What Matters

Choosing the best first antihypertensive can often be determined by patient comorbidity. An ACE-inhibitor, for example, makes sense for diabetic patients who require renovascular protection or for the heart failure patient with ventricular remodeling. We may make selections based on convenience (i.e. beta-blockers not requiring laboratory follow-up compared to ACE-inhibitors). But for patients without any prevailing medical conditions, is one antihypertensive better than another?

Dr. Atle Fretheim of the University of Oslo, and colleagues, recently published a meta-analysis assessing the comparative effectiveness of different classes of antihypertensive drugs for reduction of incident cardiovascular events among healthy people at risk of cardiovascular disease. Drugs evaluated included diuretics, beta-blockers, calcium channel blockers (CCBs), angiotensin converting enzyme inhibitors (ACE-inhibitors), angiotensin receptor blockers (ARBs), and alpha-blockers.

Centers for Disease Control and Prevention

Studies were included if they were randomized controlled trials comparing one or more drugs against each other, or no active treatment. Trials were excluded if more than half the participants had had a myocardial infarction, stroke or other significant cardiovascular event. The primary outcome of interest was cardiovascular morbidity or mortality. Twenty-five studies were included in the final analysis (BMC Med. 2012;10:33).

No clear winner emerged for outcomes of interest. But several interesting findings were suggested by this analysis. First, beta-blockers were associated with a higher risk of total mortality compared to ARBs (relative risk 1.14; 95% [credibility intervals] CrI: 1.02 to 1.28). Second, ACE-inhibitors increased the risk of stroke compared to CCBs (RR 1.19; 95% CrI 1.03 to 1.38). Third, ACE-inhibitors reduced the risk of heart failure compared to CCBs (RR 0.82; 95% CrI 0.69 to 0.94). Fourth, diuretics reduced the risk of MI compared to beta-blockers (RR 0.82; 95% CrI 0.68 to 0.98) and reduced heart failure compared to CCBs (RR 0.73; 95% CrI 0.62 to 0.84), beta-blockers (RR 0.73; 95% CrI 0.54 to 0.96) and alpha-blockers (RR 0.51; 95% CrI 0.40 to 0.64). Fifth, diuretics significantly increased the risk of diabetes relative to ACE-inhibitors (RR 1.43; 95% CrI 1.12 to 1.83) and CCB (RR 1.27; 95% CrI 1.05 to 1.57). Based upon this evidence the authors presented a ranking of the drug classes.

Some of us may still be unsure about which antihypertensive to prescribe – or to avoid – and whether these findings are relevant to clinical practice. The investigators leave us with potentially clinically useful guidance in this regard: beta-blockers (notably, all studies included atenolol) and alpha-blockers were the only drug classes not found to be significantly superior to any drug for any outcome. This suggests against recommending these two classes as first-line medications for primary prevention of cardiovascular disease.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He is an investigator on a clinical trial investigating the safety of varenicline. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

Choosing the best first antihypertensive can often be determined by patient comorbidity. An ACE-inhibitor, for example, makes sense for diabetic patients who require renovascular protection or for the heart failure patient with ventricular remodeling. We may make selections based on convenience (i.e. beta-blockers not requiring laboratory follow-up compared to ACE-inhibitors). But for patients without any prevailing medical conditions, is one antihypertensive better than another?

Dr. Atle Fretheim of the University of Oslo, and colleagues, recently published a meta-analysis assessing the comparative effectiveness of different classes of antihypertensive drugs for reduction of incident cardiovascular events among healthy people at risk of cardiovascular disease. Drugs evaluated included diuretics, beta-blockers, calcium channel blockers (CCBs), angiotensin converting enzyme inhibitors (ACE-inhibitors), angiotensin receptor blockers (ARBs), and alpha-blockers.

Centers for Disease Control and Prevention

Studies were included if they were randomized controlled trials comparing one or more drugs against each other, or no active treatment. Trials were excluded if more than half the participants had had a myocardial infarction, stroke or other significant cardiovascular event. The primary outcome of interest was cardiovascular morbidity or mortality. Twenty-five studies were included in the final analysis (BMC Med. 2012;10:33).

No clear winner emerged for outcomes of interest. But several interesting findings were suggested by this analysis. First, beta-blockers were associated with a higher risk of total mortality compared to ARBs (relative risk 1.14; 95% [credibility intervals] CrI: 1.02 to 1.28). Second, ACE-inhibitors increased the risk of stroke compared to CCBs (RR 1.19; 95% CrI 1.03 to 1.38). Third, ACE-inhibitors reduced the risk of heart failure compared to CCBs (RR 0.82; 95% CrI 0.69 to 0.94). Fourth, diuretics reduced the risk of MI compared to beta-blockers (RR 0.82; 95% CrI 0.68 to 0.98) and reduced heart failure compared to CCBs (RR 0.73; 95% CrI 0.62 to 0.84), beta-blockers (RR 0.73; 95% CrI 0.54 to 0.96) and alpha-blockers (RR 0.51; 95% CrI 0.40 to 0.64). Fifth, diuretics significantly increased the risk of diabetes relative to ACE-inhibitors (RR 1.43; 95% CrI 1.12 to 1.83) and CCB (RR 1.27; 95% CrI 1.05 to 1.57). Based upon this evidence the authors presented a ranking of the drug classes.

Some of us may still be unsure about which antihypertensive to prescribe – or to avoid – and whether these findings are relevant to clinical practice. The investigators leave us with potentially clinically useful guidance in this regard: beta-blockers (notably, all studies included atenolol) and alpha-blockers were the only drug classes not found to be significantly superior to any drug for any outcome. This suggests against recommending these two classes as first-line medications for primary prevention of cardiovascular disease.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He is an investigator on a clinical trial investigating the safety of varenicline. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

Choosing the best first antihypertensive can often be determined by patient comorbidity. An ACE-inhibitor, for example, makes sense for diabetic patients who require renovascular protection or for the heart failure patient with ventricular remodeling. We may make selections based on convenience (i.e. beta-blockers not requiring laboratory follow-up compared to ACE-inhibitors). But for patients without any prevailing medical conditions, is one antihypertensive better than another?

Dr. Atle Fretheim of the University of Oslo, and colleagues, recently published a meta-analysis assessing the comparative effectiveness of different classes of antihypertensive drugs for reduction of incident cardiovascular events among healthy people at risk of cardiovascular disease. Drugs evaluated included diuretics, beta-blockers, calcium channel blockers (CCBs), angiotensin converting enzyme inhibitors (ACE-inhibitors), angiotensin receptor blockers (ARBs), and alpha-blockers.

Centers for Disease Control and Prevention

Studies were included if they were randomized controlled trials comparing one or more drugs against each other, or no active treatment. Trials were excluded if more than half the participants had had a myocardial infarction, stroke or other significant cardiovascular event. The primary outcome of interest was cardiovascular morbidity or mortality. Twenty-five studies were included in the final analysis (BMC Med. 2012;10:33).

No clear winner emerged for outcomes of interest. But several interesting findings were suggested by this analysis. First, beta-blockers were associated with a higher risk of total mortality compared to ARBs (relative risk 1.14; 95% [credibility intervals] CrI: 1.02 to 1.28). Second, ACE-inhibitors increased the risk of stroke compared to CCBs (RR 1.19; 95% CrI 1.03 to 1.38). Third, ACE-inhibitors reduced the risk of heart failure compared to CCBs (RR 0.82; 95% CrI 0.69 to 0.94). Fourth, diuretics reduced the risk of MI compared to beta-blockers (RR 0.82; 95% CrI 0.68 to 0.98) and reduced heart failure compared to CCBs (RR 0.73; 95% CrI 0.62 to 0.84), beta-blockers (RR 0.73; 95% CrI 0.54 to 0.96) and alpha-blockers (RR 0.51; 95% CrI 0.40 to 0.64). Fifth, diuretics significantly increased the risk of diabetes relative to ACE-inhibitors (RR 1.43; 95% CrI 1.12 to 1.83) and CCB (RR 1.27; 95% CrI 1.05 to 1.57). Based upon this evidence the authors presented a ranking of the drug classes.

Some of us may still be unsure about which antihypertensive to prescribe – or to avoid – and whether these findings are relevant to clinical practice. The investigators leave us with potentially clinically useful guidance in this regard: beta-blockers (notably, all studies included atenolol) and alpha-blockers were the only drug classes not found to be significantly superior to any drug for any outcome. This suggests against recommending these two classes as first-line medications for primary prevention of cardiovascular disease.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. He is an investigator on a clinical trial investigating the safety of varenicline. The opinions expressed are solely those of the author. Contact him at ebbert.jon@mayo.edu.

About 20% of the adult population has obstructive sleep apnea (OSA), defined as apnea hypopnea index (AHI) of at least five events per hour. OSA prevalence increases from age 18 to 45 years and obesity is the most consistently documented risk factor. Untreated severe OSA is associated with a three to six times higher risk for all-cause mortality. OSA is associated with hypertension, coronary artery disease, cardiovascular disease, cardiac arrhythmias, stroke, accidents, and impaired cognitive function and quality of life.

Although a diagnosis of OSA can improve quantity of life, patients facing such a diagnosis often dread the prospect of lifelong nightly use of a continuous positive airway pressure (CPAP) device. Impact on spousal and travel considerations can be substantial.

Mandibular advancement devices (MADs) are the primary non-CPAP therapy for patients with OSA. MADs increase upper airway size and limit pharyngeal collapsibility and reduce the risk of snoring and apneas. MADs are recommended for patients with mild to moderate OSA who cannot tolerate CPAP. MADs also are an option for patients with severe sleep apnea who fail CPAP.

Marie Marklund, DDS, of Umeå University, Umeå, Sweden, and colleagues, reviewed the literature to determine the evidence base for MAD interventions. Their conclusion: For patients with mild to moderate OSA, MADS reduce apneic episodes, daytime sleepiness, and improve quality of life compared with placebo devices. In general, the reduction in overall apneic episodes is less than that achieved with traditional CPAP devices. However, emerging reports suggest that MADS are comparable to CPAP with regard to improvements in blood pressure, cardiac function, symptoms, and driving ability (Eur Respir J 2012 39:1241-7).

MADs are adjusted through titration requiring local expertise in the application and refinement of device fitting. Insurance coverage of these devices remains uncertain and requires homework on the part of the patient. MADs may be an exciting option for patients who want to travel without their CPAP devices. But for patients with mild to moderate OSA, or who have severe OSA and cannot tolerate CPAP, MADs are life-improving and life-saving devices.

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.

About 20% of the adult population has obstructive sleep apnea (OSA), defined as apnea hypopnea index (AHI) of at least five events per hour. OSA prevalence increases from age 18 to 45 years and obesity is the most consistently documented risk factor. Untreated severe OSA is associated with a three to six times higher risk for all-cause mortality. OSA is associated with hypertension, coronary artery disease, cardiovascular disease, cardiac arrhythmias, stroke, accidents, and impaired cognitive function and quality of life.

Although a diagnosis of OSA can improve quantity of life, patients facing such a diagnosis often dread the prospect of lifelong nightly use of a continuous positive airway pressure (CPAP) device. Impact on spousal and travel considerations can be substantial.

Mandibular advancement devices (MADs) are the primary non-CPAP therapy for patients with OSA. MADs increase upper airway size and limit pharyngeal collapsibility and reduce the risk of snoring and apneas. MADs are recommended for patients with mild to moderate OSA who cannot tolerate CPAP. MADs also are an option for patients with severe sleep apnea who fail CPAP.

Marie Marklund, DDS, of Umeå University, Umeå, Sweden, and colleagues, reviewed the literature to determine the evidence base for MAD interventions. Their conclusion: For patients with mild to moderate OSA, MADS reduce apneic episodes, daytime sleepiness, and improve quality of life compared with placebo devices. In general, the reduction in overall apneic episodes is less than that achieved with traditional CPAP devices. However, emerging reports suggest that MADS are comparable to CPAP with regard to improvements in blood pressure, cardiac function, symptoms, and driving ability (Eur Respir J 2012 39:1241-7).

MADs are adjusted through titration requiring local expertise in the application and refinement of device fitting. Insurance coverage of these devices remains uncertain and requires homework on the part of the patient. MADs may be an exciting option for patients who want to travel without their CPAP devices. But for patients with mild to moderate OSA, or who have severe OSA and cannot tolerate CPAP, MADs are life-improving and life-saving devices.

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.

About 20% of the adult population has obstructive sleep apnea (OSA), defined as apnea hypopnea index (AHI) of at least five events per hour. OSA prevalence increases from age 18 to 45 years and obesity is the most consistently documented risk factor. Untreated severe OSA is associated with a three to six times higher risk for all-cause mortality. OSA is associated with hypertension, coronary artery disease, cardiovascular disease, cardiac arrhythmias, stroke, accidents, and impaired cognitive function and quality of life.

Although a diagnosis of OSA can improve quantity of life, patients facing such a diagnosis often dread the prospect of lifelong nightly use of a continuous positive airway pressure (CPAP) device. Impact on spousal and travel considerations can be substantial.

Mandibular advancement devices (MADs) are the primary non-CPAP therapy for patients with OSA. MADs increase upper airway size and limit pharyngeal collapsibility and reduce the risk of snoring and apneas. MADs are recommended for patients with mild to moderate OSA who cannot tolerate CPAP. MADs also are an option for patients with severe sleep apnea who fail CPAP.

Marie Marklund, DDS, of Umeå University, Umeå, Sweden, and colleagues, reviewed the literature to determine the evidence base for MAD interventions. Their conclusion: For patients with mild to moderate OSA, MADS reduce apneic episodes, daytime sleepiness, and improve quality of life compared with placebo devices. In general, the reduction in overall apneic episodes is less than that achieved with traditional CPAP devices. However, emerging reports suggest that MADS are comparable to CPAP with regard to improvements in blood pressure, cardiac function, symptoms, and driving ability (Eur Respir J 2012 39:1241-7).

MADs are adjusted through titration requiring local expertise in the application and refinement of device fitting. Insurance coverage of these devices remains uncertain and requires homework on the part of the patient. MADs may be an exciting option for patients who want to travel without their CPAP devices. But for patients with mild to moderate OSA, or who have severe OSA and cannot tolerate CPAP, MADs are life-improving and life-saving devices.

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 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. 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.

Treating warts may not be on par with the professional challenges we face everyday – from generating differential diagnoses to judiciously applying modern diagnostic modalities, and relaying complex medical information in a patient-centered fashion. But what the cutaneous wart lacks in ability to elicit a sense of medical wonder at initial presentation, it makes up for in the ability to generate awe with its recalcitrance.

Recall that spontaneous remission of warts occurs in up to two-thirds of patients within two years. But our impatience with our own immune system has spawned an arms race against the human papillomavirus that calls on us to use everything from duct tape to immunotherapy.

We all occasionally need to be reminded of what the most effective, simple, and readily accessible approaches are for our patients presenting with a new common or plantar wart. Last week, Dr. Justin Ko at Harvard and colleagues commented on the a previously published randomized clinical trial evaluating the comparative effectiveness of cryotherapy, topical salicylic acid, and a wait-and-see approach for leading to clearance of lesions at 13 weeks (CMAJ. 2010;182: 1,624–30).

In this study, 250 patients received treatment. Observed cure rates for the common warts were 39% (30/76) for cryotherapy, 24% (20/82) for the salicylic acid arm, and 16% (13/82) for wait-and-see (P =.001). No significant differences were noted between treatments for plantar warts with cure rates of 30% (11/37) for cryotherapy, 33% (14/43) for salicylic acid, and 23% (10/44) for wait-and-see. Notably, patients with common warts were more satisfied after treatment with cryotherapy (69%) compared with salicylic acid (24%), and wait-and-see (22%; P < .001). No differences in satisfaction were observed with the treatments among patients with plantar warts.

Dr. Ko and colleagues commented that the study “calls into question the current practice of office treatment of plantar warts for curative intent with recurrent sessions.”

Indeed, but the study does not address the most common scenario in our practice, which is a patient reporting that they have exhausted all of the over-the-counter remedies and are asking us to “step up the game.”

For common warts, we will use the cryo-gun; for plantar warts we will perform curettage followed by the cryo-gun. But these studies are hard to do.
What we need is more information on the effectiveness of combination therapy for particularly recalcitrant plantar warts such as curettage and cryotherapy followed by salicylic acid treatment. The arms race continues.

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.

Treating warts may not be on par with the professional challenges we face everyday – from generating differential diagnoses to judiciously applying modern diagnostic modalities, and relaying complex medical information in a patient-centered fashion. But what the cutaneous wart lacks in ability to elicit a sense of medical wonder at initial presentation, it makes up for in the ability to generate awe with its recalcitrance.

Recall that spontaneous remission of warts occurs in up to two-thirds of patients within two years. But our impatience with our own immune system has spawned an arms race against the human papillomavirus that calls on us to use everything from duct tape to immunotherapy.

We all occasionally need to be reminded of what the most effective, simple, and readily accessible approaches are for our patients presenting with a new common or plantar wart. Last week, Dr. Justin Ko at Harvard and colleagues commented on the a previously published randomized clinical trial evaluating the comparative effectiveness of cryotherapy, topical salicylic acid, and a wait-and-see approach for leading to clearance of lesions at 13 weeks (CMAJ. 2010;182: 1,624–30).

In this study, 250 patients received treatment. Observed cure rates for the common warts were 39% (30/76) for cryotherapy, 24% (20/82) for the salicylic acid arm, and 16% (13/82) for wait-and-see (P =.001). No significant differences were noted between treatments for plantar warts with cure rates of 30% (11/37) for cryotherapy, 33% (14/43) for salicylic acid, and 23% (10/44) for wait-and-see. Notably, patients with common warts were more satisfied after treatment with cryotherapy (69%) compared with salicylic acid (24%), and wait-and-see (22%; P < .001). No differences in satisfaction were observed with the treatments among patients with plantar warts.

Dr. Ko and colleagues commented that the study “calls into question the current practice of office treatment of plantar warts for curative intent with recurrent sessions.”

Indeed, but the study does not address the most common scenario in our practice, which is a patient reporting that they have exhausted all of the over-the-counter remedies and are asking us to “step up the game.”

For common warts, we will use the cryo-gun; for plantar warts we will perform curettage followed by the cryo-gun. But these studies are hard to do.
What we need is more information on the effectiveness of combination therapy for particularly recalcitrant plantar warts such as curettage and cryotherapy followed by salicylic acid treatment. The arms race continues.

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.

Treating warts may not be on par with the professional challenges we face everyday – from generating differential diagnoses to judiciously applying modern diagnostic modalities, and relaying complex medical information in a patient-centered fashion. But what the cutaneous wart lacks in ability to elicit a sense of medical wonder at initial presentation, it makes up for in the ability to generate awe with its recalcitrance.

Recall that spontaneous remission of warts occurs in up to two-thirds of patients within two years. But our impatience with our own immune system has spawned an arms race against the human papillomavirus that calls on us to use everything from duct tape to immunotherapy.

We all occasionally need to be reminded of what the most effective, simple, and readily accessible approaches are for our patients presenting with a new common or plantar wart. Last week, Dr. Justin Ko at Harvard and colleagues commented on the a previously published randomized clinical trial evaluating the comparative effectiveness of cryotherapy, topical salicylic acid, and a wait-and-see approach for leading to clearance of lesions at 13 weeks (CMAJ. 2010;182: 1,624–30).

In this study, 250 patients received treatment. Observed cure rates for the common warts were 39% (30/76) for cryotherapy, 24% (20/82) for the salicylic acid arm, and 16% (13/82) for wait-and-see (P =.001). No significant differences were noted between treatments for plantar warts with cure rates of 30% (11/37) for cryotherapy, 33% (14/43) for salicylic acid, and 23% (10/44) for wait-and-see. Notably, patients with common warts were more satisfied after treatment with cryotherapy (69%) compared with salicylic acid (24%), and wait-and-see (22%; P < .001). No differences in satisfaction were observed with the treatments among patients with plantar warts.

Dr. Ko and colleagues commented that the study “calls into question the current practice of office treatment of plantar warts for curative intent with recurrent sessions.”

Indeed, but the study does not address the most common scenario in our practice, which is a patient reporting that they have exhausted all of the over-the-counter remedies and are asking us to “step up the game.”

For common warts, we will use the cryo-gun; for plantar warts we will perform curettage followed by the cryo-gun. But these studies are hard to do.
What we need is more information on the effectiveness of combination therapy for particularly recalcitrant plantar warts such as curettage and cryotherapy followed by salicylic acid treatment. The arms race continues.

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 grim prediction that 51% of the U.S. adult population will be obese by 2030, the U.S. Preventive Services Task Force released recommendations for obesity screening last month. Screening will lead to identification, and identification will lead to intervention. Intervention, hopefully, will lead to change.  

Keep in mind that dramatic changes are not necessarily what is needed. A 5% to 10% reduction from baseline body weight is considered to be “metabolically significant” leading to reductions in the risk for diabetes and cardiovascular events.

A lot of heat and dim light currently surrounds the debate on the best diet advice for our patients who need to overhaul their approach to food consumption. A reduction in carbohydrates and overall caloric consumption both seem to be solid advice these days. But not all carbohydrates are the same (complex vs. refined), and an absolute carbohydrate reduction necessitates an increase in another energy source, such as protein. The most readily available sources of protein in our society are animals. But animal proteins, even if lean, may be associated with adverse cardiovascular outcomes.

Dr. Pagona Lagiou of University of Athens Medical School and Harvard School of Public Health and colleagues prospectively evaluated the cardiovascular risks associated with a low-carbohydrate, high-protein diet in 43,396 Swedish women (BMJ 2012;344:e4026). Participants were aged 30-49 years randomly selected to complete an extensive baseline dietary questionnaire and followed up for an average of 15.7 years. The investigators observed that a decrease in carbohydrate intake or an increase in protein intake or an increase in the “low carbohydrate-high protein score” were all significantly associated with an increasing incidence of cardiovascular disease.

Data further suggested that the incidence of cardiovascular events was higher among women whose protein intake was mainly of animal rather than plant origin.

If we are advising our patients to decrease carbohydrates and increase protein in order to lose weight, findings from this study would suggest that we include another important bit of information. First, dietary goals should aim to reduce simple carbohydrates (e.g., sucrose, high fructose corn syrup) more than complex carbohydrates (e.g., whole grains, fruits, and vegetables). Second, increases in protein consumption should aim to include more plant (e.g., spinach, soy, beans) than animal protein (e.g., lamb, beef, pork).

Key elements of this dietary approach are nicely embodied in the South Beach Diet. Most importantly, we need to emphasize to our patients that alterations in diet should not be considered a “diet” but a lifestyle change to improve overall health and well-being.

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.

With the grim prediction that 51% of the U.S. adult population will be obese by 2030, the U.S. Preventive Services Task Force released recommendations for obesity screening last month. Screening will lead to identification, and identification will lead to intervention. Intervention, hopefully, will lead to change.  

Keep in mind that dramatic changes are not necessarily what is needed. A 5% to 10% reduction from baseline body weight is considered to be “metabolically significant” leading to reductions in the risk for diabetes and cardiovascular events.

A lot of heat and dim light currently surrounds the debate on the best diet advice for our patients who need to overhaul their approach to food consumption. A reduction in carbohydrates and overall caloric consumption both seem to be solid advice these days. But not all carbohydrates are the same (complex vs. refined), and an absolute carbohydrate reduction necessitates an increase in another energy source, such as protein. The most readily available sources of protein in our society are animals. But animal proteins, even if lean, may be associated with adverse cardiovascular outcomes.

Dr. Pagona Lagiou of University of Athens Medical School and Harvard School of Public Health and colleagues prospectively evaluated the cardiovascular risks associated with a low-carbohydrate, high-protein diet in 43,396 Swedish women (BMJ 2012;344:e4026). Participants were aged 30-49 years randomly selected to complete an extensive baseline dietary questionnaire and followed up for an average of 15.7 years. The investigators observed that a decrease in carbohydrate intake or an increase in protein intake or an increase in the “low carbohydrate-high protein score” were all significantly associated with an increasing incidence of cardiovascular disease.

Data further suggested that the incidence of cardiovascular events was higher among women whose protein intake was mainly of animal rather than plant origin.

If we are advising our patients to decrease carbohydrates and increase protein in order to lose weight, findings from this study would suggest that we include another important bit of information. First, dietary goals should aim to reduce simple carbohydrates (e.g., sucrose, high fructose corn syrup) more than complex carbohydrates (e.g., whole grains, fruits, and vegetables). Second, increases in protein consumption should aim to include more plant (e.g., spinach, soy, beans) than animal protein (e.g., lamb, beef, pork).

Key elements of this dietary approach are nicely embodied in the South Beach Diet. Most importantly, we need to emphasize to our patients that alterations in diet should not be considered a “diet” but a lifestyle change to improve overall health and well-being.

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.

With the grim prediction that 51% of the U.S. adult population will be obese by 2030, the U.S. Preventive Services Task Force released recommendations for obesity screening last month. Screening will lead to identification, and identification will lead to intervention. Intervention, hopefully, will lead to change.  

Keep in mind that dramatic changes are not necessarily what is needed. A 5% to 10% reduction from baseline body weight is considered to be “metabolically significant” leading to reductions in the risk for diabetes and cardiovascular events.

A lot of heat and dim light currently surrounds the debate on the best diet advice for our patients who need to overhaul their approach to food consumption. A reduction in carbohydrates and overall caloric consumption both seem to be solid advice these days. But not all carbohydrates are the same (complex vs. refined), and an absolute carbohydrate reduction necessitates an increase in another energy source, such as protein. The most readily available sources of protein in our society are animals. But animal proteins, even if lean, may be associated with adverse cardiovascular outcomes.

Dr. Pagona Lagiou of University of Athens Medical School and Harvard School of Public Health and colleagues prospectively evaluated the cardiovascular risks associated with a low-carbohydrate, high-protein diet in 43,396 Swedish women (BMJ 2012;344:e4026). Participants were aged 30-49 years randomly selected to complete an extensive baseline dietary questionnaire and followed up for an average of 15.7 years. The investigators observed that a decrease in carbohydrate intake or an increase in protein intake or an increase in the “low carbohydrate-high protein score” were all significantly associated with an increasing incidence of cardiovascular disease.

Data further suggested that the incidence of cardiovascular events was higher among women whose protein intake was mainly of animal rather than plant origin.

If we are advising our patients to decrease carbohydrates and increase protein in order to lose weight, findings from this study would suggest that we include another important bit of information. First, dietary goals should aim to reduce simple carbohydrates (e.g., sucrose, high fructose corn syrup) more than complex carbohydrates (e.g., whole grains, fruits, and vegetables). Second, increases in protein consumption should aim to include more plant (e.g., spinach, soy, beans) than animal protein (e.g., lamb, beef, pork).

Key elements of this dietary approach are nicely embodied in the South Beach Diet. Most importantly, we need to emphasize to our patients that alterations in diet should not be considered a “diet” but a lifestyle change to improve overall health and well-being.

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.