What Matters

As the obesity epidemic continues to rage unabated and diabetes takes its toll on nerves, I am seeing an increase in diabetic foot ulcers.

Traditionally, we have used topical therapies and dressings and pressure relief through accommodative footwear. This usually produces moderate to no effect in many of my patients. Perhaps this is because we are not monitoring in the clinic every other day, or patients are having a difficult time adhering to the complex wound care regimens we prescribe.

Then along came MIST, a proprietary, noncontact ultrasound device delivering low-frequency/low-intensity ultrasound waves via atomized sterile saline. Researchers at our institution have published data suggesting the efficacy of this treatment.

You’ll notice these data are far from new. Sorry to be late to the party, but what is new is my own case series of patients who have done astoundingly well with this therapy.

MIST Therapy heals by activating fibroblasts, reducing bacterial count, and disrupting that pernicious biofilm. The recommended regimen is three treatments per week, with treatments lasting 3-20 minutes depending on wound size. Larger wounds get longer treatments. Many centers are using this therapy exclusively when more than minimal debridement is required.

The MIST Therapy website suggests that this therapy is associated with a $2,600 cost savings over standard of care (estimated to be $10,300). In March 2013, the American Medical Association approved a CPT I code (97610) for MIST Therapy, which became effective in 2014.

Perhaps this code has resulted in more widespread use. However, my wound care colleagues said they have been using this for years prior to the code being issued, and reimbursement has not been a problem.

What I have noticed is how clean and healthy the wounds look very early in the treatment cycle. If you are not adding this therapy to your program for addressing foot ulcers, you need to. Ask your local wound care center about it, and apologize (for me) for being so late to the party.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant disclosures.

As the obesity epidemic continues to rage unabated and diabetes takes its toll on nerves, I am seeing an increase in diabetic foot ulcers.

Traditionally, we have used topical therapies and dressings and pressure relief through accommodative footwear. This usually produces moderate to no effect in many of my patients. Perhaps this is because we are not monitoring in the clinic every other day, or patients are having a difficult time adhering to the complex wound care regimens we prescribe.

Then along came MIST, a proprietary, noncontact ultrasound device delivering low-frequency/low-intensity ultrasound waves via atomized sterile saline. Researchers at our institution have published data suggesting the efficacy of this treatment.

You’ll notice these data are far from new. Sorry to be late to the party, but what is new is my own case series of patients who have done astoundingly well with this therapy.

MIST Therapy heals by activating fibroblasts, reducing bacterial count, and disrupting that pernicious biofilm. The recommended regimen is three treatments per week, with treatments lasting 3-20 minutes depending on wound size. Larger wounds get longer treatments. Many centers are using this therapy exclusively when more than minimal debridement is required.

The MIST Therapy website suggests that this therapy is associated with a $2,600 cost savings over standard of care (estimated to be $10,300). In March 2013, the American Medical Association approved a CPT I code (97610) for MIST Therapy, which became effective in 2014.

Perhaps this code has resulted in more widespread use. However, my wound care colleagues said they have been using this for years prior to the code being issued, and reimbursement has not been a problem.

What I have noticed is how clean and healthy the wounds look very early in the treatment cycle. If you are not adding this therapy to your program for addressing foot ulcers, you need to. Ask your local wound care center about it, and apologize (for me) for being so late to the party.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant disclosures.

As the obesity epidemic continues to rage unabated and diabetes takes its toll on nerves, I am seeing an increase in diabetic foot ulcers.

Traditionally, we have used topical therapies and dressings and pressure relief through accommodative footwear. This usually produces moderate to no effect in many of my patients. Perhaps this is because we are not monitoring in the clinic every other day, or patients are having a difficult time adhering to the complex wound care regimens we prescribe.

Then along came MIST, a proprietary, noncontact ultrasound device delivering low-frequency/low-intensity ultrasound waves via atomized sterile saline. Researchers at our institution have published data suggesting the efficacy of this treatment.

You’ll notice these data are far from new. Sorry to be late to the party, but what is new is my own case series of patients who have done astoundingly well with this therapy.

MIST Therapy heals by activating fibroblasts, reducing bacterial count, and disrupting that pernicious biofilm. The recommended regimen is three treatments per week, with treatments lasting 3-20 minutes depending on wound size. Larger wounds get longer treatments. Many centers are using this therapy exclusively when more than minimal debridement is required.

The MIST Therapy website suggests that this therapy is associated with a $2,600 cost savings over standard of care (estimated to be $10,300). In March 2013, the American Medical Association approved a CPT I code (97610) for MIST Therapy, which became effective in 2014.

Perhaps this code has resulted in more widespread use. However, my wound care colleagues said they have been using this for years prior to the code being issued, and reimbursement has not been a problem.

What I have noticed is how clean and healthy the wounds look very early in the treatment cycle. If you are not adding this therapy to your program for addressing foot ulcers, you need to. Ask your local wound care center about it, and apologize (for me) for being so late to the party.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant disclosures.

I freely admit I am obsessed with research articles about eating habits. I hold out hope that this will eventually unlock the magic bullet to cure us of the modern plague of obesity. At a certain level, our patients need us to be captivated by such literature. We should feel fairly comfortable with the common knowledge that diets are effective if you stay on them and reducing the caloric density of foods can result in meaningful weight loss.

But what about how quickly we eat? In our fast-paced, heavily caffeinated society, we seem to shovel rather than chew. Ever since I was a medical resident, I have practically inhaled my food. Perchance I am operating under the erroneous and illogical assumption that if I don’t taste the food it won’t register as calories. True science has now enlightened me to the error in my thinking.

Dr. Eric Robinson and his colleagues conducted a brilliant systematic review of the impact of eating rate on energy intake and hunger (Am. J. Clin. Nutr. 2014;100:123-51). They included studies for which there was at least one study arm in which participants ate a meal at a statistically significant slower rate than that of a different arm. Twenty-two studies met the criteria for inclusion.

Available evidence suggests that a slower eating rate is associated with lower intake, compared with faster eating. The effect on caloric intake was observed regardless of the intervention used to modify the eating rate, such as modifying food from soft (fast rate) to hard (slow rate) or verbal instruction. No relationship was observed between eating rate and hunger at the end of the meal or several hours later.

Intriguing to me is the hypothesis that eating rate likely affects intake through the duration and intensity of oral exposure to taste. Previous studies have shown that, when eating rate is held constant, increasing sensory exposure leads to a lower energy intake. This seems to relate to our innate wiring that gives us a “sensory specific satiety.” In my understanding, sensory specific satiety turns off appetitive drive when you have had too much chocolate or too many potato chips and you feel slightly ill. Unfortunately, the food industry is on to this game and they have designed foods to be perfectly balanced to not render satiety. These foods can tragically be eaten ceaselessly.

Take-home message: If your patients cannot control the bad foods they eat, they should try to eat them more slowly.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

I freely admit I am obsessed with research articles about eating habits. I hold out hope that this will eventually unlock the magic bullet to cure us of the modern plague of obesity. At a certain level, our patients need us to be captivated by such literature. We should feel fairly comfortable with the common knowledge that diets are effective if you stay on them and reducing the caloric density of foods can result in meaningful weight loss.

But what about how quickly we eat? In our fast-paced, heavily caffeinated society, we seem to shovel rather than chew. Ever since I was a medical resident, I have practically inhaled my food. Perchance I am operating under the erroneous and illogical assumption that if I don’t taste the food it won’t register as calories. True science has now enlightened me to the error in my thinking.

Dr. Eric Robinson and his colleagues conducted a brilliant systematic review of the impact of eating rate on energy intake and hunger (Am. J. Clin. Nutr. 2014;100:123-51). They included studies for which there was at least one study arm in which participants ate a meal at a statistically significant slower rate than that of a different arm. Twenty-two studies met the criteria for inclusion.

Available evidence suggests that a slower eating rate is associated with lower intake, compared with faster eating. The effect on caloric intake was observed regardless of the intervention used to modify the eating rate, such as modifying food from soft (fast rate) to hard (slow rate) or verbal instruction. No relationship was observed between eating rate and hunger at the end of the meal or several hours later.

Intriguing to me is the hypothesis that eating rate likely affects intake through the duration and intensity of oral exposure to taste. Previous studies have shown that, when eating rate is held constant, increasing sensory exposure leads to a lower energy intake. This seems to relate to our innate wiring that gives us a “sensory specific satiety.” In my understanding, sensory specific satiety turns off appetitive drive when you have had too much chocolate or too many potato chips and you feel slightly ill. Unfortunately, the food industry is on to this game and they have designed foods to be perfectly balanced to not render satiety. These foods can tragically be eaten ceaselessly.

Take-home message: If your patients cannot control the bad foods they eat, they should try to eat them more slowly.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

I freely admit I am obsessed with research articles about eating habits. I hold out hope that this will eventually unlock the magic bullet to cure us of the modern plague of obesity. At a certain level, our patients need us to be captivated by such literature. We should feel fairly comfortable with the common knowledge that diets are effective if you stay on them and reducing the caloric density of foods can result in meaningful weight loss.

But what about how quickly we eat? In our fast-paced, heavily caffeinated society, we seem to shovel rather than chew. Ever since I was a medical resident, I have practically inhaled my food. Perchance I am operating under the erroneous and illogical assumption that if I don’t taste the food it won’t register as calories. True science has now enlightened me to the error in my thinking.

Dr. Eric Robinson and his colleagues conducted a brilliant systematic review of the impact of eating rate on energy intake and hunger (Am. J. Clin. Nutr. 2014;100:123-51). They included studies for which there was at least one study arm in which participants ate a meal at a statistically significant slower rate than that of a different arm. Twenty-two studies met the criteria for inclusion.

Available evidence suggests that a slower eating rate is associated with lower intake, compared with faster eating. The effect on caloric intake was observed regardless of the intervention used to modify the eating rate, such as modifying food from soft (fast rate) to hard (slow rate) or verbal instruction. No relationship was observed between eating rate and hunger at the end of the meal or several hours later.

Intriguing to me is the hypothesis that eating rate likely affects intake through the duration and intensity of oral exposure to taste. Previous studies have shown that, when eating rate is held constant, increasing sensory exposure leads to a lower energy intake. This seems to relate to our innate wiring that gives us a “sensory specific satiety.” In my understanding, sensory specific satiety turns off appetitive drive when you have had too much chocolate or too many potato chips and you feel slightly ill. Unfortunately, the food industry is on to this game and they have designed foods to be perfectly balanced to not render satiety. These foods can tragically be eaten ceaselessly.

Take-home message: If your patients cannot control the bad foods they eat, they should try to eat them more slowly.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

At the risk of stating the obvious, our patients are becoming increasingly complex. Life is prolonged and comorbidities accumulate, creating dizzying laundry lists of medical problems.

Within the context of clinical or, increasingly, nonreimbursed telephonic or electronic visits, we attack the medical problem with the worst severity in an attempt to tamp it down to the level of its comorbid brethren.

Almost without exception, depression rears its ugly head in our sickest patients. Antidepressants will be started and added to the three pages (double-spaced, with 1-inch margins) of medications.

But in all of these patients, are we treating the disease or just the symptom? What if inflammation is causing the depression? Will reduction of inflammation treat the depression?

Dr. Ole Köhler of Aarhus University Hospital, Denmark, and his colleagues conducted a systematic review on the antidepressant effects of anti-inflammatory medications (JAMA Psychiatry 2014;71:1381-91). Fourteen trials informed the meta-analysis, 10 that evaluated NSAID drugs (for example, celecoxib, naproxen, ibuprofen), and 4 that investigated cytokine inhibitors (for example, etanercept, infliximab). Six of the 10 NSAID studies evaluated NSAIDs as monotherapy. All four of the cytokine-inhibitor trials evaluated them as monotherapy. Length of treatment was between 6 and 12 weeks.

The pooled effect suggests that anti-inflammatory treatment reduced depressive symptoms. Celecoxib seemed to have the strongest effect on remission and clinical response. No increase in adverse events was reported.

We know that proinflammatory drugs can induce depression. So the opposite is quite possibly true, and these data suggest it to be so. Findings suggest that reducing the inflammatory state among our patients with depression may be a useful adjunct to antidepressant therapy, at least in the initial period.

Whatever we can do to facilitate depressive symptom relief seems a worthy goal. So, here again, we could tell our patients presenting with depression to take two (with an SSRI, perhaps) and call us in the morning. But how best to do this and in what patients remains uncertain.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified, practicing clinician.

At the risk of stating the obvious, our patients are becoming increasingly complex. Life is prolonged and comorbidities accumulate, creating dizzying laundry lists of medical problems.

Within the context of clinical or, increasingly, nonreimbursed telephonic or electronic visits, we attack the medical problem with the worst severity in an attempt to tamp it down to the level of its comorbid brethren.

Almost without exception, depression rears its ugly head in our sickest patients. Antidepressants will be started and added to the three pages (double-spaced, with 1-inch margins) of medications.

But in all of these patients, are we treating the disease or just the symptom? What if inflammation is causing the depression? Will reduction of inflammation treat the depression?

Dr. Ole Köhler of Aarhus University Hospital, Denmark, and his colleagues conducted a systematic review on the antidepressant effects of anti-inflammatory medications (JAMA Psychiatry 2014;71:1381-91). Fourteen trials informed the meta-analysis, 10 that evaluated NSAID drugs (for example, celecoxib, naproxen, ibuprofen), and 4 that investigated cytokine inhibitors (for example, etanercept, infliximab). Six of the 10 NSAID studies evaluated NSAIDs as monotherapy. All four of the cytokine-inhibitor trials evaluated them as monotherapy. Length of treatment was between 6 and 12 weeks.

The pooled effect suggests that anti-inflammatory treatment reduced depressive symptoms. Celecoxib seemed to have the strongest effect on remission and clinical response. No increase in adverse events was reported.

We know that proinflammatory drugs can induce depression. So the opposite is quite possibly true, and these data suggest it to be so. Findings suggest that reducing the inflammatory state among our patients with depression may be a useful adjunct to antidepressant therapy, at least in the initial period.

Whatever we can do to facilitate depressive symptom relief seems a worthy goal. So, here again, we could tell our patients presenting with depression to take two (with an SSRI, perhaps) and call us in the morning. But how best to do this and in what patients remains uncertain.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified, practicing clinician.

At the risk of stating the obvious, our patients are becoming increasingly complex. Life is prolonged and comorbidities accumulate, creating dizzying laundry lists of medical problems.

Within the context of clinical or, increasingly, nonreimbursed telephonic or electronic visits, we attack the medical problem with the worst severity in an attempt to tamp it down to the level of its comorbid brethren.

Almost without exception, depression rears its ugly head in our sickest patients. Antidepressants will be started and added to the three pages (double-spaced, with 1-inch margins) of medications.

But in all of these patients, are we treating the disease or just the symptom? What if inflammation is causing the depression? Will reduction of inflammation treat the depression?

Dr. Ole Köhler of Aarhus University Hospital, Denmark, and his colleagues conducted a systematic review on the antidepressant effects of anti-inflammatory medications (JAMA Psychiatry 2014;71:1381-91). Fourteen trials informed the meta-analysis, 10 that evaluated NSAID drugs (for example, celecoxib, naproxen, ibuprofen), and 4 that investigated cytokine inhibitors (for example, etanercept, infliximab). Six of the 10 NSAID studies evaluated NSAIDs as monotherapy. All four of the cytokine-inhibitor trials evaluated them as monotherapy. Length of treatment was between 6 and 12 weeks.

The pooled effect suggests that anti-inflammatory treatment reduced depressive symptoms. Celecoxib seemed to have the strongest effect on remission and clinical response. No increase in adverse events was reported.

We know that proinflammatory drugs can induce depression. So the opposite is quite possibly true, and these data suggest it to be so. Findings suggest that reducing the inflammatory state among our patients with depression may be a useful adjunct to antidepressant therapy, at least in the initial period.

Whatever we can do to facilitate depressive symptom relief seems a worthy goal. So, here again, we could tell our patients presenting with depression to take two (with an SSRI, perhaps) and call us in the morning. But how best to do this and in what patients remains uncertain.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified, practicing clinician.

In the realm of screening routinely offered to our patients in primary care, colon cancer screening stands with cervical cancer screening with a grade A recommendation from the U.S. Preventive Services Task Force. As such, our systems have been set up to gently remind us of colon cancer screening when it is due. If your practice is like mine, it has been almost exclusively colonoscopy. As such, I hear a lot of patient complaints about the colonoscopy prep.

Recently, one of our patients had uncontrolled vomiting with one of the commonly used polyethylene glycol (PEG) 3350 preparations. Many of us may have been aware of the Miralax and Gatorade (M-G) colon prep, and I considered recommending it to my patient. But is it just as good?

Dr. Sameer Siddique of the University of Missouri, Columbia, and colleagues published a systematic review evaluating the comparability of the M-G prep (238-255 g in 1.9 L) to PEG (3.8-4 L) (Am. J. Gastroenterol. 2014;109:1566-74).

The investigators identified five articles and observed that the M-G prep was associated with significantly fewer satisfactory bowel preparations, compared with PEG (odds ratio, 0.65; 95% confidence interval, 0.43-0.98; P = .04). In a subgroup analysis, split-dose M-G was inferior to split-dose PEG in the number of satisfactory preparations.

Patients, however, had a greater willingness to repeat the preparation (OR, 7.32; 95% CI, 4.88-10.98; P <.01). No significant differences were observed with polyp detection or in side effects such as nausea, cramping, or bloating.

The study authors point out that the dose of Miralax in the M-G prep is not FDA approved (because it is 15 times higher than the dose for constipation), and that the solution is hypotonic and can potentially cause hyponatremia. Furthermore, the cost of a colonoscopy ranges from $600 to more than $5,400. At those prices, patient agreeableness to repeat the test does not mean the health care system can bear a deluge of re-do’s.

Remember that split-dose PEG (one half the day before and one half the day of) has been shown to be superior to the night-before preparation, and it can increase tolerability. If a patient has time to get the job done the day of the colonoscopy, maybe this is the way to go.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

In the realm of screening routinely offered to our patients in primary care, colon cancer screening stands with cervical cancer screening with a grade A recommendation from the U.S. Preventive Services Task Force. As such, our systems have been set up to gently remind us of colon cancer screening when it is due. If your practice is like mine, it has been almost exclusively colonoscopy. As such, I hear a lot of patient complaints about the colonoscopy prep.

Recently, one of our patients had uncontrolled vomiting with one of the commonly used polyethylene glycol (PEG) 3350 preparations. Many of us may have been aware of the Miralax and Gatorade (M-G) colon prep, and I considered recommending it to my patient. But is it just as good?

Dr. Sameer Siddique of the University of Missouri, Columbia, and colleagues published a systematic review evaluating the comparability of the M-G prep (238-255 g in 1.9 L) to PEG (3.8-4 L) (Am. J. Gastroenterol. 2014;109:1566-74).

The investigators identified five articles and observed that the M-G prep was associated with significantly fewer satisfactory bowel preparations, compared with PEG (odds ratio, 0.65; 95% confidence interval, 0.43-0.98; P = .04). In a subgroup analysis, split-dose M-G was inferior to split-dose PEG in the number of satisfactory preparations.

Patients, however, had a greater willingness to repeat the preparation (OR, 7.32; 95% CI, 4.88-10.98; P <.01). No significant differences were observed with polyp detection or in side effects such as nausea, cramping, or bloating.

The study authors point out that the dose of Miralax in the M-G prep is not FDA approved (because it is 15 times higher than the dose for constipation), and that the solution is hypotonic and can potentially cause hyponatremia. Furthermore, the cost of a colonoscopy ranges from $600 to more than $5,400. At those prices, patient agreeableness to repeat the test does not mean the health care system can bear a deluge of re-do’s.

Remember that split-dose PEG (one half the day before and one half the day of) has been shown to be superior to the night-before preparation, and it can increase tolerability. If a patient has time to get the job done the day of the colonoscopy, maybe this is the way to go.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

In the realm of screening routinely offered to our patients in primary care, colon cancer screening stands with cervical cancer screening with a grade A recommendation from the U.S. Preventive Services Task Force. As such, our systems have been set up to gently remind us of colon cancer screening when it is due. If your practice is like mine, it has been almost exclusively colonoscopy. As such, I hear a lot of patient complaints about the colonoscopy prep.

Recently, one of our patients had uncontrolled vomiting with one of the commonly used polyethylene glycol (PEG) 3350 preparations. Many of us may have been aware of the Miralax and Gatorade (M-G) colon prep, and I considered recommending it to my patient. But is it just as good?

Dr. Sameer Siddique of the University of Missouri, Columbia, and colleagues published a systematic review evaluating the comparability of the M-G prep (238-255 g in 1.9 L) to PEG (3.8-4 L) (Am. J. Gastroenterol. 2014;109:1566-74).

The investigators identified five articles and observed that the M-G prep was associated with significantly fewer satisfactory bowel preparations, compared with PEG (odds ratio, 0.65; 95% confidence interval, 0.43-0.98; P = .04). In a subgroup analysis, split-dose M-G was inferior to split-dose PEG in the number of satisfactory preparations.

Patients, however, had a greater willingness to repeat the preparation (OR, 7.32; 95% CI, 4.88-10.98; P <.01). No significant differences were observed with polyp detection or in side effects such as nausea, cramping, or bloating.

The study authors point out that the dose of Miralax in the M-G prep is not FDA approved (because it is 15 times higher than the dose for constipation), and that the solution is hypotonic and can potentially cause hyponatremia. Furthermore, the cost of a colonoscopy ranges from $600 to more than $5,400. At those prices, patient agreeableness to repeat the test does not mean the health care system can bear a deluge of re-do’s.

Remember that split-dose PEG (one half the day before and one half the day of) has been shown to be superior to the night-before preparation, and it can increase tolerability. If a patient has time to get the job done the day of the colonoscopy, maybe this is the way to go.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

Alcohol is a drug, the abuse of which is the third leading cause of preventable death and disability in the United States. Most clinicians intuitively appreciate that 80% of drinkers consume only 20% of all the alcohol consumed in the United States. In other words, most problem drinkers consume most of the alcohol and most drinkers are not problem drinkers. Perhaps as a result, clinicians may recommend the consumption of alcohol in moderation for its putative health promoting effects (e.g., reduction in cardiovascular events and increases in HDL), hoping that patients can benefit without being put at risk.

I am personally guilty of such allowances among patients who already consume modestly. With all the potential negative consequences of alcohol use, it might not have taken much for me to change my clinical advice-giving.

Knott and colleagues conducted a population based study from the Health Survey for England encompassing the years 1998-2008 linked to national mortality data. The investigators observed that compared with never drinkers, protective effects of alcohol were limited to younger men (aged 50-64 years) and older women (≥ 65 years).

What this study adds to the literature is a cleaner comparison between alcohol consumers and never drinkers and adjustments for additional confounders. Many of the previous studies showing alcohol’s beneficial effects have included former drinkers in the nondrinker comparison group; however, former drinkers have a higher mortality risk than do never drinkers because they tend to be unhealthier than never drinkers. Compared to a healthier population of never drinkers, alcohol’s effects attenuate. The use of additional adjustment variables not used in previous studies also attenuated the effect of alcohol.

As patients age, their ability to metabolize and eliminate alcohol changes. Such alterations can lead to increased adverse health consequences and accidents. If the benefit of alcohol is not as great as we previously thought, maybe the time has come to change our advice on alcohol.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

Alcohol is a drug, the abuse of which is the third leading cause of preventable death and disability in the United States. Most clinicians intuitively appreciate that 80% of drinkers consume only 20% of all the alcohol consumed in the United States. In other words, most problem drinkers consume most of the alcohol and most drinkers are not problem drinkers. Perhaps as a result, clinicians may recommend the consumption of alcohol in moderation for its putative health promoting effects (e.g., reduction in cardiovascular events and increases in HDL), hoping that patients can benefit without being put at risk.

I am personally guilty of such allowances among patients who already consume modestly. With all the potential negative consequences of alcohol use, it might not have taken much for me to change my clinical advice-giving.

Knott and colleagues conducted a population based study from the Health Survey for England encompassing the years 1998-2008 linked to national mortality data. The investigators observed that compared with never drinkers, protective effects of alcohol were limited to younger men (aged 50-64 years) and older women (≥ 65 years).

What this study adds to the literature is a cleaner comparison between alcohol consumers and never drinkers and adjustments for additional confounders. Many of the previous studies showing alcohol’s beneficial effects have included former drinkers in the nondrinker comparison group; however, former drinkers have a higher mortality risk than do never drinkers because they tend to be unhealthier than never drinkers. Compared to a healthier population of never drinkers, alcohol’s effects attenuate. The use of additional adjustment variables not used in previous studies also attenuated the effect of alcohol.

As patients age, their ability to metabolize and eliminate alcohol changes. Such alterations can lead to increased adverse health consequences and accidents. If the benefit of alcohol is not as great as we previously thought, maybe the time has come to change our advice on alcohol.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

Alcohol is a drug, the abuse of which is the third leading cause of preventable death and disability in the United States. Most clinicians intuitively appreciate that 80% of drinkers consume only 20% of all the alcohol consumed in the United States. In other words, most problem drinkers consume most of the alcohol and most drinkers are not problem drinkers. Perhaps as a result, clinicians may recommend the consumption of alcohol in moderation for its putative health promoting effects (e.g., reduction in cardiovascular events and increases in HDL), hoping that patients can benefit without being put at risk.

I am personally guilty of such allowances among patients who already consume modestly. With all the potential negative consequences of alcohol use, it might not have taken much for me to change my clinical advice-giving.

Knott and colleagues conducted a population based study from the Health Survey for England encompassing the years 1998-2008 linked to national mortality data. The investigators observed that compared with never drinkers, protective effects of alcohol were limited to younger men (aged 50-64 years) and older women (≥ 65 years).

What this study adds to the literature is a cleaner comparison between alcohol consumers and never drinkers and adjustments for additional confounders. Many of the previous studies showing alcohol’s beneficial effects have included former drinkers in the nondrinker comparison group; however, former drinkers have a higher mortality risk than do never drinkers because they tend to be unhealthier than never drinkers. Compared to a healthier population of never drinkers, alcohol’s effects attenuate. The use of additional adjustment variables not used in previous studies also attenuated the effect of alcohol.

As patients age, their ability to metabolize and eliminate alcohol changes. Such alterations can lead to increased adverse health consequences and accidents. If the benefit of alcohol is not as great as we previously thought, maybe the time has come to change our advice on alcohol.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

One out of every 10 adults in the United States has diabetes, and the percentage of Americans aged 65 years or older who have diabetes continues to increase. The treatment of diabetes consumes an enormous amount of health care and personal resources. This would palatable if such expenditures did nothing but improve outcomes and reduce morbidity and mortality.

But they don’t.

Compared with young healthy patients with diabetes, older patients with diabetes and complex medical conditions may derive little benefit from intensive management but may incur harm. Hypoglycemia is associated with significant medical costs and adverse health consequences among older patients. Hypoglycemic agents (oral and injectable) are implicated in one-fourth of emergency hospitalizations for adverse drugs events in this population.

Dr. Kasia J. Lipska of Yale University, New Haven, Conn., and her colleagues evaluated the potential overtreatment of diabetes in older patients (at least 65 years) by examining participants in the National Health and Nutrition Examination Survey from 2001 through 2010 who had an HbA_1c measurement. Participants were grouped into different health status categories using available data: very complex/poor, complex/intermediate, and relatively healthy (JAMA Intern. Med. 2015 [doi:10.1001/jamainternmed.2014.7345]).

The investigators found that almost two-thirds of this population had an HbA_1c less than 7% (i.e., tight control), which did not differ across health status categories. Of the adults with an HbA_1c less than 7%, more than one-half were treated with insulin or sulfonylureas, and this was similar across health status categories. During the 10 study years, no changes were observed in the proportion with an HbA_1c less than 7% or the proportion of patients with an HbA_1c less than 7% who were treated with insulin or a sulfonylurea.

These data tell us we are not racheting our care back when patients reach an age when aggressive care does more harm than good. We may feel hamstrung by quality metrics, a limited ability to manage large populations using health management approach, algorithmic approaches to facilitate appropriate de-escalations in medication management, and lack of time to engage in these discussions with our patients. What we tend to do is decrease these medications after patients have an office or emergency department visit for a hypoglycemic event or complication.

Moving forward, we need to embrace more liberal HbA_1c goals for our patients at least 65 years of age. Most important, yet most challenging, we need to have ongoing goals of care discussions with our patients, and comorbidities need to be considered when setting such goals. Decision aids would be helpful tools in this space.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

One out of every 10 adults in the United States has diabetes, and the percentage of Americans aged 65 years or older who have diabetes continues to increase. The treatment of diabetes consumes an enormous amount of health care and personal resources. This would palatable if such expenditures did nothing but improve outcomes and reduce morbidity and mortality.

But they don’t.

Compared with young healthy patients with diabetes, older patients with diabetes and complex medical conditions may derive little benefit from intensive management but may incur harm. Hypoglycemia is associated with significant medical costs and adverse health consequences among older patients. Hypoglycemic agents (oral and injectable) are implicated in one-fourth of emergency hospitalizations for adverse drugs events in this population.

Dr. Kasia J. Lipska of Yale University, New Haven, Conn., and her colleagues evaluated the potential overtreatment of diabetes in older patients (at least 65 years) by examining participants in the National Health and Nutrition Examination Survey from 2001 through 2010 who had an HbA_1c measurement. Participants were grouped into different health status categories using available data: very complex/poor, complex/intermediate, and relatively healthy (JAMA Intern. Med. 2015 [doi:10.1001/jamainternmed.2014.7345]).

The investigators found that almost two-thirds of this population had an HbA_1c less than 7% (i.e., tight control), which did not differ across health status categories. Of the adults with an HbA_1c less than 7%, more than one-half were treated with insulin or sulfonylureas, and this was similar across health status categories. During the 10 study years, no changes were observed in the proportion with an HbA_1c less than 7% or the proportion of patients with an HbA_1c less than 7% who were treated with insulin or a sulfonylurea.

These data tell us we are not racheting our care back when patients reach an age when aggressive care does more harm than good. We may feel hamstrung by quality metrics, a limited ability to manage large populations using health management approach, algorithmic approaches to facilitate appropriate de-escalations in medication management, and lack of time to engage in these discussions with our patients. What we tend to do is decrease these medications after patients have an office or emergency department visit for a hypoglycemic event or complication.

Moving forward, we need to embrace more liberal HbA_1c goals for our patients at least 65 years of age. Most important, yet most challenging, we need to have ongoing goals of care discussions with our patients, and comorbidities need to be considered when setting such goals. Decision aids would be helpful tools in this space.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

One out of every 10 adults in the United States has diabetes, and the percentage of Americans aged 65 years or older who have diabetes continues to increase. The treatment of diabetes consumes an enormous amount of health care and personal resources. This would palatable if such expenditures did nothing but improve outcomes and reduce morbidity and mortality.

But they don’t.

Compared with young healthy patients with diabetes, older patients with diabetes and complex medical conditions may derive little benefit from intensive management but may incur harm. Hypoglycemia is associated with significant medical costs and adverse health consequences among older patients. Hypoglycemic agents (oral and injectable) are implicated in one-fourth of emergency hospitalizations for adverse drugs events in this population.

Dr. Kasia J. Lipska of Yale University, New Haven, Conn., and her colleagues evaluated the potential overtreatment of diabetes in older patients (at least 65 years) by examining participants in the National Health and Nutrition Examination Survey from 2001 through 2010 who had an HbA_1c measurement. Participants were grouped into different health status categories using available data: very complex/poor, complex/intermediate, and relatively healthy (JAMA Intern. Med. 2015 [doi:10.1001/jamainternmed.2014.7345]).

The investigators found that almost two-thirds of this population had an HbA_1c less than 7% (i.e., tight control), which did not differ across health status categories. Of the adults with an HbA_1c less than 7%, more than one-half were treated with insulin or sulfonylureas, and this was similar across health status categories. During the 10 study years, no changes were observed in the proportion with an HbA_1c less than 7% or the proportion of patients with an HbA_1c less than 7% who were treated with insulin or a sulfonylurea.

These data tell us we are not racheting our care back when patients reach an age when aggressive care does more harm than good. We may feel hamstrung by quality metrics, a limited ability to manage large populations using health management approach, algorithmic approaches to facilitate appropriate de-escalations in medication management, and lack of time to engage in these discussions with our patients. What we tend to do is decrease these medications after patients have an office or emergency department visit for a hypoglycemic event or complication.

Moving forward, we need to embrace more liberal HbA_1c goals for our patients at least 65 years of age. Most important, yet most challenging, we need to have ongoing goals of care discussions with our patients, and comorbidities need to be considered when setting such goals. Decision aids would be helpful tools in this space.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

Like many groups, our practice shares backup call on a rotational basis. This week-long pleasure cruise is characterized by phone calls throughout the night (“Why are we checking a temperature on a comfortably sleeping 85-year-old at 2 a.m. again?”), dubious requests (“I am still unclear why you were cleaning out your medicine cabinet at 4 a.m. Even so, I cannot refill the oxycodone you just flushed down the toilet.”), and fragmented sleep associated with clinically significant carbohydrate cravings.

In the old days, this indispensable community service could be handled without the need for remoting into the practice. But most calls these days require that our computers be close at hand. As such, we find ourselves in the wee hours of morning staring at computer screens that, we are increasingly aware, emit melatonin-killing blue wavelengths of light. This makes it that much harder to go back to sleep after triaging colonoscopy-preps-gone-wrong calls.

Several months ago, one of my patients gave me orange-tinted, blue light–blocking (BB) glasses as a gift. These glasses are designed to filter out the blue wavelength (480 nm), which most strongly impacts alertness, cognitive performance, and circadian physiology.

They have collected dust on my desk. … until last week while on call.

In a recently published study, Stéphanie van der Lely of the University of Basel, Switzerland, and colleagues evaluated the impact of blue-blocker glasses as a countermeasure to evening computer screen time among adolescents (J. Adolesc. Health 2015;56:113-9). Thirteen adolescents with a mean age of 16 years participated in this crossover study over 16 days. Blue blockers were provided from 6 p.m. to sleep onset. Glasses reduced the blue light transmission to 30%.

Compared with clear lenses, BB significantly attenuated LED-induced melatonin suppression in the evening. BB glasses also decreased vigilant attention and subjective alertness before bedtime.

This article would suggest that my melatonin is not being suppressed while I wear the glasses as I do my evening article writing and answer phone calls. The color shifts take some getting used to, but the glasses are comfortable. In addition to sleeping in the attic, my backup call routine will include these glasses.

Now, if we can just find something to filter out midnight acetaminophen requests. At least I’ll fall back asleep quickly after telling them to take two and call me in the morning.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

Like many groups, our practice shares backup call on a rotational basis. This week-long pleasure cruise is characterized by phone calls throughout the night (“Why are we checking a temperature on a comfortably sleeping 85-year-old at 2 a.m. again?”), dubious requests (“I am still unclear why you were cleaning out your medicine cabinet at 4 a.m. Even so, I cannot refill the oxycodone you just flushed down the toilet.”), and fragmented sleep associated with clinically significant carbohydrate cravings.

In the old days, this indispensable community service could be handled without the need for remoting into the practice. But most calls these days require that our computers be close at hand. As such, we find ourselves in the wee hours of morning staring at computer screens that, we are increasingly aware, emit melatonin-killing blue wavelengths of light. This makes it that much harder to go back to sleep after triaging colonoscopy-preps-gone-wrong calls.

Several months ago, one of my patients gave me orange-tinted, blue light–blocking (BB) glasses as a gift. These glasses are designed to filter out the blue wavelength (480 nm), which most strongly impacts alertness, cognitive performance, and circadian physiology.

They have collected dust on my desk. … until last week while on call.

In a recently published study, Stéphanie van der Lely of the University of Basel, Switzerland, and colleagues evaluated the impact of blue-blocker glasses as a countermeasure to evening computer screen time among adolescents (J. Adolesc. Health 2015;56:113-9). Thirteen adolescents with a mean age of 16 years participated in this crossover study over 16 days. Blue blockers were provided from 6 p.m. to sleep onset. Glasses reduced the blue light transmission to 30%.

Compared with clear lenses, BB significantly attenuated LED-induced melatonin suppression in the evening. BB glasses also decreased vigilant attention and subjective alertness before bedtime.

This article would suggest that my melatonin is not being suppressed while I wear the glasses as I do my evening article writing and answer phone calls. The color shifts take some getting used to, but the glasses are comfortable. In addition to sleeping in the attic, my backup call routine will include these glasses.

Now, if we can just find something to filter out midnight acetaminophen requests. At least I’ll fall back asleep quickly after telling them to take two and call me in the morning.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

Like many groups, our practice shares backup call on a rotational basis. This week-long pleasure cruise is characterized by phone calls throughout the night (“Why are we checking a temperature on a comfortably sleeping 85-year-old at 2 a.m. again?”), dubious requests (“I am still unclear why you were cleaning out your medicine cabinet at 4 a.m. Even so, I cannot refill the oxycodone you just flushed down the toilet.”), and fragmented sleep associated with clinically significant carbohydrate cravings.

In the old days, this indispensable community service could be handled without the need for remoting into the practice. But most calls these days require that our computers be close at hand. As such, we find ourselves in the wee hours of morning staring at computer screens that, we are increasingly aware, emit melatonin-killing blue wavelengths of light. This makes it that much harder to go back to sleep after triaging colonoscopy-preps-gone-wrong calls.

Several months ago, one of my patients gave me orange-tinted, blue light–blocking (BB) glasses as a gift. These glasses are designed to filter out the blue wavelength (480 nm), which most strongly impacts alertness, cognitive performance, and circadian physiology.

They have collected dust on my desk. … until last week while on call.

In a recently published study, Stéphanie van der Lely of the University of Basel, Switzerland, and colleagues evaluated the impact of blue-blocker glasses as a countermeasure to evening computer screen time among adolescents (J. Adolesc. Health 2015;56:113-9). Thirteen adolescents with a mean age of 16 years participated in this crossover study over 16 days. Blue blockers were provided from 6 p.m. to sleep onset. Glasses reduced the blue light transmission to 30%.

Compared with clear lenses, BB significantly attenuated LED-induced melatonin suppression in the evening. BB glasses also decreased vigilant attention and subjective alertness before bedtime.

This article would suggest that my melatonin is not being suppressed while I wear the glasses as I do my evening article writing and answer phone calls. The color shifts take some getting used to, but the glasses are comfortable. In addition to sleeping in the attic, my backup call routine will include these glasses.

Now, if we can just find something to filter out midnight acetaminophen requests. At least I’ll fall back asleep quickly after telling them to take two and call me in the morning.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

Seems that none of my patients sleeps, or at least not very well. Indeed, population-based studies suggest that almost one-third of adults report difficulty initiating or maintaining sleep, waking up too early, and/or nonrestorative or poor quality of sleep.

Light-emitting electronic “e-readers” or “e-books” have exploded as a favorite medium for reading. Many of my patients tell me that when they are unable to sleep, they read. Much of this reading occurs on e-books. But artificial light can produce alerting effects and suppress melatonin. This might be causing or worsening the national insomnia epidemic.

Dr. Anne-Marie Chang and colleagues conducted a randomized, crossover study evaluating the impact of an e-book and a traditional book on sleep (PNAS 2014 Dec. 22 [doi:10.1073/pnas.1418490112]). In the study, 12 healthy young adults were randomized to two conditions: 1) reading an e-book for 4 hours before bedtime; or 2) reading a printed book for 4 hours before bedtime on 5 consecutive evenings. Participants then switched conditions.

The e-book suppressed evening levels of melatonin by 55%, whereas the printed book showed no suppression, and the e-book shifted the melatonin onset to more than 1.5 hours later. Compared with the printed book, the e-book also significantly increased sleep latency (10 minutes longer), decreased REM sleep by11 minutes, decreased evening sleepiness, and increased morning sleepiness.

But not all e-book readers are created equal. Screens of devices used in the current study emit blue light (wavelength 452 nm), the type of light most implicated in melatonin suppression. Newer “e-ink” readers do not emit this light and are “front lit,” with light cast inward rather than outward.

People struggling with insomnia should be encouraged to explore the e-ink options. The table included in the study can provide some guidance as to the type of e-book that may be most beneficial to our sleepy patients.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

Seems that none of my patients sleeps, or at least not very well. Indeed, population-based studies suggest that almost one-third of adults report difficulty initiating or maintaining sleep, waking up too early, and/or nonrestorative or poor quality of sleep.

Light-emitting electronic “e-readers” or “e-books” have exploded as a favorite medium for reading. Many of my patients tell me that when they are unable to sleep, they read. Much of this reading occurs on e-books. But artificial light can produce alerting effects and suppress melatonin. This might be causing or worsening the national insomnia epidemic.

Dr. Anne-Marie Chang and colleagues conducted a randomized, crossover study evaluating the impact of an e-book and a traditional book on sleep (PNAS 2014 Dec. 22 [doi:10.1073/pnas.1418490112]). In the study, 12 healthy young adults were randomized to two conditions: 1) reading an e-book for 4 hours before bedtime; or 2) reading a printed book for 4 hours before bedtime on 5 consecutive evenings. Participants then switched conditions.

The e-book suppressed evening levels of melatonin by 55%, whereas the printed book showed no suppression, and the e-book shifted the melatonin onset to more than 1.5 hours later. Compared with the printed book, the e-book also significantly increased sleep latency (10 minutes longer), decreased REM sleep by11 minutes, decreased evening sleepiness, and increased morning sleepiness.

But not all e-book readers are created equal. Screens of devices used in the current study emit blue light (wavelength 452 nm), the type of light most implicated in melatonin suppression. Newer “e-ink” readers do not emit this light and are “front lit,” with light cast inward rather than outward.

People struggling with insomnia should be encouraged to explore the e-ink options. The table included in the study can provide some guidance as to the type of e-book that may be most beneficial to our sleepy patients.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

Seems that none of my patients sleeps, or at least not very well. Indeed, population-based studies suggest that almost one-third of adults report difficulty initiating or maintaining sleep, waking up too early, and/or nonrestorative or poor quality of sleep.

Light-emitting electronic “e-readers” or “e-books” have exploded as a favorite medium for reading. Many of my patients tell me that when they are unable to sleep, they read. Much of this reading occurs on e-books. But artificial light can produce alerting effects and suppress melatonin. This might be causing or worsening the national insomnia epidemic.

Dr. Anne-Marie Chang and colleagues conducted a randomized, crossover study evaluating the impact of an e-book and a traditional book on sleep (PNAS 2014 Dec. 22 [doi:10.1073/pnas.1418490112]). In the study, 12 healthy young adults were randomized to two conditions: 1) reading an e-book for 4 hours before bedtime; or 2) reading a printed book for 4 hours before bedtime on 5 consecutive evenings. Participants then switched conditions.

The e-book suppressed evening levels of melatonin by 55%, whereas the printed book showed no suppression, and the e-book shifted the melatonin onset to more than 1.5 hours later. Compared with the printed book, the e-book also significantly increased sleep latency (10 minutes longer), decreased REM sleep by11 minutes, decreased evening sleepiness, and increased morning sleepiness.

But not all e-book readers are created equal. Screens of devices used in the current study emit blue light (wavelength 452 nm), the type of light most implicated in melatonin suppression. Newer “e-ink” readers do not emit this light and are “front lit,” with light cast inward rather than outward.

People struggling with insomnia should be encouraged to explore the e-ink options. The table included in the study can provide some guidance as to the type of e-book that may be most beneficial to our sleepy patients.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

While typing this column, I could not recall the last time I saw a patient with “tennis elbow” (lateral epicondylitis) from actual tennis. Lateral epicondylitis peaks between the ages of 30 and 65 years and affects about 1.3% of this group – the vast majority of whom, I am quite suddenly convinced, do not play tennis. Pain is worse with wrist extension and typically affects the dominant hand. The most likely etiology is repeated microtrauma.

The examination is straightforward and about 90% will recover by 1 year without a surgical procedure. The unhappy customers who darken our doorways with worsening or nonimproving symptoms are the ones who make us wonder if we gave them effective conservative measures to begin with.

So what conservative measures are effective?

Sims and colleagues published a meta-analysis evaluating nonsurgical treatments for lateral epicondylitis. The review involved 58 studies (Hand 2014.9:419-46).

The investigators concluded that steroid injections provide relief only for the short term. The authors suggest that this may related to lateral epicondylitis being caused by repeated microtrauma rather than inflammation (perhaps this is why NSAIDs are not always beneficial either). Botulinum A, which works by paralyzing the extensor muscles, thereby allowing them to heal, is comparable to steroids. But patients may not love the experience of extensor muscle paralysis. Prolotherapy, injection of osmotics or irritants to promote inflammation in the target tissue, is also comparable to steroids. Platelet-rich plasma or autologous blood injections have uncertain relative benefit compared to steroids. Bracing with a counterforce brace (i.e., “tennis elbow strap”) or wrist extension splint, physical therapy, and shock wave therapy do not lessen pain or improve function in a dependable way.

This review leaves primary care clinicians who are uncomfortable injecting steroids into the arm with not much in the way of clearly effective evidence-based therapies. Personally, I ask my Ortho Hand colleagues to help me with the injection part. But only when patients fail to respond to what I give them.

So if this is a self-limited disease that gets better in 12-18 months, should we just be offering nothing more than activity modification? Patients will not accept this. My read on the data Sims collected is that there weren’t any quality studies comparing the elbow strap to offering nothing and patients tended to improve with it – although admittedly not clearly more than other therapies such as strengthening exercises. So for now, I will continue to recommend: 1) the elbow strap; 2) home exercises, and 3) lots and lots of reassurance. It’s all I got to give.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

While typing this column, I could not recall the last time I saw a patient with “tennis elbow” (lateral epicondylitis) from actual tennis. Lateral epicondylitis peaks between the ages of 30 and 65 years and affects about 1.3% of this group – the vast majority of whom, I am quite suddenly convinced, do not play tennis. Pain is worse with wrist extension and typically affects the dominant hand. The most likely etiology is repeated microtrauma.

The examination is straightforward and about 90% will recover by 1 year without a surgical procedure. The unhappy customers who darken our doorways with worsening or nonimproving symptoms are the ones who make us wonder if we gave them effective conservative measures to begin with.

So what conservative measures are effective?

Sims and colleagues published a meta-analysis evaluating nonsurgical treatments for lateral epicondylitis. The review involved 58 studies (Hand 2014.9:419-46).

The investigators concluded that steroid injections provide relief only for the short term. The authors suggest that this may related to lateral epicondylitis being caused by repeated microtrauma rather than inflammation (perhaps this is why NSAIDs are not always beneficial either). Botulinum A, which works by paralyzing the extensor muscles, thereby allowing them to heal, is comparable to steroids. But patients may not love the experience of extensor muscle paralysis. Prolotherapy, injection of osmotics or irritants to promote inflammation in the target tissue, is also comparable to steroids. Platelet-rich plasma or autologous blood injections have uncertain relative benefit compared to steroids. Bracing with a counterforce brace (i.e., “tennis elbow strap”) or wrist extension splint, physical therapy, and shock wave therapy do not lessen pain or improve function in a dependable way.

This review leaves primary care clinicians who are uncomfortable injecting steroids into the arm with not much in the way of clearly effective evidence-based therapies. Personally, I ask my Ortho Hand colleagues to help me with the injection part. But only when patients fail to respond to what I give them.

So if this is a self-limited disease that gets better in 12-18 months, should we just be offering nothing more than activity modification? Patients will not accept this. My read on the data Sims collected is that there weren’t any quality studies comparing the elbow strap to offering nothing and patients tended to improve with it – although admittedly not clearly more than other therapies such as strengthening exercises. So for now, I will continue to recommend: 1) the elbow strap; 2) home exercises, and 3) lots and lots of reassurance. It’s all I got to give.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

While typing this column, I could not recall the last time I saw a patient with “tennis elbow” (lateral epicondylitis) from actual tennis. Lateral epicondylitis peaks between the ages of 30 and 65 years and affects about 1.3% of this group – the vast majority of whom, I am quite suddenly convinced, do not play tennis. Pain is worse with wrist extension and typically affects the dominant hand. The most likely etiology is repeated microtrauma.

The examination is straightforward and about 90% will recover by 1 year without a surgical procedure. The unhappy customers who darken our doorways with worsening or nonimproving symptoms are the ones who make us wonder if we gave them effective conservative measures to begin with.

So what conservative measures are effective?

Sims and colleagues published a meta-analysis evaluating nonsurgical treatments for lateral epicondylitis. The review involved 58 studies (Hand 2014.9:419-46).

The investigators concluded that steroid injections provide relief only for the short term. The authors suggest that this may related to lateral epicondylitis being caused by repeated microtrauma rather than inflammation (perhaps this is why NSAIDs are not always beneficial either). Botulinum A, which works by paralyzing the extensor muscles, thereby allowing them to heal, is comparable to steroids. But patients may not love the experience of extensor muscle paralysis. Prolotherapy, injection of osmotics or irritants to promote inflammation in the target tissue, is also comparable to steroids. Platelet-rich plasma or autologous blood injections have uncertain relative benefit compared to steroids. Bracing with a counterforce brace (i.e., “tennis elbow strap”) or wrist extension splint, physical therapy, and shock wave therapy do not lessen pain or improve function in a dependable way.

This review leaves primary care clinicians who are uncomfortable injecting steroids into the arm with not much in the way of clearly effective evidence-based therapies. Personally, I ask my Ortho Hand colleagues to help me with the injection part. But only when patients fail to respond to what I give them.

So if this is a self-limited disease that gets better in 12-18 months, should we just be offering nothing more than activity modification? Patients will not accept this. My read on the data Sims collected is that there weren’t any quality studies comparing the elbow strap to offering nothing and patients tended to improve with it – although admittedly not clearly more than other therapies such as strengthening exercises. So for now, I will continue to recommend: 1) the elbow strap; 2) home exercises, and 3) lots and lots of reassurance. It’s all I got to give.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

Most of my counseling to patients about lowering blood pressure through self management is heavy on weight loss and light on dietary causes of high blood pressure – other than the obvious ones that make people gain weight.

Denial of the effects of dietary salt on blood pressure is not the issue. Rather, it is a time-hewn lack of confidence in the ability of patients to significantly and consistently modify their diet. Part of this may also relate to our inability to provide useful lifestyle tips on how to do so, other than the obvious referral to a dietitian. Telling them not to eat out does not solve this problem, because they can just as easily add salt at home.

However, a recent meta-analysis evaluating the effect of salt substitutes on blood pressure has reinvigorated my desire to counsel my patients on blood pressure self-management.

In this study, the investigators sought randomized, controlled trials with interventions lasting at least 6 months in duration (Am. J. Clin. Nutr. 2014;100:1448-54). Six cohorts were identified in the literature involving a total of 1,974 participants. Included studies took place in China and the Netherlands. Three studies used 65% NaCl/25% KCl/10% MgSO₂, one used 41% NaCl/41% KCl/17% magnesium salt/trace minerals, and one used 65% NaCl/30% KCl/5% calcium salt and folic acid.

Salt substitutes had significant effects on systolic blood pressure with a mean difference of –4.9 mm Hg and on diastolic blood pressure with a mean difference of –1.5 mm Hg.

Overall, one may not be impressed with a 5–mm Hg change in systolic blood pressure. But this is the mean difference – and we presume population heterogeneity in response to salt substitution, such that some patients will respond to a higher degree than this and some to a lower degree. But we do not know which ones are which.

Population interventions aimed at reducing salt intake have been shown to be effective. The Finnish government, for example, collaborated with private industry and was able to achieve reductions in sodium content of food. That initiative resulted in a 33% reduction in the population’s average salt intake, a greater than 10–mm Hg decrease in the population average of both systolic BP and diastolic BP, and a 75%-80% decrease in both stroke and coronary artery disease mortality. Australia, Japan, and the United Kingdom were able to do similar things.

Because we are unlikely to ever see such organized political will exercised in the United States, it seems reasonable to recommend salt substitutes to our patients on an individual level. Adverse effects have been noted with salt substitutes in patients with kidney disease, however, which will have to be considered in that specific population of patients.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

Most of my counseling to patients about lowering blood pressure through self management is heavy on weight loss and light on dietary causes of high blood pressure – other than the obvious ones that make people gain weight.

Denial of the effects of dietary salt on blood pressure is not the issue. Rather, it is a time-hewn lack of confidence in the ability of patients to significantly and consistently modify their diet. Part of this may also relate to our inability to provide useful lifestyle tips on how to do so, other than the obvious referral to a dietitian. Telling them not to eat out does not solve this problem, because they can just as easily add salt at home.

However, a recent meta-analysis evaluating the effect of salt substitutes on blood pressure has reinvigorated my desire to counsel my patients on blood pressure self-management.

In this study, the investigators sought randomized, controlled trials with interventions lasting at least 6 months in duration (Am. J. Clin. Nutr. 2014;100:1448-54). Six cohorts were identified in the literature involving a total of 1,974 participants. Included studies took place in China and the Netherlands. Three studies used 65% NaCl/25% KCl/10% MgSO₂, one used 41% NaCl/41% KCl/17% magnesium salt/trace minerals, and one used 65% NaCl/30% KCl/5% calcium salt and folic acid.

Salt substitutes had significant effects on systolic blood pressure with a mean difference of –4.9 mm Hg and on diastolic blood pressure with a mean difference of –1.5 mm Hg.

Overall, one may not be impressed with a 5–mm Hg change in systolic blood pressure. But this is the mean difference – and we presume population heterogeneity in response to salt substitution, such that some patients will respond to a higher degree than this and some to a lower degree. But we do not know which ones are which.

Population interventions aimed at reducing salt intake have been shown to be effective. The Finnish government, for example, collaborated with private industry and was able to achieve reductions in sodium content of food. That initiative resulted in a 33% reduction in the population’s average salt intake, a greater than 10–mm Hg decrease in the population average of both systolic BP and diastolic BP, and a 75%-80% decrease in both stroke and coronary artery disease mortality. Australia, Japan, and the United Kingdom were able to do similar things.

Because we are unlikely to ever see such organized political will exercised in the United States, it seems reasonable to recommend salt substitutes to our patients on an individual level. Adverse effects have been noted with salt substitutes in patients with kidney disease, however, which will have to be considered in that specific population of patients.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

Most of my counseling to patients about lowering blood pressure through self management is heavy on weight loss and light on dietary causes of high blood pressure – other than the obvious ones that make people gain weight.

Denial of the effects of dietary salt on blood pressure is not the issue. Rather, it is a time-hewn lack of confidence in the ability of patients to significantly and consistently modify their diet. Part of this may also relate to our inability to provide useful lifestyle tips on how to do so, other than the obvious referral to a dietitian. Telling them not to eat out does not solve this problem, because they can just as easily add salt at home.

However, a recent meta-analysis evaluating the effect of salt substitutes on blood pressure has reinvigorated my desire to counsel my patients on blood pressure self-management.

In this study, the investigators sought randomized, controlled trials with interventions lasting at least 6 months in duration (Am. J. Clin. Nutr. 2014;100:1448-54). Six cohorts were identified in the literature involving a total of 1,974 participants. Included studies took place in China and the Netherlands. Three studies used 65% NaCl/25% KCl/10% MgSO₂, one used 41% NaCl/41% KCl/17% magnesium salt/trace minerals, and one used 65% NaCl/30% KCl/5% calcium salt and folic acid.

Salt substitutes had significant effects on systolic blood pressure with a mean difference of –4.9 mm Hg and on diastolic blood pressure with a mean difference of –1.5 mm Hg.

Overall, one may not be impressed with a 5–mm Hg change in systolic blood pressure. But this is the mean difference – and we presume population heterogeneity in response to salt substitution, such that some patients will respond to a higher degree than this and some to a lower degree. But we do not know which ones are which.

Population interventions aimed at reducing salt intake have been shown to be effective. The Finnish government, for example, collaborated with private industry and was able to achieve reductions in sodium content of food. That initiative resulted in a 33% reduction in the population’s average salt intake, a greater than 10–mm Hg decrease in the population average of both systolic BP and diastolic BP, and a 75%-80% decrease in both stroke and coronary artery disease mortality. Australia, Japan, and the United Kingdom were able to do similar things.

Because we are unlikely to ever see such organized political will exercised in the United States, it seems reasonable to recommend salt substitutes to our patients on an individual level. Adverse effects have been noted with salt substitutes in patients with kidney disease, however, which will have to be considered in that specific population of patients.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.