The United States Preventive Services Task Force noted only limited evidence suggesting that sunscreen decreases melanoma incidence (Ann. Intern. Med. 2011;154:190-201).

However, a randomized trial involving more than 1,600 patients, aged 25 to 75 years, conducted in Queensland, Australia, suggested that sunscreen is very effective for reducing melanoma incidence. In this study, subjects were randomized to daily sunscreen (SPF 15+) use to head and arms over a 5-year period combined with 30 mg beta carotene or discretionary sunscreen application plus placebo supplements. After 10 years, 11 primary melanomas were diagnosed in the daily sunscreen group while 22 were diagnosed in the discretionary group (hazard ratio [HR], 0.50; 95% CI, 0.24 to 1.02; P = .051). A substantial reduction in invasive melanomas also was observed (3 active vs. 11 control; HR, 0.27; 95% CI, 0.08 to 0.97) (JCO 2011;29:257-63).

Only sun avoidance affords the best protection against melanoma. But for many of our patients this is not realistic. The best “skin tips” include: 1) use at least an SPF 15 (additional UVB protection above this rating is minimal); 2) apply at least a shot-glass full of sunscreen to cover exposed areas; and 3) re-apply sunscreen if out for several hours or if in contact with water.

Jon O. Ebbert, M.D. is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He declares having no conflict of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

With the droughts and record temperatures throughout the U.S., many of our patients are wisely staying in the air conditioned indoors. Yet invariably, we will find ourselves dispensing advice on the use of sunscreens to prevent the development of skin cancer. But before we do, it may be important to remind ourselves of the controversial link between solar ultraviolet (UV) exposure and melanoma, and the utility of sunscreen to protect against its development.

The evidence is overwhelming that UV radiation is a risk factor for melanoma. UV-B causes the most DNA damage and may be more closely associated with melanoma than UV-A. Sun protection factor (SPF) measures the protection against UVB. SPF refers to the ratio of the minimal dose of solar radiation producing perceptible erythema (minimal erythema dose, MED) on sunscreen-protected skin and the MED for unprotected skin. New FDA regulations slated to take effect last month allow sunscreens to be labeled “broad spectrum” if they protect against both UVA and UVB. Products may only be called a “sunscreen” if they decrease the risk of cancer and premature skin aging.

Courtesy of the Food and Drug Administration

The effectiveness of sunscreen for the prevention of melanoma has been controversial. The United States Preventive Services Task Force noted only limited evidence suggesting that sunscreen decreases melanoma incidence (Ann. Intern. Med. 2011;154:190-201).

However, a randomized trial involving more than 1,600 patients, aged 25 to 75 years, conducted in Queensland, Australia, suggested that sunscreen is very effective for reducing melanoma incidence. In this study, subjects were randomized to daily sunscreen (SPF 15+) use to head and arms over a 5-year period combined with 30 mg beta carotene or discretionary sunscreen application plus placebo supplements. After 10 years, 11 primary melanomas were diagnosed in the daily sunscreen group while 22 were diagnosed in the discretionary group (hazard ratio [HR], 0.50; 95% CI, 0.24 to 1.02; P = .051). A substantial reduction in invasive melanomas also was observed (3 active vs. 11 control; HR, 0.27; 95% CI, 0.08 to 0.97) (JCO 2011;29:257-63).

Only sun avoidance affords the best protection against melanoma. But for many of our patients this is not realistic. The best “skin tips” include: 1) use at least an SPF 15 (additional UVB protection above this rating is minimal); 2) apply at least a shot-glass full of sunscreen to cover exposed areas; and 3) re-apply sunscreen if out for several hours or if in contact with water.

Jon O. Ebbert, M.D. is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He declares having no conflict of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

The Food and Drug Administration’s recent approval of lorcaserin (Belviq) for the treatment of obesity is going to have an inevitable – and unavoidable – impact on our practices. You may have already talked yourself into not prescribing it, or you may practice the “5-year rule,” deciding not to prescribe a medication until it has been on the market for at least 5 years.

Either way, now is the time to develop your clinical stump speech because once the company starts its direct-to-consumer advertising campaign, your patients are going to ask you about it when you start counseling them about their weight.

So what is lorcaserin and how good are the data to support its use?
Lorcaserin is a “super selective” serotonin receptor agonist working predominantly at the 5-HT2C receptor. The theoretical mechanism of action is through an enhancement of satiety, an “anorectic effect.”

The safety and efficacy of lorcaserin has been evaluated in three phase III studies: BLOSSOM (Behavioral Modification and Lorcaserin Second Study for Obesity Management), BLOOM (Behavioral Modification and Lorcaserin for Overweight and Obesity Management), and BLOOM-DM (Diabetes Management).

The BLOSSOM trial randomized 4,008 adults aged 18-65 years with a body mass index of 30-45 kg/m2 or with a body mass index of 27-29.9 kg/m2 and a comorbid, obesity-related condition. Participants received lorcaserin 10 mg twice daily, 10 mg once daily, or placebo for 52 weeks. All patients received physical activity counseling to exercise moderately for 30 minutes per day and dietary counseling that included a reduction of 600 kcal below estimated energy requirements (JCEM 2011;96:3067-77).

At one year, lorcaserin was associated with a significantly higher proportion of patients losing at least 5% baseline body weight (47% on 10 mg b.i.d. and 40% on 10 mg once daily) compared to placebo (25%; P < .001 verses lorcaserin b.i.d.).

Weight loss of at least 10% of baseline body weight was achieved by 23% and 17% in the lorcaserin 10 mg b.i.d. and 10 mg once daily groups, respectively, compared with about 10% of those in the placebo group (P < .001 vs. lorcaserin b.i.d.). Lorcaserin b.i.d. was associated with significantly greater weight loss than once daily dosing (P < .01).

The most common side effects were headache, nausea, and dizziness. Valvulopathy was observed in 2% of the placebo and lorcaserin b.i.d. groups each. Patients taking lorcaserin lost an average of 5.8 kgs at 52 weeks.

Recall that fenfluramine (the “fen” in “fen-phen”) was a serotonergic agent that caused cardiac valvulopathy and was withdrawn from the market. But fenfluramine was a potent agonist of the serotonin 5-HT2B receptor, which are plentiful in cardiac valves. By contrast, lorcaserin binds strongly to 5-HT2C at a ratio of 100:1 to other receptors. No increased risk of valvulopathy has been observed with lorcaserin.

Another 4 to 6 months will pass before this drug comes to market. Being the first obesity drug to be approved in 13 years, pent-up demand combined with a likely aggressive advertising campaign will result in a deluge of patient inquiries.

Keep in mind that the FDA recommended restrictions on the drug by limiting approval to patients with a BMI greater than 30 kg/m2 or a BMI greater than 27 kg/m2 with other medical co-morbidities related to obesity.

Whatever we decide to do, patients need to be reminded that lifestyle change including diet and exercise remain the cornerstone of any successful weight-loss attempt and for the maintenance of those results.

Dr. Jon O. Ebbert is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He declares having no conflicts of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

The Food and Drug Administration’s recent approval of lorcaserin (Belviq) for the treatment of obesity is going to have an inevitable – and unavoidable – impact on our practices. You may have already talked yourself into not prescribing it, or you may practice the “5-year rule,” deciding not to prescribe a medication until it has been on the market for at least 5 years.

Either way, now is the time to develop your clinical stump speech because once the company starts its direct-to-consumer advertising campaign, your patients are going to ask you about it when you start counseling them about their weight.

So what is lorcaserin and how good are the data to support its use?
Lorcaserin is a “super selective” serotonin receptor agonist working predominantly at the 5-HT2C receptor. The theoretical mechanism of action is through an enhancement of satiety, an “anorectic effect.”

The safety and efficacy of lorcaserin has been evaluated in three phase III studies: BLOSSOM (Behavioral Modification and Lorcaserin Second Study for Obesity Management), BLOOM (Behavioral Modification and Lorcaserin for Overweight and Obesity Management), and BLOOM-DM (Diabetes Management).

The BLOSSOM trial randomized 4,008 adults aged 18-65 years with a body mass index of 30-45 kg/m2 or with a body mass index of 27-29.9 kg/m2 and a comorbid, obesity-related condition. Participants received lorcaserin 10 mg twice daily, 10 mg once daily, or placebo for 52 weeks. All patients received physical activity counseling to exercise moderately for 30 minutes per day and dietary counseling that included a reduction of 600 kcal below estimated energy requirements (JCEM 2011;96:3067-77).

At one year, lorcaserin was associated with a significantly higher proportion of patients losing at least 5% baseline body weight (47% on 10 mg b.i.d. and 40% on 10 mg once daily) compared to placebo (25%; P < .001 verses lorcaserin b.i.d.).

Weight loss of at least 10% of baseline body weight was achieved by 23% and 17% in the lorcaserin 10 mg b.i.d. and 10 mg once daily groups, respectively, compared with about 10% of those in the placebo group (P < .001 vs. lorcaserin b.i.d.). Lorcaserin b.i.d. was associated with significantly greater weight loss than once daily dosing (P < .01).

The most common side effects were headache, nausea, and dizziness. Valvulopathy was observed in 2% of the placebo and lorcaserin b.i.d. groups each. Patients taking lorcaserin lost an average of 5.8 kgs at 52 weeks.

Recall that fenfluramine (the “fen” in “fen-phen”) was a serotonergic agent that caused cardiac valvulopathy and was withdrawn from the market. But fenfluramine was a potent agonist of the serotonin 5-HT2B receptor, which are plentiful in cardiac valves. By contrast, lorcaserin binds strongly to 5-HT2C at a ratio of 100:1 to other receptors. No increased risk of valvulopathy has been observed with lorcaserin.

Another 4 to 6 months will pass before this drug comes to market. Being the first obesity drug to be approved in 13 years, pent-up demand combined with a likely aggressive advertising campaign will result in a deluge of patient inquiries.

Keep in mind that the FDA recommended restrictions on the drug by limiting approval to patients with a BMI greater than 30 kg/m2 or a BMI greater than 27 kg/m2 with other medical co-morbidities related to obesity.

Whatever we decide to do, patients need to be reminded that lifestyle change including diet and exercise remain the cornerstone of any successful weight-loss attempt and for the maintenance of those results.

Dr. Jon O. Ebbert is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He declares having no conflicts of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

The Food and Drug Administration’s recent approval of lorcaserin (Belviq) for the treatment of obesity is going to have an inevitable – and unavoidable – impact on our practices. You may have already talked yourself into not prescribing it, or you may practice the “5-year rule,” deciding not to prescribe a medication until it has been on the market for at least 5 years.

Either way, now is the time to develop your clinical stump speech because once the company starts its direct-to-consumer advertising campaign, your patients are going to ask you about it when you start counseling them about their weight.

So what is lorcaserin and how good are the data to support its use?
Lorcaserin is a “super selective” serotonin receptor agonist working predominantly at the 5-HT2C receptor. The theoretical mechanism of action is through an enhancement of satiety, an “anorectic effect.”

The safety and efficacy of lorcaserin has been evaluated in three phase III studies: BLOSSOM (Behavioral Modification and Lorcaserin Second Study for Obesity Management), BLOOM (Behavioral Modification and Lorcaserin for Overweight and Obesity Management), and BLOOM-DM (Diabetes Management).

The BLOSSOM trial randomized 4,008 adults aged 18-65 years with a body mass index of 30-45 kg/m2 or with a body mass index of 27-29.9 kg/m2 and a comorbid, obesity-related condition. Participants received lorcaserin 10 mg twice daily, 10 mg once daily, or placebo for 52 weeks. All patients received physical activity counseling to exercise moderately for 30 minutes per day and dietary counseling that included a reduction of 600 kcal below estimated energy requirements (JCEM 2011;96:3067-77).

At one year, lorcaserin was associated with a significantly higher proportion of patients losing at least 5% baseline body weight (47% on 10 mg b.i.d. and 40% on 10 mg once daily) compared to placebo (25%; P < .001 verses lorcaserin b.i.d.).

Weight loss of at least 10% of baseline body weight was achieved by 23% and 17% in the lorcaserin 10 mg b.i.d. and 10 mg once daily groups, respectively, compared with about 10% of those in the placebo group (P < .001 vs. lorcaserin b.i.d.). Lorcaserin b.i.d. was associated with significantly greater weight loss than once daily dosing (P < .01).

The most common side effects were headache, nausea, and dizziness. Valvulopathy was observed in 2% of the placebo and lorcaserin b.i.d. groups each. Patients taking lorcaserin lost an average of 5.8 kgs at 52 weeks.

Recall that fenfluramine (the “fen” in “fen-phen”) was a serotonergic agent that caused cardiac valvulopathy and was withdrawn from the market. But fenfluramine was a potent agonist of the serotonin 5-HT2B receptor, which are plentiful in cardiac valves. By contrast, lorcaserin binds strongly to 5-HT2C at a ratio of 100:1 to other receptors. No increased risk of valvulopathy has been observed with lorcaserin.

Another 4 to 6 months will pass before this drug comes to market. Being the first obesity drug to be approved in 13 years, pent-up demand combined with a likely aggressive advertising campaign will result in a deluge of patient inquiries.

Keep in mind that the FDA recommended restrictions on the drug by limiting approval to patients with a BMI greater than 30 kg/m2 or a BMI greater than 27 kg/m2 with other medical co-morbidities related to obesity.

Whatever we decide to do, patients need to be reminded that lifestyle change including diet and exercise remain the cornerstone of any successful weight-loss attempt and for the maintenance of those results.

Dr. Jon O. Ebbert is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He declares having no conflicts of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

Updated 7/6/12

As pressures to control medical costs intensify, more light will be shed on the clinical reality of overdiagnosis and overtreatment, which I have recently discussed. With modern medicine falsely suggesting that death is optional, we continue to expand the indications for expensive procedures.

Hemodialysis (HD) is one of these procedures. The rate at which it is administered has increased rapidly in recent decades, and individuals at least aged 65 years are the largest driver of utilization. Additional pressures to increase HD use arise from data suggesting improved outcomes if started in patients with higher glomerular filtration rates and if it is conducted more frequently.

But among the elderly with chronic kidney disease (CKD), no significant changes in the one-year dialysis survival rate have been observed over the past several decades. Ninety-day mortality is almost 33% among individuals older than 84 years and almost half have died by one year. Functional decline accelerates and the burden of treatment increases precipitously after HD initiation. A minority of patients (13%) maintain pre-dialysis levels of functioning at 12 months. Six months after starting dialysis, patients report more symptoms; only half report HD to be an acceptable treatment. Perceived survival “benefits” are frequently spent in the hospital or in the dialysis unit. Are we really serving the best interests of our patients? If not, what is the alternative?

Dr. Bjorg Thorsteinsdottir and colleagues from the Mayo Clinic challenge us to consider palliative care strategies instead of, or in conjunction with, HD for our elderly patients (Mayo Clinic Proceedings 2012;87:514-6). The group reports that patients are comfortable discussing end-of-life issues with the nephrology and primary care teams. The vast majority (97%) prefer detailed survival information before consenting to HD. Shared decision-making tools have been developed that may facilitate this process with patients and their families.

Palliative medicine programs need to be expanded for elderly patients in our nephrology training and clinical programs. We need to get beyond the mentality that these decisions are driven by limited resources. Informed, evidence-based, patient-centered decisions about HD incorporating discussions about palliative care are truly the best medicine for our elderly with CKD.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, MN. He declares having no conflicts of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

Update: A citation and a link to Dr. Bjorg Thorsteinsdottir's study was added to this blog entry.

Updated 7/6/12

As pressures to control medical costs intensify, more light will be shed on the clinical reality of overdiagnosis and overtreatment, which I have recently discussed. With modern medicine falsely suggesting that death is optional, we continue to expand the indications for expensive procedures.

Hemodialysis (HD) is one of these procedures. The rate at which it is administered has increased rapidly in recent decades, and individuals at least aged 65 years are the largest driver of utilization. Additional pressures to increase HD use arise from data suggesting improved outcomes if started in patients with higher glomerular filtration rates and if it is conducted more frequently.

But among the elderly with chronic kidney disease (CKD), no significant changes in the one-year dialysis survival rate have been observed over the past several decades. Ninety-day mortality is almost 33% among individuals older than 84 years and almost half have died by one year. Functional decline accelerates and the burden of treatment increases precipitously after HD initiation. A minority of patients (13%) maintain pre-dialysis levels of functioning at 12 months. Six months after starting dialysis, patients report more symptoms; only half report HD to be an acceptable treatment. Perceived survival “benefits” are frequently spent in the hospital or in the dialysis unit. Are we really serving the best interests of our patients? If not, what is the alternative?

Dr. Bjorg Thorsteinsdottir and colleagues from the Mayo Clinic challenge us to consider palliative care strategies instead of, or in conjunction with, HD for our elderly patients (Mayo Clinic Proceedings 2012;87:514-6). The group reports that patients are comfortable discussing end-of-life issues with the nephrology and primary care teams. The vast majority (97%) prefer detailed survival information before consenting to HD. Shared decision-making tools have been developed that may facilitate this process with patients and their families.

Palliative medicine programs need to be expanded for elderly patients in our nephrology training and clinical programs. We need to get beyond the mentality that these decisions are driven by limited resources. Informed, evidence-based, patient-centered decisions about HD incorporating discussions about palliative care are truly the best medicine for our elderly with CKD.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, MN. He declares having no conflicts of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

Update: A citation and a link to Dr. Bjorg Thorsteinsdottir's study was added to this blog entry.

Updated 7/6/12

As pressures to control medical costs intensify, more light will be shed on the clinical reality of overdiagnosis and overtreatment, which I have recently discussed. With modern medicine falsely suggesting that death is optional, we continue to expand the indications for expensive procedures.

Hemodialysis (HD) is one of these procedures. The rate at which it is administered has increased rapidly in recent decades, and individuals at least aged 65 years are the largest driver of utilization. Additional pressures to increase HD use arise from data suggesting improved outcomes if started in patients with higher glomerular filtration rates and if it is conducted more frequently.

But among the elderly with chronic kidney disease (CKD), no significant changes in the one-year dialysis survival rate have been observed over the past several decades. Ninety-day mortality is almost 33% among individuals older than 84 years and almost half have died by one year. Functional decline accelerates and the burden of treatment increases precipitously after HD initiation. A minority of patients (13%) maintain pre-dialysis levels of functioning at 12 months. Six months after starting dialysis, patients report more symptoms; only half report HD to be an acceptable treatment. Perceived survival “benefits” are frequently spent in the hospital or in the dialysis unit. Are we really serving the best interests of our patients? If not, what is the alternative?

Dr. Bjorg Thorsteinsdottir and colleagues from the Mayo Clinic challenge us to consider palliative care strategies instead of, or in conjunction with, HD for our elderly patients (Mayo Clinic Proceedings 2012;87:514-6). The group reports that patients are comfortable discussing end-of-life issues with the nephrology and primary care teams. The vast majority (97%) prefer detailed survival information before consenting to HD. Shared decision-making tools have been developed that may facilitate this process with patients and their families.

Palliative medicine programs need to be expanded for elderly patients in our nephrology training and clinical programs. We need to get beyond the mentality that these decisions are driven by limited resources. Informed, evidence-based, patient-centered decisions about HD incorporating discussions about palliative care are truly the best medicine for our elderly with CKD.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, MN. He declares having no conflicts of interest. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

Update: A citation and a link to Dr. Bjorg Thorsteinsdottir's study was added to this blog entry.

Americans are very tired. The National Sleep Foundation recommends that adults sleep 7 to 9 hours per day, yet the percentage of U.S. adults securing at least 8 hours of sleep on weeknights has fallen from 38% to 27% since 2001. Sleep promotion is a recognized national health agenda with a Healthy People 2020 objective to increase the proportion of adults who get sufficient sleep to 71%.

CDC released a report last month on the prevalence of short sleep duration among U.S. workers. Short sleep duration (average ≤ 6 hours per 24-hour period) was reported by 30% of employed U.S. adults (approximately 40.6 million workers). The prevalence of short sleep duration was especially high among night shift workers in the transportation and warehousing (70%) and healthcare and social assistance (52%) industries. Sleep deprivation has been linked to adverse health consequences, such as obesity. But how does sleep deprivation lead to obesity?

Dr. Nathaniel Watson from the University of Washington and colleagues recently published a population-based twin-study evaluating the link between sleep duration and BMI (Sleep. 2012 May 1;35(5):597-603) that begins to unlock the sleep-BMI mystery. Investigators analyzed data from a twin registry involving 1,088 complete twin pairs. Normal sleep duration was considered 7 to 8.9 hours. Findings from this study suggest that restricting sleep provides a permissive environment for the expression of genes promoting obesity. The flipside is that extending sleep suppresses the expression of obesity genes.

The study adds to extant data suggesting that people who sleep six or fewer hours are at greater risk for obesity. Other published data suggest that too much sleep may increase the risk for cardiovascular disease, insulin resistance, and mortality. One may find it helpful to think of the relationship between nightly sleep duration and BMI as a U-shaped curve – both short and long sleepers weigh more than those in the sweet spot around 7 to 9 hours.

This study does not inform us about whether an intervention aimed at increasing sleep will result in clinically significant weight loss. But it does suggest that behavioral measures to lose weight may be more effective when genetic drivers of body weight are ratcheted down through sleep extension.
This knowledge may prove useful to our patients who are trying to get a handle on their body weight and literally feel tired doing so. Evidence is now mounting that a component of obesity treatment may be to tell our patients to get some sleep.

Jon O. Ebbert, M.D. is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, MN. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

Americans are very tired. The National Sleep Foundation recommends that adults sleep 7 to 9 hours per day, yet the percentage of U.S. adults securing at least 8 hours of sleep on weeknights has fallen from 38% to 27% since 2001. Sleep promotion is a recognized national health agenda with a Healthy People 2020 objective to increase the proportion of adults who get sufficient sleep to 71%.

CDC released a report last month on the prevalence of short sleep duration among U.S. workers. Short sleep duration (average ≤ 6 hours per 24-hour period) was reported by 30% of employed U.S. adults (approximately 40.6 million workers). The prevalence of short sleep duration was especially high among night shift workers in the transportation and warehousing (70%) and healthcare and social assistance (52%) industries. Sleep deprivation has been linked to adverse health consequences, such as obesity. But how does sleep deprivation lead to obesity?

Dr. Nathaniel Watson from the University of Washington and colleagues recently published a population-based twin-study evaluating the link between sleep duration and BMI (Sleep. 2012 May 1;35(5):597-603) that begins to unlock the sleep-BMI mystery. Investigators analyzed data from a twin registry involving 1,088 complete twin pairs. Normal sleep duration was considered 7 to 8.9 hours. Findings from this study suggest that restricting sleep provides a permissive environment for the expression of genes promoting obesity. The flipside is that extending sleep suppresses the expression of obesity genes.

The study adds to extant data suggesting that people who sleep six or fewer hours are at greater risk for obesity. Other published data suggest that too much sleep may increase the risk for cardiovascular disease, insulin resistance, and mortality. One may find it helpful to think of the relationship between nightly sleep duration and BMI as a U-shaped curve – both short and long sleepers weigh more than those in the sweet spot around 7 to 9 hours.

This study does not inform us about whether an intervention aimed at increasing sleep will result in clinically significant weight loss. But it does suggest that behavioral measures to lose weight may be more effective when genetic drivers of body weight are ratcheted down through sleep extension.
This knowledge may prove useful to our patients who are trying to get a handle on their body weight and literally feel tired doing so. Evidence is now mounting that a component of obesity treatment may be to tell our patients to get some sleep.

Jon O. Ebbert, M.D. is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, MN. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

Americans are very tired. The National Sleep Foundation recommends that adults sleep 7 to 9 hours per day, yet the percentage of U.S. adults securing at least 8 hours of sleep on weeknights has fallen from 38% to 27% since 2001. Sleep promotion is a recognized national health agenda with a Healthy People 2020 objective to increase the proportion of adults who get sufficient sleep to 71%.

CDC released a report last month on the prevalence of short sleep duration among U.S. workers. Short sleep duration (average ≤ 6 hours per 24-hour period) was reported by 30% of employed U.S. adults (approximately 40.6 million workers). The prevalence of short sleep duration was especially high among night shift workers in the transportation and warehousing (70%) and healthcare and social assistance (52%) industries. Sleep deprivation has been linked to adverse health consequences, such as obesity. But how does sleep deprivation lead to obesity?

Dr. Nathaniel Watson from the University of Washington and colleagues recently published a population-based twin-study evaluating the link between sleep duration and BMI (Sleep. 2012 May 1;35(5):597-603) that begins to unlock the sleep-BMI mystery. Investigators analyzed data from a twin registry involving 1,088 complete twin pairs. Normal sleep duration was considered 7 to 8.9 hours. Findings from this study suggest that restricting sleep provides a permissive environment for the expression of genes promoting obesity. The flipside is that extending sleep suppresses the expression of obesity genes.

The study adds to extant data suggesting that people who sleep six or fewer hours are at greater risk for obesity. Other published data suggest that too much sleep may increase the risk for cardiovascular disease, insulin resistance, and mortality. One may find it helpful to think of the relationship between nightly sleep duration and BMI as a U-shaped curve – both short and long sleepers weigh more than those in the sweet spot around 7 to 9 hours.

This study does not inform us about whether an intervention aimed at increasing sleep will result in clinically significant weight loss. But it does suggest that behavioral measures to lose weight may be more effective when genetic drivers of body weight are ratcheted down through sleep extension.
This knowledge may prove useful to our patients who are trying to get a handle on their body weight and literally feel tired doing so. Evidence is now mounting that a component of obesity treatment may be to tell our patients to get some sleep.

Jon O. Ebbert, M.D. is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, MN. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.