Child Psychiatry Consult

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 [email protected].

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 [email protected].

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 [email protected].

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 [email protected].

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 [email protected].

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 [email protected].

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 [email protected].

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 [email protected].

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 [email protected].

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

Our toolbox for preventing cardiovascular disease just became a whole lot richer.

The Latin name for cacao, Theobroma, literally means “food of the gods.” Dark chocolate is produced by adding fat and sugar to cacao, or cocoa, which contains flavonoids that exert antihypertensive, anti-inflammatory, and antithrombotic effects.

This month, Ella Zomer and colleagues of Monash University in Melbourne, Australia, attempted to put a dollar amount on dark chocolate’s health benefits (BMJ 2012;344:e3657).

Using statistical modeling, the investigators evaluated the health effects and costs associated with daily plain dark chocolate consumption compared with no such consumption in a population of 2,013 people with hypertension who met criteria for metabolic syndrome, but who had no history of cardiovascular disease and were not receiving antihypertensive therapy.

The analysis focused on people in the Australian Diabetes Obesity and Lifestyle (AusDiab) study and the effects of chocolate were informed by randomized trials and meta-analyses.

Assuming 100% adherence, daily dark chocolate consumption was estimated to prevent 70 non-fatal and 15 fatal cardiovascular events per 10,000 people treated over 10 years. This would occur at a cost of $52,500 per year of life saved when $42 was spent per person per year on dark chocolate.

Available evidence suggests that dark chocolate needs to be at least 60%-70% cacao to exert beneficial health effects. Higher levels of cacao adds bitterness, an acquired taste that may not be tolerated by many of our American patients raised on milk chocolate. Clinical recommendations need to take into consideration that palatable dark chocolate contains fat and sugar that may increase the risk for weight gain, but dark chocolate increases satiety, which may help decrease snacking.

The general notion that dark chocolate may be beneficial for our patients is provocative, but taking it a step further and actually prescribing chocolate is tricky given that the optimal dose is unclear. Many of us may be reluctant to encourage chocolate consumption in our patients with metabolic syndrome for fear that they will over do it. Perhaps its time to extrapolate these findings and test the health benefits of dark chocolate for ourselves.

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. Contact him at [email protected].

Our toolbox for preventing cardiovascular disease just became a whole lot richer.

The Latin name for cacao, Theobroma, literally means “food of the gods.” Dark chocolate is produced by adding fat and sugar to cacao, or cocoa, which contains flavonoids that exert antihypertensive, anti-inflammatory, and antithrombotic effects.

This month, Ella Zomer and colleagues of Monash University in Melbourne, Australia, attempted to put a dollar amount on dark chocolate’s health benefits (BMJ 2012;344:e3657).

Using statistical modeling, the investigators evaluated the health effects and costs associated with daily plain dark chocolate consumption compared with no such consumption in a population of 2,013 people with hypertension who met criteria for metabolic syndrome, but who had no history of cardiovascular disease and were not receiving antihypertensive therapy.

The analysis focused on people in the Australian Diabetes Obesity and Lifestyle (AusDiab) study and the effects of chocolate were informed by randomized trials and meta-analyses.

Assuming 100% adherence, daily dark chocolate consumption was estimated to prevent 70 non-fatal and 15 fatal cardiovascular events per 10,000 people treated over 10 years. This would occur at a cost of $52,500 per year of life saved when $42 was spent per person per year on dark chocolate.

Available evidence suggests that dark chocolate needs to be at least 60%-70% cacao to exert beneficial health effects. Higher levels of cacao adds bitterness, an acquired taste that may not be tolerated by many of our American patients raised on milk chocolate. Clinical recommendations need to take into consideration that palatable dark chocolate contains fat and sugar that may increase the risk for weight gain, but dark chocolate increases satiety, which may help decrease snacking.

The general notion that dark chocolate may be beneficial for our patients is provocative, but taking it a step further and actually prescribing chocolate is tricky given that the optimal dose is unclear. Many of us may be reluctant to encourage chocolate consumption in our patients with metabolic syndrome for fear that they will over do it. Perhaps its time to extrapolate these findings and test the health benefits of dark chocolate for ourselves.

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. Contact him at [email protected].

Our toolbox for preventing cardiovascular disease just became a whole lot richer.

The Latin name for cacao, Theobroma, literally means “food of the gods.” Dark chocolate is produced by adding fat and sugar to cacao, or cocoa, which contains flavonoids that exert antihypertensive, anti-inflammatory, and antithrombotic effects.

This month, Ella Zomer and colleagues of Monash University in Melbourne, Australia, attempted to put a dollar amount on dark chocolate’s health benefits (BMJ 2012;344:e3657).

Using statistical modeling, the investigators evaluated the health effects and costs associated with daily plain dark chocolate consumption compared with no such consumption in a population of 2,013 people with hypertension who met criteria for metabolic syndrome, but who had no history of cardiovascular disease and were not receiving antihypertensive therapy.

The analysis focused on people in the Australian Diabetes Obesity and Lifestyle (AusDiab) study and the effects of chocolate were informed by randomized trials and meta-analyses.

Assuming 100% adherence, daily dark chocolate consumption was estimated to prevent 70 non-fatal and 15 fatal cardiovascular events per 10,000 people treated over 10 years. This would occur at a cost of $52,500 per year of life saved when $42 was spent per person per year on dark chocolate.

Available evidence suggests that dark chocolate needs to be at least 60%-70% cacao to exert beneficial health effects. Higher levels of cacao adds bitterness, an acquired taste that may not be tolerated by many of our American patients raised on milk chocolate. Clinical recommendations need to take into consideration that palatable dark chocolate contains fat and sugar that may increase the risk for weight gain, but dark chocolate increases satiety, which may help decrease snacking.

The general notion that dark chocolate may be beneficial for our patients is provocative, but taking it a step further and actually prescribing chocolate is tricky given that the optimal dose is unclear. Many of us may be reluctant to encourage chocolate consumption in our patients with metabolic syndrome for fear that they will over do it. Perhaps its time to extrapolate these findings and test the health benefits of dark chocolate for ourselves.

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. Contact him at [email protected].

The recent release of the U.S. Preventive Services Task Force (USPSTF) recommendations on prostate specific-antigen (PSA) screening, anticipated as they may have been, necessitated prolonged visits with concerned men demanding explanations for why it was no longer recommended regardless of age.

Discussions about “turning off” screening are frequently more challenging than ones explaining why screening should not be “turned on” at all. But for some of us who continue to screen informed and requesting men, we will be haunted by the imperfection of the PSA as a screening modality. We cannot escape our inability to distinguish between indolent and aggressive prostate cancer with the PSA.

Ray Moynihan of Bond University in Australia and colleagues recently explored the causes and possible solutions to the “overdiagnosis” and “medicalization” of healthy individuals (BMJ. 2012;344:e3502. PubMed PMID: 22645185). At stake is potentially more than $200 billion U.S. dollars spent on unnecessary treatment for early cancers and other diseases based on broader diagnostic criteria that capture low-risk individuals. Also at risk is the health of the healthy.

Technology is a double-edged sword. Sensitive testing modalities detect cancers that may regress, remain indolent, or grow so slowly as to not cause problems if left untreated. The ever increasing use of imaging spurs the detection of incidental findings in up to 40% of patients, who then require additional testing for issues that most often turn out to be benign.

Labeling otherwise mild clinical problems as a “dysfunction” (e.g., sexual dysfunction) increases medication use and the possibility of adverse effects. Mr. Moynihan and colleagues provide a provocative “hit list” of conditions for which sensitive screening and expanding disease definitions result in overdiagnosis and overtreatment. The list includes: 1) asthma; 2) attention deficit hyperactivity disorder; 3) breast cancer; 4) chronic kidney disease; 5) gestational diabetes; 6) hypertension; 7) hyperlipidemia; 8) osteoporosis; 9) prostate cancer; 10) pulmonary embolism; and 11) thyroid cancer.

Combating the overdiagnosis and overtreatment trends will require a cultural shift. Enabled by medical technology, many medical practitioners strongly believe that early detection is beneficial for their patients. Medical advancement is increasingly driven by the question “can we?” instead of the more important question “should we?” But when we can, we sometimes cause harm when we do.

Awareness about the need to address unnecessary care is growing. The “Choosing Wisely” campaign attempts to decrease unnecessary testing and treatments. In September 2013, an international scientific conference called “Preventing Overdiagnosis” will attempt to advance our understanding of how this issue. The conference will be hosted by Dartmouth, BMJ, Consumer Reports, and Bond University. Perhaps we will see you there.

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 [email protected].

The recent release of the U.S. Preventive Services Task Force (USPSTF) recommendations on prostate specific-antigen (PSA) screening, anticipated as they may have been, necessitated prolonged visits with concerned men demanding explanations for why it was no longer recommended regardless of age.

Discussions about “turning off” screening are frequently more challenging than ones explaining why screening should not be “turned on” at all. But for some of us who continue to screen informed and requesting men, we will be haunted by the imperfection of the PSA as a screening modality. We cannot escape our inability to distinguish between indolent and aggressive prostate cancer with the PSA.

Ray Moynihan of Bond University in Australia and colleagues recently explored the causes and possible solutions to the “overdiagnosis” and “medicalization” of healthy individuals (BMJ. 2012;344:e3502. PubMed PMID: 22645185). At stake is potentially more than $200 billion U.S. dollars spent on unnecessary treatment for early cancers and other diseases based on broader diagnostic criteria that capture low-risk individuals. Also at risk is the health of the healthy.

Technology is a double-edged sword. Sensitive testing modalities detect cancers that may regress, remain indolent, or grow so slowly as to not cause problems if left untreated. The ever increasing use of imaging spurs the detection of incidental findings in up to 40% of patients, who then require additional testing for issues that most often turn out to be benign.

Labeling otherwise mild clinical problems as a “dysfunction” (e.g., sexual dysfunction) increases medication use and the possibility of adverse effects. Mr. Moynihan and colleagues provide a provocative “hit list” of conditions for which sensitive screening and expanding disease definitions result in overdiagnosis and overtreatment. The list includes: 1) asthma; 2) attention deficit hyperactivity disorder; 3) breast cancer; 4) chronic kidney disease; 5) gestational diabetes; 6) hypertension; 7) hyperlipidemia; 8) osteoporosis; 9) prostate cancer; 10) pulmonary embolism; and 11) thyroid cancer.

Combating the overdiagnosis and overtreatment trends will require a cultural shift. Enabled by medical technology, many medical practitioners strongly believe that early detection is beneficial for their patients. Medical advancement is increasingly driven by the question “can we?” instead of the more important question “should we?” But when we can, we sometimes cause harm when we do.

Awareness about the need to address unnecessary care is growing. The “Choosing Wisely” campaign attempts to decrease unnecessary testing and treatments. In September 2013, an international scientific conference called “Preventing Overdiagnosis” will attempt to advance our understanding of how this issue. The conference will be hosted by Dartmouth, BMJ, Consumer Reports, and Bond University. Perhaps we will see you there.

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 [email protected].

The recent release of the U.S. Preventive Services Task Force (USPSTF) recommendations on prostate specific-antigen (PSA) screening, anticipated as they may have been, necessitated prolonged visits with concerned men demanding explanations for why it was no longer recommended regardless of age.

Discussions about “turning off” screening are frequently more challenging than ones explaining why screening should not be “turned on” at all. But for some of us who continue to screen informed and requesting men, we will be haunted by the imperfection of the PSA as a screening modality. We cannot escape our inability to distinguish between indolent and aggressive prostate cancer with the PSA.

Ray Moynihan of Bond University in Australia and colleagues recently explored the causes and possible solutions to the “overdiagnosis” and “medicalization” of healthy individuals (BMJ. 2012;344:e3502. PubMed PMID: 22645185). At stake is potentially more than $200 billion U.S. dollars spent on unnecessary treatment for early cancers and other diseases based on broader diagnostic criteria that capture low-risk individuals. Also at risk is the health of the healthy.

Technology is a double-edged sword. Sensitive testing modalities detect cancers that may regress, remain indolent, or grow so slowly as to not cause problems if left untreated. The ever increasing use of imaging spurs the detection of incidental findings in up to 40% of patients, who then require additional testing for issues that most often turn out to be benign.

Labeling otherwise mild clinical problems as a “dysfunction” (e.g., sexual dysfunction) increases medication use and the possibility of adverse effects. Mr. Moynihan and colleagues provide a provocative “hit list” of conditions for which sensitive screening and expanding disease definitions result in overdiagnosis and overtreatment. The list includes: 1) asthma; 2) attention deficit hyperactivity disorder; 3) breast cancer; 4) chronic kidney disease; 5) gestational diabetes; 6) hypertension; 7) hyperlipidemia; 8) osteoporosis; 9) prostate cancer; 10) pulmonary embolism; and 11) thyroid cancer.

Combating the overdiagnosis and overtreatment trends will require a cultural shift. Enabled by medical technology, many medical practitioners strongly believe that early detection is beneficial for their patients. Medical advancement is increasingly driven by the question “can we?” instead of the more important question “should we?” But when we can, we sometimes cause harm when we do.

Awareness about the need to address unnecessary care is growing. The “Choosing Wisely” campaign attempts to decrease unnecessary testing and treatments. In September 2013, an international scientific conference called “Preventing Overdiagnosis” will attempt to advance our understanding of how this issue. The conference will be hosted by Dartmouth, BMJ, Consumer Reports, and Bond University. Perhaps we will see you there.

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 [email protected].

Despite solid clinical evidence that most sinusitis is caused by viral infections – 99% of which will improve without therapy – we frequently prescribe antibiotics. Some clinicians attempt to put the breaks on using antibiotics by reserving them for patients with “chronic sinusitis” (defined as at least 12 weeks of symptoms) or for those who fail conservative therapy with oral and nasal decongestants.

Others have proposed using intranasal steroids as an adjunctive therapy for sinusitis. But how effective are steroids alone or in combination with antibiotics?

Dr. Gail Hayward and colleagues at Oxford University, England, conducted an updated systematic review of the literature evaluating the efficacy of intranasal corticosteroids for acute sinusitis (Ann. Fam. Med. 2012;10:241-9). Their investigation focused on six randomized controlled trials (RCTs) comparing intranasal corticosteroids with placebo in 2,495 children or adults who had symptoms consistent with sinusitis and who presented to various ambulatory settings. Studies were excluded if they enrolled patients with chronic/allergic sinusitis or those with chronic underlying health conditions.

Corticosteroids used were budesonide (2 studies), fluticasone propionate (1 study), and mometasone furoate (3 studies). Five trials involved the antibiotics amoxicillin, amoxicillin/clavulanic acid, or cefuroxime. One study prescribed intranasal xylometazoline.

Five of the trials showed that intranasal steroids improved or resolved symptoms at 14 to 21 days (risk difference 0.08; 95% CI, 0.03-0.13; P = .004) with a number needed to treat of 14. Studies did not demonstrate improvement at 14 to 15 days. Higher doses of mometasone (800 µg) were associated with greater symptom improvement than lower doses (400 µg). Steroids were associated with improvement in facial pain, congestion, rhinorrhea, headache, and post-nasal drip. No significant increases in adverse symptoms were observed.

Although the number needed to treat for intranasal steroids is reasonable, patients may not want to pay the cost, or even the co-pay, for a medication that requires 2 to 3 weeks to lead to symptoms improvement or resolution. Cheaper options exist (i.e., decongestants). Questions remain as to whether we can use steroids instead of antibiotics for the treatment of sinusitis in selected patients. Until we have these data, tension between the clinician’s desire to judiciously prescribe antibiotics and the patient’s expectations for them will persist.

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 [email protected].

Despite solid clinical evidence that most sinusitis is caused by viral infections – 99% of which will improve without therapy – we frequently prescribe antibiotics. Some clinicians attempt to put the breaks on using antibiotics by reserving them for patients with “chronic sinusitis” (defined as at least 12 weeks of symptoms) or for those who fail conservative therapy with oral and nasal decongestants.

Others have proposed using intranasal steroids as an adjunctive therapy for sinusitis. But how effective are steroids alone or in combination with antibiotics?

Dr. Gail Hayward and colleagues at Oxford University, England, conducted an updated systematic review of the literature evaluating the efficacy of intranasal corticosteroids for acute sinusitis (Ann. Fam. Med. 2012;10:241-9). Their investigation focused on six randomized controlled trials (RCTs) comparing intranasal corticosteroids with placebo in 2,495 children or adults who had symptoms consistent with sinusitis and who presented to various ambulatory settings. Studies were excluded if they enrolled patients with chronic/allergic sinusitis or those with chronic underlying health conditions.

Corticosteroids used were budesonide (2 studies), fluticasone propionate (1 study), and mometasone furoate (3 studies). Five trials involved the antibiotics amoxicillin, amoxicillin/clavulanic acid, or cefuroxime. One study prescribed intranasal xylometazoline.

Five of the trials showed that intranasal steroids improved or resolved symptoms at 14 to 21 days (risk difference 0.08; 95% CI, 0.03-0.13; P = .004) with a number needed to treat of 14. Studies did not demonstrate improvement at 14 to 15 days. Higher doses of mometasone (800 µg) were associated with greater symptom improvement than lower doses (400 µg). Steroids were associated with improvement in facial pain, congestion, rhinorrhea, headache, and post-nasal drip. No significant increases in adverse symptoms were observed.

Although the number needed to treat for intranasal steroids is reasonable, patients may not want to pay the cost, or even the co-pay, for a medication that requires 2 to 3 weeks to lead to symptoms improvement or resolution. Cheaper options exist (i.e., decongestants). Questions remain as to whether we can use steroids instead of antibiotics for the treatment of sinusitis in selected patients. Until we have these data, tension between the clinician’s desire to judiciously prescribe antibiotics and the patient’s expectations for them will persist.

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 [email protected].

Despite solid clinical evidence that most sinusitis is caused by viral infections – 99% of which will improve without therapy – we frequently prescribe antibiotics. Some clinicians attempt to put the breaks on using antibiotics by reserving them for patients with “chronic sinusitis” (defined as at least 12 weeks of symptoms) or for those who fail conservative therapy with oral and nasal decongestants.

Others have proposed using intranasal steroids as an adjunctive therapy for sinusitis. But how effective are steroids alone or in combination with antibiotics?

Dr. Gail Hayward and colleagues at Oxford University, England, conducted an updated systematic review of the literature evaluating the efficacy of intranasal corticosteroids for acute sinusitis (Ann. Fam. Med. 2012;10:241-9). Their investigation focused on six randomized controlled trials (RCTs) comparing intranasal corticosteroids with placebo in 2,495 children or adults who had symptoms consistent with sinusitis and who presented to various ambulatory settings. Studies were excluded if they enrolled patients with chronic/allergic sinusitis or those with chronic underlying health conditions.

Corticosteroids used were budesonide (2 studies), fluticasone propionate (1 study), and mometasone furoate (3 studies). Five trials involved the antibiotics amoxicillin, amoxicillin/clavulanic acid, or cefuroxime. One study prescribed intranasal xylometazoline.

Five of the trials showed that intranasal steroids improved or resolved symptoms at 14 to 21 days (risk difference 0.08; 95% CI, 0.03-0.13; P = .004) with a number needed to treat of 14. Studies did not demonstrate improvement at 14 to 15 days. Higher doses of mometasone (800 µg) were associated with greater symptom improvement than lower doses (400 µg). Steroids were associated with improvement in facial pain, congestion, rhinorrhea, headache, and post-nasal drip. No significant increases in adverse symptoms were observed.

Although the number needed to treat for intranasal steroids is reasonable, patients may not want to pay the cost, or even the co-pay, for a medication that requires 2 to 3 weeks to lead to symptoms improvement or resolution. Cheaper options exist (i.e., decongestants). Questions remain as to whether we can use steroids instead of antibiotics for the treatment of sinusitis in selected patients. Until we have these data, tension between the clinician’s desire to judiciously prescribe antibiotics and the patient’s expectations for them will persist.

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 [email protected].

Syncope is an abrupt, transient loss of consciousness and postural tone followed by spontaneous recovery associated with profound anxiety in the patient, family, and, not too infrequently, the clinician. For patients receiving the “rule out” diagnosis of vasovagal syncope (VVS), treatment options are commonly of uncertain value, and often are dissatisfying because they are not typically curative. 

Dr. Ankur Vyas of the University of Iowa, and colleagues, conducted a systematic review to shed light on the various options for vasovagal syncope (Int J Cardiol. 2012 May 22 doi:10.1016/j.ijcard.2012.04.144).

Among other studies, their analysis focused on seven randomized controlled trials involving 400 patients. End points for four of the studies looked at repeat positive tilt tests; three evaluated spontaneous symptom recurrence. Among their findings:
•    Alpha-adrenergic agonists were found to be effective in preventing recurrence (7 studies, n = 400; OR 0.19, CI 0.06–0.62, P < 0.05). Among the alpha-adrenergic agonists, midodrine was found to be effective (4 studies, n = 136, OR 0.12, CI 0.05–0.26, P < 0.05), but etilefrine was not.
•    Beta-blockers were found to be ineffective for reducing VVS when only randomized studies comparing them to non-pharmacologic agents were analyzed (9 studies, n = 583, OR 0.48, CI 0.22–1.04, P = 0.06).
•    SSRI’s were ineffective for reducing recurrence (2 studies, n = 131, OR 0.28, CI 0.10–0.74, P< 0.05).
•    When only randomized trials were included, tilt training was not found to be effective for reducing recurrence of VVS.
•    Pacemakers appeared to be effective for preventing syncope recurrence (6 studies, n = 463, OR 0.13, CI 0.05–0.36, P < 0.05). And specifically, when pacemakers were compared to medical therapy they were more effective at preventing syncope (4 studies, n = 209, OR 0.09, CI 0.04–0.22, P < 0.05).

Vasovagal syncope is clinically challenging especially for our patients who have recurrent symptoms. “High risk” patients, defined as those whose events occur without warning and in any position with no clear precipitating causes, and/or frequent occurrence, need to be counseled against driving. Unfortunately, adherence to this recommendation is low. Only 35% of patients with VVS are symptom free after a median of five years of follow-up, regardless of presenting symptoms or treatment. For patients with VVS, reassurance and education regarding the nature, risks, and prognosis of the condition may be just as important as the medical therapy we provide.

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 [email protected].

Syncope is an abrupt, transient loss of consciousness and postural tone followed by spontaneous recovery associated with profound anxiety in the patient, family, and, not too infrequently, the clinician. For patients receiving the “rule out” diagnosis of vasovagal syncope (VVS), treatment options are commonly of uncertain value, and often are dissatisfying because they are not typically curative. 

Dr. Ankur Vyas of the University of Iowa, and colleagues, conducted a systematic review to shed light on the various options for vasovagal syncope (Int J Cardiol. 2012 May 22 doi:10.1016/j.ijcard.2012.04.144).

Among other studies, their analysis focused on seven randomized controlled trials involving 400 patients. End points for four of the studies looked at repeat positive tilt tests; three evaluated spontaneous symptom recurrence. Among their findings:
•    Alpha-adrenergic agonists were found to be effective in preventing recurrence (7 studies, n = 400; OR 0.19, CI 0.06–0.62, P < 0.05). Among the alpha-adrenergic agonists, midodrine was found to be effective (4 studies, n = 136, OR 0.12, CI 0.05–0.26, P < 0.05), but etilefrine was not.
•    Beta-blockers were found to be ineffective for reducing VVS when only randomized studies comparing them to non-pharmacologic agents were analyzed (9 studies, n = 583, OR 0.48, CI 0.22–1.04, P = 0.06).
•    SSRI’s were ineffective for reducing recurrence (2 studies, n = 131, OR 0.28, CI 0.10–0.74, P< 0.05).
•    When only randomized trials were included, tilt training was not found to be effective for reducing recurrence of VVS.
•    Pacemakers appeared to be effective for preventing syncope recurrence (6 studies, n = 463, OR 0.13, CI 0.05–0.36, P < 0.05). And specifically, when pacemakers were compared to medical therapy they were more effective at preventing syncope (4 studies, n = 209, OR 0.09, CI 0.04–0.22, P < 0.05).

Vasovagal syncope is clinically challenging especially for our patients who have recurrent symptoms. “High risk” patients, defined as those whose events occur without warning and in any position with no clear precipitating causes, and/or frequent occurrence, need to be counseled against driving. Unfortunately, adherence to this recommendation is low. Only 35% of patients with VVS are symptom free after a median of five years of follow-up, regardless of presenting symptoms or treatment. For patients with VVS, reassurance and education regarding the nature, risks, and prognosis of the condition may be just as important as the medical therapy we provide.

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 [email protected].

Syncope is an abrupt, transient loss of consciousness and postural tone followed by spontaneous recovery associated with profound anxiety in the patient, family, and, not too infrequently, the clinician. For patients receiving the “rule out” diagnosis of vasovagal syncope (VVS), treatment options are commonly of uncertain value, and often are dissatisfying because they are not typically curative. 

Dr. Ankur Vyas of the University of Iowa, and colleagues, conducted a systematic review to shed light on the various options for vasovagal syncope (Int J Cardiol. 2012 May 22 doi:10.1016/j.ijcard.2012.04.144).

Among other studies, their analysis focused on seven randomized controlled trials involving 400 patients. End points for four of the studies looked at repeat positive tilt tests; three evaluated spontaneous symptom recurrence. Among their findings:
•    Alpha-adrenergic agonists were found to be effective in preventing recurrence (7 studies, n = 400; OR 0.19, CI 0.06–0.62, P < 0.05). Among the alpha-adrenergic agonists, midodrine was found to be effective (4 studies, n = 136, OR 0.12, CI 0.05–0.26, P < 0.05), but etilefrine was not.
•    Beta-blockers were found to be ineffective for reducing VVS when only randomized studies comparing them to non-pharmacologic agents were analyzed (9 studies, n = 583, OR 0.48, CI 0.22–1.04, P = 0.06).
•    SSRI’s were ineffective for reducing recurrence (2 studies, n = 131, OR 0.28, CI 0.10–0.74, P< 0.05).
•    When only randomized trials were included, tilt training was not found to be effective for reducing recurrence of VVS.
•    Pacemakers appeared to be effective for preventing syncope recurrence (6 studies, n = 463, OR 0.13, CI 0.05–0.36, P < 0.05). And specifically, when pacemakers were compared to medical therapy they were more effective at preventing syncope (4 studies, n = 209, OR 0.09, CI 0.04–0.22, P < 0.05).

Vasovagal syncope is clinically challenging especially for our patients who have recurrent symptoms. “High risk” patients, defined as those whose events occur without warning and in any position with no clear precipitating causes, and/or frequent occurrence, need to be counseled against driving. Unfortunately, adherence to this recommendation is low. Only 35% of patients with VVS are symptom free after a median of five years of follow-up, regardless of presenting symptoms or treatment. For patients with VVS, reassurance and education regarding the nature, risks, and prognosis of the condition may be just as important as the medical therapy we provide.

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 [email protected].

Antibiotic-associated diarrhea (AAD) is an unfortunate clinical morbidity associated with our attempts to treat another clinical problem (i.e., infection). The most serious AAD is associated with Clostridium difficile; historically high rates of this infection have resulted in increased calls for “antibiotic stewardship.”

Despite our appropriate apprehensions about C. difficile, we commonly need to prescribe antibiotics in clinical practice. So what do we do to prevent “run of the mill” AAD? Although AAD does not occur in the majority of patients (~ 20%), we have patients who express concern about its occurrence and request advice on how to prevent it. Perhaps many of us have told our patients to eat yogurt or purchase over-the-counter probiotics. The efficacy of this approach has been controversial both because of uncertainty about effectiveness and concerns about side effects.

Earlier this month, Dr. Susanne Hempel of RAND Health and colleagues published a systematic review exploring the evidence for probiotic use in the prevention and treatment of AAD (JAMA. 2012;307:1959-69).

Recall that probiotics are micro-organisms intended to provide health benefits when consumed. Investigators searched for randomized controlled trials (RCTs) for both prevention and treatment. Probiotic interventions were primarily Lactobacillus-based, either alone or combined with other genera such as Bifidobacterium. Most studies explicitly administered probiotics to prevent or treat AAD. Across 63 RCTs (11,811 participants), probiotic use was associated with a lower relative risk (RR) of developing diarrhea compared to a control group not using a probiotic (RR, 0.58; 95% CI: 0.50 to 0.68; P< .001).

The exclusively Lactobacillus-based interventions (17 RCTs) reduced AAD [RR = 0.64; 95% CI: 0.47 to 0.86; P = .004; number needed to treat (NNT) = 14] and the exclusively yeast-based interventions (15 RCTs, Saccharomyces) reduced AAD (RR = 0.48; 95% CI: 0.35 to 0.65; P < .001; NNT = 10).
Adjunctive probiotic use for the treatment of Helicobacter pylori also was associated with benefit (RR = 0.55; 95% CI: 0.35 to 0.86; P = .009; NNT = 17).

In 14 RCTs, probiotics reduced the risk for C. difficile diarrhea (RR = 0.29; 95% CI: 0.17 to 0.48; P < .001; NNT = 25). Nineteen RCTs reported that no adverse events were judged to be associated with the use of probiotics.
Findings from this study are useful for clinicians alleviating patient concerns about AAD. Findings also may provide us with an intervention that may reduce infection with C. difficile.

So why are more of us not recommending probiotics? Perhaps our lack of familiarity with the variety of different products and the unavailability of standardized prescribing information are the most significant barriers to wider use. Companies with “skin in the game” on probiotics need to make this information more readily accessible to clinicians in order to increase recommendations for use of what appears to be a very effective intervention.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. The opinions expressed are solely those of the author. Reach him by e-mail at [email protected].

Antibiotic-associated diarrhea (AAD) is an unfortunate clinical morbidity associated with our attempts to treat another clinical problem (i.e., infection). The most serious AAD is associated with Clostridium difficile; historically high rates of this infection have resulted in increased calls for “antibiotic stewardship.”

Despite our appropriate apprehensions about C. difficile, we commonly need to prescribe antibiotics in clinical practice. So what do we do to prevent “run of the mill” AAD? Although AAD does not occur in the majority of patients (~ 20%), we have patients who express concern about its occurrence and request advice on how to prevent it. Perhaps many of us have told our patients to eat yogurt or purchase over-the-counter probiotics. The efficacy of this approach has been controversial both because of uncertainty about effectiveness and concerns about side effects.

Earlier this month, Dr. Susanne Hempel of RAND Health and colleagues published a systematic review exploring the evidence for probiotic use in the prevention and treatment of AAD (JAMA. 2012;307:1959-69).

Recall that probiotics are micro-organisms intended to provide health benefits when consumed. Investigators searched for randomized controlled trials (RCTs) for both prevention and treatment. Probiotic interventions were primarily Lactobacillus-based, either alone or combined with other genera such as Bifidobacterium. Most studies explicitly administered probiotics to prevent or treat AAD. Across 63 RCTs (11,811 participants), probiotic use was associated with a lower relative risk (RR) of developing diarrhea compared to a control group not using a probiotic (RR, 0.58; 95% CI: 0.50 to 0.68; P< .001).

The exclusively Lactobacillus-based interventions (17 RCTs) reduced AAD [RR = 0.64; 95% CI: 0.47 to 0.86; P = .004; number needed to treat (NNT) = 14] and the exclusively yeast-based interventions (15 RCTs, Saccharomyces) reduced AAD (RR = 0.48; 95% CI: 0.35 to 0.65; P < .001; NNT = 10).
Adjunctive probiotic use for the treatment of Helicobacter pylori also was associated with benefit (RR = 0.55; 95% CI: 0.35 to 0.86; P = .009; NNT = 17).

In 14 RCTs, probiotics reduced the risk for C. difficile diarrhea (RR = 0.29; 95% CI: 0.17 to 0.48; P < .001; NNT = 25). Nineteen RCTs reported that no adverse events were judged to be associated with the use of probiotics.
Findings from this study are useful for clinicians alleviating patient concerns about AAD. Findings also may provide us with an intervention that may reduce infection with C. difficile.

So why are more of us not recommending probiotics? Perhaps our lack of familiarity with the variety of different products and the unavailability of standardized prescribing information are the most significant barriers to wider use. Companies with “skin in the game” on probiotics need to make this information more readily accessible to clinicians in order to increase recommendations for use of what appears to be a very effective intervention.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. The opinions expressed are solely those of the author. Reach him by e-mail at [email protected].

Antibiotic-associated diarrhea (AAD) is an unfortunate clinical morbidity associated with our attempts to treat another clinical problem (i.e., infection). The most serious AAD is associated with Clostridium difficile; historically high rates of this infection have resulted in increased calls for “antibiotic stewardship.”

Despite our appropriate apprehensions about C. difficile, we commonly need to prescribe antibiotics in clinical practice. So what do we do to prevent “run of the mill” AAD? Although AAD does not occur in the majority of patients (~ 20%), we have patients who express concern about its occurrence and request advice on how to prevent it. Perhaps many of us have told our patients to eat yogurt or purchase over-the-counter probiotics. The efficacy of this approach has been controversial both because of uncertainty about effectiveness and concerns about side effects.

Earlier this month, Dr. Susanne Hempel of RAND Health and colleagues published a systematic review exploring the evidence for probiotic use in the prevention and treatment of AAD (JAMA. 2012;307:1959-69).

Recall that probiotics are micro-organisms intended to provide health benefits when consumed. Investigators searched for randomized controlled trials (RCTs) for both prevention and treatment. Probiotic interventions were primarily Lactobacillus-based, either alone or combined with other genera such as Bifidobacterium. Most studies explicitly administered probiotics to prevent or treat AAD. Across 63 RCTs (11,811 participants), probiotic use was associated with a lower relative risk (RR) of developing diarrhea compared to a control group not using a probiotic (RR, 0.58; 95% CI: 0.50 to 0.68; P< .001).

The exclusively Lactobacillus-based interventions (17 RCTs) reduced AAD [RR = 0.64; 95% CI: 0.47 to 0.86; P = .004; number needed to treat (NNT) = 14] and the exclusively yeast-based interventions (15 RCTs, Saccharomyces) reduced AAD (RR = 0.48; 95% CI: 0.35 to 0.65; P < .001; NNT = 10).
Adjunctive probiotic use for the treatment of Helicobacter pylori also was associated with benefit (RR = 0.55; 95% CI: 0.35 to 0.86; P = .009; NNT = 17).

In 14 RCTs, probiotics reduced the risk for C. difficile diarrhea (RR = 0.29; 95% CI: 0.17 to 0.48; P < .001; NNT = 25). Nineteen RCTs reported that no adverse events were judged to be associated with the use of probiotics.
Findings from this study are useful for clinicians alleviating patient concerns about AAD. Findings also may provide us with an intervention that may reduce infection with C. difficile.

So why are more of us not recommending probiotics? Perhaps our lack of familiarity with the variety of different products and the unavailability of standardized prescribing information are the most significant barriers to wider use. Companies with “skin in the game” on probiotics need to make this information more readily accessible to clinicians in order to increase recommendations for use of what appears to be a very effective intervention.

Jon O. Ebbert, M.D., is a professor of medicine and a primary care clinician at the Mayo Clinic in Rochester, Minn. The opinions expressed are solely those of the author. Reach him by e-mail at [email protected].

When the Surgeon General released its 31st report on Preventing Tobacco Use Among Youth and Young Adults: A Report of the Surgeon General earlier this year, media outlets picked up on the slowing of declines in youth cigarette smoking and the stalling of declines in smokeless tobacco use. The report estimated that more than 3 million high school students – 80% of high school smokers – will continue to smoke into adulthood.

Tobacco use prevention is indeed critical for the health of our youth and practicing clinicians need to be ready to treat these newly minted tobacco users when they walk into our offices. To do this, we need accurate information on the efficacy and safety of pharmacotherapy for the treatment of tobacco dependence.

Varenicline (Chantix) is arguably the most effective medication for the treatment of tobacco dependence. But as with many new medications, metaanalyses of published clinical data are conducted as both formal and informal components of postmarketing surveillance. Some findings regarding varenicline have struck the bell of alarm. 

Dr. Sonal Singh of Johns Hopkins University School of Medicine, Baltimore, and colleagues published a metaanalysis suggesting that varenicline may increase the risk for cardiovascular events (CMAJ 2011;183:1359-66). This study was controversial primarily because it included events beyond the period of drug exposure and excluded trials with no events. The findings, however, were the basis for including information about cardiovascular risk on the Chantix drug label.

New data published last week by Judith J. Prochaska, Ph.D., of the University of California, San Francisco, and a colleague (BMJ 2012; 344 doi: 10.1136/bmj.e2856) suggest that varenicline does not increase the risk for cardiovascular events. This metaanalysis analyzed serious cardiovascular events occurring during treatment or within 30 days of discontinuation. Twenty-two randomized, controlled clinical trials were included. No significant difference in risk for cardiovascular events was observed between the varenicline and placebo groups.

The critical difference between the two metaanalyses is that Dr. Prochaska’s analysis focused on events during drug exposure. On balance, it’s only reasonable to expect that the safety of a drug administered for a short period of time be evaluated in the time frame that the drug is given. This is especially true for a drug that is given to a population that is at notably high risk for the disease of interest (i.e., cardiovascular disease event risk in smokers).

Smoking is the most important risk factor for cardiovascular disease and varenicline is the most effective medication for the treatment of tobacco dependence. Perhaps the real risk is that patients who would benefit the most from this medication may not receive it because it’s hard to unring the bell of alarm.

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 clinical trials investigating the safety of varenicline. The opinions expressed are solely those of the author. Contact him at [email protected].

When the Surgeon General released its 31st report on Preventing Tobacco Use Among Youth and Young Adults: A Report of the Surgeon General earlier this year, media outlets picked up on the slowing of declines in youth cigarette smoking and the stalling of declines in smokeless tobacco use. The report estimated that more than 3 million high school students – 80% of high school smokers – will continue to smoke into adulthood.

Tobacco use prevention is indeed critical for the health of our youth and practicing clinicians need to be ready to treat these newly minted tobacco users when they walk into our offices. To do this, we need accurate information on the efficacy and safety of pharmacotherapy for the treatment of tobacco dependence.

Varenicline (Chantix) is arguably the most effective medication for the treatment of tobacco dependence. But as with many new medications, metaanalyses of published clinical data are conducted as both formal and informal components of postmarketing surveillance. Some findings regarding varenicline have struck the bell of alarm. 

Dr. Sonal Singh of Johns Hopkins University School of Medicine, Baltimore, and colleagues published a metaanalysis suggesting that varenicline may increase the risk for cardiovascular events (CMAJ 2011;183:1359-66). This study was controversial primarily because it included events beyond the period of drug exposure and excluded trials with no events. The findings, however, were the basis for including information about cardiovascular risk on the Chantix drug label.

New data published last week by Judith J. Prochaska, Ph.D., of the University of California, San Francisco, and a colleague (BMJ 2012; 344 doi: 10.1136/bmj.e2856) suggest that varenicline does not increase the risk for cardiovascular events. This metaanalysis analyzed serious cardiovascular events occurring during treatment or within 30 days of discontinuation. Twenty-two randomized, controlled clinical trials were included. No significant difference in risk for cardiovascular events was observed between the varenicline and placebo groups.

The critical difference between the two metaanalyses is that Dr. Prochaska’s analysis focused on events during drug exposure. On balance, it’s only reasonable to expect that the safety of a drug administered for a short period of time be evaluated in the time frame that the drug is given. This is especially true for a drug that is given to a population that is at notably high risk for the disease of interest (i.e., cardiovascular disease event risk in smokers).

Smoking is the most important risk factor for cardiovascular disease and varenicline is the most effective medication for the treatment of tobacco dependence. Perhaps the real risk is that patients who would benefit the most from this medication may not receive it because it’s hard to unring the bell of alarm.

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 clinical trials investigating the safety of varenicline. The opinions expressed are solely those of the author. Contact him at [email protected].

When the Surgeon General released its 31st report on Preventing Tobacco Use Among Youth and Young Adults: A Report of the Surgeon General earlier this year, media outlets picked up on the slowing of declines in youth cigarette smoking and the stalling of declines in smokeless tobacco use. The report estimated that more than 3 million high school students – 80% of high school smokers – will continue to smoke into adulthood.

Tobacco use prevention is indeed critical for the health of our youth and practicing clinicians need to be ready to treat these newly minted tobacco users when they walk into our offices. To do this, we need accurate information on the efficacy and safety of pharmacotherapy for the treatment of tobacco dependence.

Varenicline (Chantix) is arguably the most effective medication for the treatment of tobacco dependence. But as with many new medications, metaanalyses of published clinical data are conducted as both formal and informal components of postmarketing surveillance. Some findings regarding varenicline have struck the bell of alarm. 

Dr. Sonal Singh of Johns Hopkins University School of Medicine, Baltimore, and colleagues published a metaanalysis suggesting that varenicline may increase the risk for cardiovascular events (CMAJ 2011;183:1359-66). This study was controversial primarily because it included events beyond the period of drug exposure and excluded trials with no events. The findings, however, were the basis for including information about cardiovascular risk on the Chantix drug label.

New data published last week by Judith J. Prochaska, Ph.D., of the University of California, San Francisco, and a colleague (BMJ 2012; 344 doi: 10.1136/bmj.e2856) suggest that varenicline does not increase the risk for cardiovascular events. This metaanalysis analyzed serious cardiovascular events occurring during treatment or within 30 days of discontinuation. Twenty-two randomized, controlled clinical trials were included. No significant difference in risk for cardiovascular events was observed between the varenicline and placebo groups.

The critical difference between the two metaanalyses is that Dr. Prochaska’s analysis focused on events during drug exposure. On balance, it’s only reasonable to expect that the safety of a drug administered for a short period of time be evaluated in the time frame that the drug is given. This is especially true for a drug that is given to a population that is at notably high risk for the disease of interest (i.e., cardiovascular disease event risk in smokers).

Smoking is the most important risk factor for cardiovascular disease and varenicline is the most effective medication for the treatment of tobacco dependence. Perhaps the real risk is that patients who would benefit the most from this medication may not receive it because it’s hard to unring the bell of alarm.

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 clinical trials investigating the safety of varenicline. The opinions expressed are solely those of the author. Contact him at [email protected].

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 [email protected].

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 [email protected].

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 [email protected].