What Matters

We are a product of our environment. But we shan’t forget that we are a product of the critical interaction between our environment and our evolutionary biology.

Back when we were roaming the plains searching for food, we likely experienced “forced fasts” (that is, we had no food). Our ancestors who were the best at surviving these periods of scarcity lived to bear us into our current period of staggering abundance. Now, we are the unhealthiest humans in history.

Is part of the answer to our current health problems to return to our roots and ... fast?

In a recent article by Catherine Marinac and her colleagues, patients aged 27-70 years with breast cancer in the Women’s Healthy Eating and Living study were analyzed to uncover the relationship between nightly fasting duration and new primary breast tumors and death (JAMA Oncol. 2016 Mar 31. doi: 10.1001/jamaoncol.2016.0164). Fasting was assessed through use of 24-hour dietary recall.

Fasting less than 13 hours per night was associated with an increased risk of breast cancer, compared with fasting at least 13 hours (hazard ratio, 1.36; 95% confidence interval, 1.05-1.76). Different fasting durations were not associated with breast cancer mortality.

Additional analyses demonstrated that each 2-hour increase in fasting duration was associated with significantly lower hemoglobin A_1c levels and a longer duration of nighttime sleep.

The positive health benefits of fasting have become increasingly “discussed,” albeit commonly on websites advertising for fasting cookbooks. Benefits of fasting include weight loss, improved insulin sensitivity, reductions in inflammation, improved cardiovascular risk factors, enhanced brain function, reductions in Alzheimer’s disease symptoms, and extended life span.

Many of these data are preliminary, and some are based upon animal models, such as the prolonged lifespan. In one study, rats undergoing alternate-day fasting lived 83% longer than rats who were not fasted. Interestingly, human data suggest that food consumption on the nonfasting days does not result in caloric consumption to cover the caloric deficit on the fasted day.

I have to admit that I am intrigued. I am not hearing much discussion about fasting among my colleagues – although a lot them skip meals, I know. But nobody is discussing it as a recommendation to appropriately selected patients (for example, not on insulin) to combat obesity and other diseases. I tried to suggest it to a patient the other day, who had a staggering amount of central adiposity, and he laughed at me. Is the thought of skipping eating for a day so anathema to our modern consumptive culture that we can’t even consider it?

Depending on the type of fasting that one is doing, one does not have to count calories on the fasting days, because there aren’t any. That makes it easy.

In a world of abundance and limitless food options, it may seem strange (self-indulgent?) to fast. But perhaps it will be a key to help us continue the species for a couple more generations.

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 financial disclosures about this article.

We are a product of our environment. But we shan’t forget that we are a product of the critical interaction between our environment and our evolutionary biology.

Back when we were roaming the plains searching for food, we likely experienced “forced fasts” (that is, we had no food). Our ancestors who were the best at surviving these periods of scarcity lived to bear us into our current period of staggering abundance. Now, we are the unhealthiest humans in history.

Is part of the answer to our current health problems to return to our roots and ... fast?

In a recent article by Catherine Marinac and her colleagues, patients aged 27-70 years with breast cancer in the Women’s Healthy Eating and Living study were analyzed to uncover the relationship between nightly fasting duration and new primary breast tumors and death (JAMA Oncol. 2016 Mar 31. doi: 10.1001/jamaoncol.2016.0164). Fasting was assessed through use of 24-hour dietary recall.

Fasting less than 13 hours per night was associated with an increased risk of breast cancer, compared with fasting at least 13 hours (hazard ratio, 1.36; 95% confidence interval, 1.05-1.76). Different fasting durations were not associated with breast cancer mortality.

Additional analyses demonstrated that each 2-hour increase in fasting duration was associated with significantly lower hemoglobin A_1c levels and a longer duration of nighttime sleep.

The positive health benefits of fasting have become increasingly “discussed,” albeit commonly on websites advertising for fasting cookbooks. Benefits of fasting include weight loss, improved insulin sensitivity, reductions in inflammation, improved cardiovascular risk factors, enhanced brain function, reductions in Alzheimer’s disease symptoms, and extended life span.

Many of these data are preliminary, and some are based upon animal models, such as the prolonged lifespan. In one study, rats undergoing alternate-day fasting lived 83% longer than rats who were not fasted. Interestingly, human data suggest that food consumption on the nonfasting days does not result in caloric consumption to cover the caloric deficit on the fasted day.

I have to admit that I am intrigued. I am not hearing much discussion about fasting among my colleagues – although a lot them skip meals, I know. But nobody is discussing it as a recommendation to appropriately selected patients (for example, not on insulin) to combat obesity and other diseases. I tried to suggest it to a patient the other day, who had a staggering amount of central adiposity, and he laughed at me. Is the thought of skipping eating for a day so anathema to our modern consumptive culture that we can’t even consider it?

Depending on the type of fasting that one is doing, one does not have to count calories on the fasting days, because there aren’t any. That makes it easy.

In a world of abundance and limitless food options, it may seem strange (self-indulgent?) to fast. But perhaps it will be a key to help us continue the species for a couple more generations.

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 financial disclosures about this article.

We are a product of our environment. But we shan’t forget that we are a product of the critical interaction between our environment and our evolutionary biology.

Back when we were roaming the plains searching for food, we likely experienced “forced fasts” (that is, we had no food). Our ancestors who were the best at surviving these periods of scarcity lived to bear us into our current period of staggering abundance. Now, we are the unhealthiest humans in history.

Is part of the answer to our current health problems to return to our roots and ... fast?

In a recent article by Catherine Marinac and her colleagues, patients aged 27-70 years with breast cancer in the Women’s Healthy Eating and Living study were analyzed to uncover the relationship between nightly fasting duration and new primary breast tumors and death (JAMA Oncol. 2016 Mar 31. doi: 10.1001/jamaoncol.2016.0164). Fasting was assessed through use of 24-hour dietary recall.

Fasting less than 13 hours per night was associated with an increased risk of breast cancer, compared with fasting at least 13 hours (hazard ratio, 1.36; 95% confidence interval, 1.05-1.76). Different fasting durations were not associated with breast cancer mortality.

Additional analyses demonstrated that each 2-hour increase in fasting duration was associated with significantly lower hemoglobin A_1c levels and a longer duration of nighttime sleep.

The positive health benefits of fasting have become increasingly “discussed,” albeit commonly on websites advertising for fasting cookbooks. Benefits of fasting include weight loss, improved insulin sensitivity, reductions in inflammation, improved cardiovascular risk factors, enhanced brain function, reductions in Alzheimer’s disease symptoms, and extended life span.

Many of these data are preliminary, and some are based upon animal models, such as the prolonged lifespan. In one study, rats undergoing alternate-day fasting lived 83% longer than rats who were not fasted. Interestingly, human data suggest that food consumption on the nonfasting days does not result in caloric consumption to cover the caloric deficit on the fasted day.

I have to admit that I am intrigued. I am not hearing much discussion about fasting among my colleagues – although a lot them skip meals, I know. But nobody is discussing it as a recommendation to appropriately selected patients (for example, not on insulin) to combat obesity and other diseases. I tried to suggest it to a patient the other day, who had a staggering amount of central adiposity, and he laughed at me. Is the thought of skipping eating for a day so anathema to our modern consumptive culture that we can’t even consider it?

Depending on the type of fasting that one is doing, one does not have to count calories on the fasting days, because there aren’t any. That makes it easy.

In a world of abundance and limitless food options, it may seem strange (self-indulgent?) to fast. But perhaps it will be a key to help us continue the species for a couple more generations.

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 financial disclosures about this article.

Sometimes, you come across an article that makes you cringe. After this initial reaction – and if we are up for the challenge – we realize that this information can help us grow by pushing our clinical approach in new directions.

This is the experience I had with an article by Dr. Daniel Bouland and colleagues that explored the ways in which people struggling with addiction obtain prescription medications (J Addict Med. 2015 Jul-Aug;9[4]:281-5).

In this semiquantitative qualitative study, investigators interviewed 36 patients in a residential addiction treatment program who obtained prescriptions from clinicians in support of an addiction. Types of medications obtained by respondents were opioids (97.2%), sedative hypnotics (47.4%), and amphetamines (5.5%).

Patients reported obtaining prescriptions from clinicians because it was perceived to be “legal” – even though 75% of them faked symptoms, several falsified MRI images of an injury, and some used old or forged prescriptions. One patient paid a physician outright for the medication.

Eight percent of patients physically harmed themselves to obtain prescriptions by doing things such as cutting themselves to put blood in the urine, hitting their head against the wall to the point of unconsciousness, and undergoing unnecessary surgery.

Primary care clinicians and pain specialists were viewed as the easiest sources of medication. Most patients used “mom and pop” pharmacies, visited multiple pharmacies, and paid in cash. Importantly, 67% of patients said that an intervention could have changed their behaviors.

I think I knew this, but it challenged me to see it in writing. I appreciated the honesty of these individuals and was struck by the fact that almost two-thirds suggested that an intervention could have transformed them.

But how to start this conversation?

The last time I expressed concern about a patient’s allergy to any pain medication – except oxycodone and the potentially toxic doses of ibuprofen and acetaminophen that didn’t “touch it” – I was the recipient of seething rage and hostility.

Addiction treatment is hard, diagnosing addiction in daily primary care practice is harder, and holding up a mirror to a patient’s prescription drug habits requires protective body armor. That’s why not many of us do it.

So, now that we have guidelines for chronic opioids, we need best practices for acute visits presenting with x-rays of broken animal bones labeled with their name handwritten on duct tape.

Are we up for urine drug screens for every controlled substance prescription on nonestablished patients every time? Probably not, but we have to start somewhere.

At least it might start a conversation when we can say: “We do this for all of our patients, we are not singling you out. Is there anything you would like to talk about before we complete this test?”

Most importantly, once we make a diagnosis of prescription drug abuse, we need resources to which to refer them and health insurance to help cover the cost for this care.

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 financial disclosures about this article.

Sometimes, you come across an article that makes you cringe. After this initial reaction – and if we are up for the challenge – we realize that this information can help us grow by pushing our clinical approach in new directions.

This is the experience I had with an article by Dr. Daniel Bouland and colleagues that explored the ways in which people struggling with addiction obtain prescription medications (J Addict Med. 2015 Jul-Aug;9[4]:281-5).

In this semiquantitative qualitative study, investigators interviewed 36 patients in a residential addiction treatment program who obtained prescriptions from clinicians in support of an addiction. Types of medications obtained by respondents were opioids (97.2%), sedative hypnotics (47.4%), and amphetamines (5.5%).

Patients reported obtaining prescriptions from clinicians because it was perceived to be “legal” – even though 75% of them faked symptoms, several falsified MRI images of an injury, and some used old or forged prescriptions. One patient paid a physician outright for the medication.

Eight percent of patients physically harmed themselves to obtain prescriptions by doing things such as cutting themselves to put blood in the urine, hitting their head against the wall to the point of unconsciousness, and undergoing unnecessary surgery.

Primary care clinicians and pain specialists were viewed as the easiest sources of medication. Most patients used “mom and pop” pharmacies, visited multiple pharmacies, and paid in cash. Importantly, 67% of patients said that an intervention could have changed their behaviors.

I think I knew this, but it challenged me to see it in writing. I appreciated the honesty of these individuals and was struck by the fact that almost two-thirds suggested that an intervention could have transformed them.

But how to start this conversation?

The last time I expressed concern about a patient’s allergy to any pain medication – except oxycodone and the potentially toxic doses of ibuprofen and acetaminophen that didn’t “touch it” – I was the recipient of seething rage and hostility.

Addiction treatment is hard, diagnosing addiction in daily primary care practice is harder, and holding up a mirror to a patient’s prescription drug habits requires protective body armor. That’s why not many of us do it.

So, now that we have guidelines for chronic opioids, we need best practices for acute visits presenting with x-rays of broken animal bones labeled with their name handwritten on duct tape.

Are we up for urine drug screens for every controlled substance prescription on nonestablished patients every time? Probably not, but we have to start somewhere.

At least it might start a conversation when we can say: “We do this for all of our patients, we are not singling you out. Is there anything you would like to talk about before we complete this test?”

Most importantly, once we make a diagnosis of prescription drug abuse, we need resources to which to refer them and health insurance to help cover the cost for this care.

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 financial disclosures about this article.

Sometimes, you come across an article that makes you cringe. After this initial reaction – and if we are up for the challenge – we realize that this information can help us grow by pushing our clinical approach in new directions.

This is the experience I had with an article by Dr. Daniel Bouland and colleagues that explored the ways in which people struggling with addiction obtain prescription medications (J Addict Med. 2015 Jul-Aug;9[4]:281-5).

In this semiquantitative qualitative study, investigators interviewed 36 patients in a residential addiction treatment program who obtained prescriptions from clinicians in support of an addiction. Types of medications obtained by respondents were opioids (97.2%), sedative hypnotics (47.4%), and amphetamines (5.5%).

Patients reported obtaining prescriptions from clinicians because it was perceived to be “legal” – even though 75% of them faked symptoms, several falsified MRI images of an injury, and some used old or forged prescriptions. One patient paid a physician outright for the medication.

Eight percent of patients physically harmed themselves to obtain prescriptions by doing things such as cutting themselves to put blood in the urine, hitting their head against the wall to the point of unconsciousness, and undergoing unnecessary surgery.

Primary care clinicians and pain specialists were viewed as the easiest sources of medication. Most patients used “mom and pop” pharmacies, visited multiple pharmacies, and paid in cash. Importantly, 67% of patients said that an intervention could have changed their behaviors.

I think I knew this, but it challenged me to see it in writing. I appreciated the honesty of these individuals and was struck by the fact that almost two-thirds suggested that an intervention could have transformed them.

But how to start this conversation?

The last time I expressed concern about a patient’s allergy to any pain medication – except oxycodone and the potentially toxic doses of ibuprofen and acetaminophen that didn’t “touch it” – I was the recipient of seething rage and hostility.

Addiction treatment is hard, diagnosing addiction in daily primary care practice is harder, and holding up a mirror to a patient’s prescription drug habits requires protective body armor. That’s why not many of us do it.

So, now that we have guidelines for chronic opioids, we need best practices for acute visits presenting with x-rays of broken animal bones labeled with their name handwritten on duct tape.

Are we up for urine drug screens for every controlled substance prescription on nonestablished patients every time? Probably not, but we have to start somewhere.

At least it might start a conversation when we can say: “We do this for all of our patients, we are not singling you out. Is there anything you would like to talk about before we complete this test?”

Most importantly, once we make a diagnosis of prescription drug abuse, we need resources to which to refer them and health insurance to help cover the cost for this care.

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 financial disclosures about this article.

In the era of individualized (or precision) medicine, we are presented with a unique opportunity to peer into the genetic “maps” of our patients. Through this window, we can envision the self-evident present or predict a possible future.

For the front-line provider, knowing that we could someday have a large amount of these data to deal with can be overwhelming. We may be loath to think that, amongst all the other daily battles we wage with current disease states, we may now need to understand and explain risk for future disease states.

But would we be more likely to use these data if we thought that they would change patient behavior? Maybe.

So does it?

Gareth Hollands, Ph.D., of the University of Cambridge, England, and his colleagues conducted a brilliantly timed and welcome systematic review of the literature assessing the impact of communicating DNA-based disease risk estimates on risk-reducing health behaviors and motivation to engage in such behaviors (BMJ. 2016 Mar 15;352:i1102).

Eighteen studies were found reporting on seven behavioral outcomes, including smoking cessation (six studies, n = 2,663), diet (seven studies, n = 1,784), and physical activity (six studies, n = 1,704). The smoking studies related genetic risk for lung or esophageal cancer; the diet studies related risk for diabetes, obesity, cardiovascular disease, hypertension, hyperlipidemia, and Alzheimer’s disease; and the physical activity studies related risks similar to the diet studies.

No evidence was found that communicating DNA-based risk increased smoking cessation or led to positive changes in diet or physical activity. Nor did the investigators find any effects on motivation to change behavior. Although this information is not motivating to patients, no evidence was found suggesting that it is demotivating, either.

If neither behavior nor motivation is modified by DNA-based risk assessment, what is it good for? As the authors pointed out, this information can be used for clinical risk stratification and for refining screening and treatment procedures.

It’s important to note that this puts the responsibility for the required action in response to DNA data in the hands of medical providers – sadly reminding us that the list of ways to motivate patients to change behavior remains frustratingly short.

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 financial disclosures about this article.

In the era of individualized (or precision) medicine, we are presented with a unique opportunity to peer into the genetic “maps” of our patients. Through this window, we can envision the self-evident present or predict a possible future.

For the front-line provider, knowing that we could someday have a large amount of these data to deal with can be overwhelming. We may be loath to think that, amongst all the other daily battles we wage with current disease states, we may now need to understand and explain risk for future disease states.

But would we be more likely to use these data if we thought that they would change patient behavior? Maybe.

So does it?

Gareth Hollands, Ph.D., of the University of Cambridge, England, and his colleagues conducted a brilliantly timed and welcome systematic review of the literature assessing the impact of communicating DNA-based disease risk estimates on risk-reducing health behaviors and motivation to engage in such behaviors (BMJ. 2016 Mar 15;352:i1102).

Eighteen studies were found reporting on seven behavioral outcomes, including smoking cessation (six studies, n = 2,663), diet (seven studies, n = 1,784), and physical activity (six studies, n = 1,704). The smoking studies related genetic risk for lung or esophageal cancer; the diet studies related risk for diabetes, obesity, cardiovascular disease, hypertension, hyperlipidemia, and Alzheimer’s disease; and the physical activity studies related risks similar to the diet studies.

No evidence was found that communicating DNA-based risk increased smoking cessation or led to positive changes in diet or physical activity. Nor did the investigators find any effects on motivation to change behavior. Although this information is not motivating to patients, no evidence was found suggesting that it is demotivating, either.

If neither behavior nor motivation is modified by DNA-based risk assessment, what is it good for? As the authors pointed out, this information can be used for clinical risk stratification and for refining screening and treatment procedures.

It’s important to note that this puts the responsibility for the required action in response to DNA data in the hands of medical providers – sadly reminding us that the list of ways to motivate patients to change behavior remains frustratingly short.

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 financial disclosures about this article.

In the era of individualized (or precision) medicine, we are presented with a unique opportunity to peer into the genetic “maps” of our patients. Through this window, we can envision the self-evident present or predict a possible future.

For the front-line provider, knowing that we could someday have a large amount of these data to deal with can be overwhelming. We may be loath to think that, amongst all the other daily battles we wage with current disease states, we may now need to understand and explain risk for future disease states.

But would we be more likely to use these data if we thought that they would change patient behavior? Maybe.

So does it?

Gareth Hollands, Ph.D., of the University of Cambridge, England, and his colleagues conducted a brilliantly timed and welcome systematic review of the literature assessing the impact of communicating DNA-based disease risk estimates on risk-reducing health behaviors and motivation to engage in such behaviors (BMJ. 2016 Mar 15;352:i1102).

Eighteen studies were found reporting on seven behavioral outcomes, including smoking cessation (six studies, n = 2,663), diet (seven studies, n = 1,784), and physical activity (six studies, n = 1,704). The smoking studies related genetic risk for lung or esophageal cancer; the diet studies related risk for diabetes, obesity, cardiovascular disease, hypertension, hyperlipidemia, and Alzheimer’s disease; and the physical activity studies related risks similar to the diet studies.

No evidence was found that communicating DNA-based risk increased smoking cessation or led to positive changes in diet or physical activity. Nor did the investigators find any effects on motivation to change behavior. Although this information is not motivating to patients, no evidence was found suggesting that it is demotivating, either.

If neither behavior nor motivation is modified by DNA-based risk assessment, what is it good for? As the authors pointed out, this information can be used for clinical risk stratification and for refining screening and treatment procedures.

It’s important to note that this puts the responsibility for the required action in response to DNA data in the hands of medical providers – sadly reminding us that the list of ways to motivate patients to change behavior remains frustratingly short.

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 financial disclosures about this article.

A fair number of my patients have had or are undergoing bariatric surgery. Disconcertingly, a not insignificant number of them are regaining the weight after surgery. Weight regain will occur in 20% of patients undergoing bariatric surgery after initial weight loss.

When this occurs, not only do we have a patient with an altered gut putting them at risk for nutritional deficiencies if we are not fastidious in our follow-up, but they are discouraged and overweight again.

Add this to the concern that bariatric surgery has been associated with an increase in suicides (2.33-3.63 per 1000 patient-years), and we may have some cause for alarm.

So, what predicts success – and can we facilitate it?

Several factors have been shown to predict successful weight loss after bariatric surgery. An “active coping style” (that is, planning vs. denial) and adherence to follow-up after bariatric surgery have both been shown to be associated with a higher percentage of excess weight loss. Interestingly, psychological burden and motivation have not been associated with weight loss.

In a recent article, Lori Liebl, Ph.D., and her colleagues conducted a qualitative study of the experiences of adults who successfully maintained weight loss after bariatric surgery (J Clin Nurs. 2016 Feb 23. doi: 10.1111/jocn.13129). Success was defined as 50% or more of the excessive weight loss 24 months after bariatric surgery.

The voice of the successful bariatric patient is an interesting and important one. Several themes were identified: 1) taking life back (“I did it for myself”); 2) a new lease on life (“There are things I can do now that I am not exhausted”); 3) the importance of social support; 4) avoiding the negative (terminating unhealthy relationships in which “food is love”); 5) the void (food addiction and sense of loss); 6) fighting food demons; 7) finding the happy weight; and 8) a ripple effect (that is, if you don’t eat it, the rest of family doesn’t, either).

I was left wondering how I can best help my patients using this information.

First, I think the themes can mature our empathy for the struggles that these patients face, and perhaps help us combat bias. Second, I think this knowledge can inform early discussions around what sorts of things need to be lined up for after the procedure, such as social support.

Finally, I think the themes can be universalized and help us counsel patients who may be struggling with weight, but who are otherwise not candidates for bariatric surgery.

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 financial disclosures about this article.

A fair number of my patients have had or are undergoing bariatric surgery. Disconcertingly, a not insignificant number of them are regaining the weight after surgery. Weight regain will occur in 20% of patients undergoing bariatric surgery after initial weight loss.

When this occurs, not only do we have a patient with an altered gut putting them at risk for nutritional deficiencies if we are not fastidious in our follow-up, but they are discouraged and overweight again.

Add this to the concern that bariatric surgery has been associated with an increase in suicides (2.33-3.63 per 1000 patient-years), and we may have some cause for alarm.

So, what predicts success – and can we facilitate it?

Several factors have been shown to predict successful weight loss after bariatric surgery. An “active coping style” (that is, planning vs. denial) and adherence to follow-up after bariatric surgery have both been shown to be associated with a higher percentage of excess weight loss. Interestingly, psychological burden and motivation have not been associated with weight loss.

In a recent article, Lori Liebl, Ph.D., and her colleagues conducted a qualitative study of the experiences of adults who successfully maintained weight loss after bariatric surgery (J Clin Nurs. 2016 Feb 23. doi: 10.1111/jocn.13129). Success was defined as 50% or more of the excessive weight loss 24 months after bariatric surgery.

The voice of the successful bariatric patient is an interesting and important one. Several themes were identified: 1) taking life back (“I did it for myself”); 2) a new lease on life (“There are things I can do now that I am not exhausted”); 3) the importance of social support; 4) avoiding the negative (terminating unhealthy relationships in which “food is love”); 5) the void (food addiction and sense of loss); 6) fighting food demons; 7) finding the happy weight; and 8) a ripple effect (that is, if you don’t eat it, the rest of family doesn’t, either).

I was left wondering how I can best help my patients using this information.

First, I think the themes can mature our empathy for the struggles that these patients face, and perhaps help us combat bias. Second, I think this knowledge can inform early discussions around what sorts of things need to be lined up for after the procedure, such as social support.

Finally, I think the themes can be universalized and help us counsel patients who may be struggling with weight, but who are otherwise not candidates for bariatric surgery.

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 financial disclosures about this article.

A fair number of my patients have had or are undergoing bariatric surgery. Disconcertingly, a not insignificant number of them are regaining the weight after surgery. Weight regain will occur in 20% of patients undergoing bariatric surgery after initial weight loss.

When this occurs, not only do we have a patient with an altered gut putting them at risk for nutritional deficiencies if we are not fastidious in our follow-up, but they are discouraged and overweight again.

Add this to the concern that bariatric surgery has been associated with an increase in suicides (2.33-3.63 per 1000 patient-years), and we may have some cause for alarm.

So, what predicts success – and can we facilitate it?

Several factors have been shown to predict successful weight loss after bariatric surgery. An “active coping style” (that is, planning vs. denial) and adherence to follow-up after bariatric surgery have both been shown to be associated with a higher percentage of excess weight loss. Interestingly, psychological burden and motivation have not been associated with weight loss.

In a recent article, Lori Liebl, Ph.D., and her colleagues conducted a qualitative study of the experiences of adults who successfully maintained weight loss after bariatric surgery (J Clin Nurs. 2016 Feb 23. doi: 10.1111/jocn.13129). Success was defined as 50% or more of the excessive weight loss 24 months after bariatric surgery.

The voice of the successful bariatric patient is an interesting and important one. Several themes were identified: 1) taking life back (“I did it for myself”); 2) a new lease on life (“There are things I can do now that I am not exhausted”); 3) the importance of social support; 4) avoiding the negative (terminating unhealthy relationships in which “food is love”); 5) the void (food addiction and sense of loss); 6) fighting food demons; 7) finding the happy weight; and 8) a ripple effect (that is, if you don’t eat it, the rest of family doesn’t, either).

I was left wondering how I can best help my patients using this information.

First, I think the themes can mature our empathy for the struggles that these patients face, and perhaps help us combat bias. Second, I think this knowledge can inform early discussions around what sorts of things need to be lined up for after the procedure, such as social support.

Finally, I think the themes can be universalized and help us counsel patients who may be struggling with weight, but who are otherwise not candidates for bariatric surgery.

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 financial disclosures about this article.

In the midst of the cold and flu season, we should reflect on the fact that our patients are laying down billions of dollars annually on preventions and cures for respiratory tract infections.

An aside: I am frequently turned down on my offer of the influenza vaccine, for which we probably have the best evidence. But $60 per month for a completely unproven preventive/curative agent made in some random factory in some random foreign land with no guarantee of good manufacturing practices (never mind the lack of active ingredients)? Stores can’t keep it in stock.

But I digress.

Our patients may lack the awareness of where to access evidence-based information when seeking answers about efficacy for cold remedies. So, it’s up to us to have at least some sense of where to get reliable information.

Truth be told, I am an enormous fan of safe and effective nonmedication therapies for the treatment and prevention of disease. So, when time permits, I will do a quick PubMed.gov search limiting my articles to randomized trials or systematic reviews on the latest and greatest home remedy.

Probiotics have been around for a while, and I think of them as a cure in search of a disease. The Cochrane Collaboration conducted a systematic review evaluating probiotics for the prevention of upper respiratory tract infection. In this review, 13 randomized, controlled trials were included (Explore [NY]. 2015 Sep-Oct;11[5]:418-20).

Probiotics were observed to be significantly better than placebo for reducing episodes of upper respiratory tract infection, the mean duration of episodes, antibiotic prescription rates, and cold-related absences. The evidence was of moderate to low quality.

Some may wonder how an ingested probiotic helps the respiratory tract stave off or fight infection. The prevailing theory appears to be that probiotics may function by mobilizing cells from the intestine to immunomodulate respiratory mucosa.

As for what probiotic/organism to prescribe? On this issue, there is a lot of smoke and not a lot of heat.

In general, the product should be encapsulated, and the label should include the genus and species of the strains (e.g., Lactobacillus acidophilus), the number of organisms (e.g., 5 billion), storage conditions (e.g., refrigerated or room temperature), and the shelf life. Pharmacy chain house brands may be cheaper. Gummy and chewable products tend to have 92% fewer beneficial bacteria than standard formulations.

How can we ensure purity?

That is tough, because supplements like probiotics are not regulated by the Food and Drug Administration above and beyond the agency’s trying to ensure good manufacturing practices. However, companies such as LabDoor (which generates revenue through affiliate links) test and grade supplements for label accuracy and purity. Websites like this might be the best place to start.

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 financial disclosures relevant to this article.

In the midst of the cold and flu season, we should reflect on the fact that our patients are laying down billions of dollars annually on preventions and cures for respiratory tract infections.

An aside: I am frequently turned down on my offer of the influenza vaccine, for which we probably have the best evidence. But $60 per month for a completely unproven preventive/curative agent made in some random factory in some random foreign land with no guarantee of good manufacturing practices (never mind the lack of active ingredients)? Stores can’t keep it in stock.

But I digress.

Our patients may lack the awareness of where to access evidence-based information when seeking answers about efficacy for cold remedies. So, it’s up to us to have at least some sense of where to get reliable information.

Truth be told, I am an enormous fan of safe and effective nonmedication therapies for the treatment and prevention of disease. So, when time permits, I will do a quick PubMed.gov search limiting my articles to randomized trials or systematic reviews on the latest and greatest home remedy.

Probiotics have been around for a while, and I think of them as a cure in search of a disease. The Cochrane Collaboration conducted a systematic review evaluating probiotics for the prevention of upper respiratory tract infection. In this review, 13 randomized, controlled trials were included (Explore [NY]. 2015 Sep-Oct;11[5]:418-20).

Probiotics were observed to be significantly better than placebo for reducing episodes of upper respiratory tract infection, the mean duration of episodes, antibiotic prescription rates, and cold-related absences. The evidence was of moderate to low quality.

Some may wonder how an ingested probiotic helps the respiratory tract stave off or fight infection. The prevailing theory appears to be that probiotics may function by mobilizing cells from the intestine to immunomodulate respiratory mucosa.

As for what probiotic/organism to prescribe? On this issue, there is a lot of smoke and not a lot of heat.

In general, the product should be encapsulated, and the label should include the genus and species of the strains (e.g., Lactobacillus acidophilus), the number of organisms (e.g., 5 billion), storage conditions (e.g., refrigerated or room temperature), and the shelf life. Pharmacy chain house brands may be cheaper. Gummy and chewable products tend to have 92% fewer beneficial bacteria than standard formulations.

How can we ensure purity?

That is tough, because supplements like probiotics are not regulated by the Food and Drug Administration above and beyond the agency’s trying to ensure good manufacturing practices. However, companies such as LabDoor (which generates revenue through affiliate links) test and grade supplements for label accuracy and purity. Websites like this might be the best place to start.

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 financial disclosures relevant to this article.

In the midst of the cold and flu season, we should reflect on the fact that our patients are laying down billions of dollars annually on preventions and cures for respiratory tract infections.

An aside: I am frequently turned down on my offer of the influenza vaccine, for which we probably have the best evidence. But $60 per month for a completely unproven preventive/curative agent made in some random factory in some random foreign land with no guarantee of good manufacturing practices (never mind the lack of active ingredients)? Stores can’t keep it in stock.

But I digress.

Our patients may lack the awareness of where to access evidence-based information when seeking answers about efficacy for cold remedies. So, it’s up to us to have at least some sense of where to get reliable information.

Truth be told, I am an enormous fan of safe and effective nonmedication therapies for the treatment and prevention of disease. So, when time permits, I will do a quick PubMed.gov search limiting my articles to randomized trials or systematic reviews on the latest and greatest home remedy.

Probiotics have been around for a while, and I think of them as a cure in search of a disease. The Cochrane Collaboration conducted a systematic review evaluating probiotics for the prevention of upper respiratory tract infection. In this review, 13 randomized, controlled trials were included (Explore [NY]. 2015 Sep-Oct;11[5]:418-20).

Probiotics were observed to be significantly better than placebo for reducing episodes of upper respiratory tract infection, the mean duration of episodes, antibiotic prescription rates, and cold-related absences. The evidence was of moderate to low quality.

Some may wonder how an ingested probiotic helps the respiratory tract stave off or fight infection. The prevailing theory appears to be that probiotics may function by mobilizing cells from the intestine to immunomodulate respiratory mucosa.

As for what probiotic/organism to prescribe? On this issue, there is a lot of smoke and not a lot of heat.

In general, the product should be encapsulated, and the label should include the genus and species of the strains (e.g., Lactobacillus acidophilus), the number of organisms (e.g., 5 billion), storage conditions (e.g., refrigerated or room temperature), and the shelf life. Pharmacy chain house brands may be cheaper. Gummy and chewable products tend to have 92% fewer beneficial bacteria than standard formulations.

How can we ensure purity?

That is tough, because supplements like probiotics are not regulated by the Food and Drug Administration above and beyond the agency’s trying to ensure good manufacturing practices. However, companies such as LabDoor (which generates revenue through affiliate links) test and grade supplements for label accuracy and purity. Websites like this might be the best place to start.

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 financial disclosures relevant to this article.

Urinary tract infections (UTIs) unfortunately present an abundant opportunity for us to reflexively and mindlessly contribute to filling up the globe with multidrug resistant bacteria. Many of us have patients with recurrent UTIs, who, despite our best efforts at trying to reduce recurrence through non–medication approaches, frequently call for treatment. We stand by helplessly as we watch the resistance of these organisms increase.

Is there another way?

Investigators in Germany evaluated the benefit and harms of prescribing ibuprofen in place of an antibiotic in women with symptoms of a UTI and no risk factors (BMC Med. 2010 May 26;8:30). Women aged 18-65 years were randomized to a single dose of the broad-spectrum antibiotic fosfomycin 3 g (n = 246) or ibuprofen three 400-mg doses (n = 248) for 3 days. Patients were excluded if they had any signs of upper urinary tract infection, pregnancy, urinary catheterization, gastrointestinal ulcers, or chronic conditions. Antibiotics were prescribed for persistent, worsening, or recurrent symptoms.

Women in the ibuprofen group received significantly fewer antibiotic prescriptions (283 in the fosfomycin group and 94 in the ibuprofen group; incidence rate reduction of 66.5%; 95% confidence interval, 58.8%-74.4%; P less than .001). The ibuprofen group had more symptoms that lasted a day longer. On day 4, 56% of women in the fosfomycin vs. 39% of participants in the ibuprofen group were symptom free, which increased to 82% and 70% by day 7. The ibuprofen group were more likely to develop pyelonephritis (five cases in the ibuprofen group and one in the fosfomycin group; P = .12), but all women were treated and recovered fully. Four events led to “hospital referrals,” only one of which was related to trial drug (gastrointestinal hemorrhage).

In summary, two-thirds of women in the ibuprofen group recovered without antibiotic treatment and one-third received antibiotics for persistent or worsening symptoms. The authors concluded that ibuprofen was inferior to fosfomycin for initial symptomatic treatment. The nonstatistically higher rate of upper urinary tract infection with ibuprofen may make some clinicians nervous.

However, perhaps this is worth exploring for select patients with mild symptoms. The investigators mention data suggesting women may be aware of disadvantages of antibiotics and may be open to the idea of delaying or avoiding treatment, which opens the door to informed discussions. I am planning to discuss it with my patient who has frequent UTIs to see if we can delay intravenous antibiotics for UTI. Intravenous antibiotics for UTI make me uncomfortable for a variety of reasons.

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 financial disclosures about this article.

Urinary tract infections (UTIs) unfortunately present an abundant opportunity for us to reflexively and mindlessly contribute to filling up the globe with multidrug resistant bacteria. Many of us have patients with recurrent UTIs, who, despite our best efforts at trying to reduce recurrence through non–medication approaches, frequently call for treatment. We stand by helplessly as we watch the resistance of these organisms increase.

Is there another way?

Investigators in Germany evaluated the benefit and harms of prescribing ibuprofen in place of an antibiotic in women with symptoms of a UTI and no risk factors (BMC Med. 2010 May 26;8:30). Women aged 18-65 years were randomized to a single dose of the broad-spectrum antibiotic fosfomycin 3 g (n = 246) or ibuprofen three 400-mg doses (n = 248) for 3 days. Patients were excluded if they had any signs of upper urinary tract infection, pregnancy, urinary catheterization, gastrointestinal ulcers, or chronic conditions. Antibiotics were prescribed for persistent, worsening, or recurrent symptoms.

Women in the ibuprofen group received significantly fewer antibiotic prescriptions (283 in the fosfomycin group and 94 in the ibuprofen group; incidence rate reduction of 66.5%; 95% confidence interval, 58.8%-74.4%; P less than .001). The ibuprofen group had more symptoms that lasted a day longer. On day 4, 56% of women in the fosfomycin vs. 39% of participants in the ibuprofen group were symptom free, which increased to 82% and 70% by day 7. The ibuprofen group were more likely to develop pyelonephritis (five cases in the ibuprofen group and one in the fosfomycin group; P = .12), but all women were treated and recovered fully. Four events led to “hospital referrals,” only one of which was related to trial drug (gastrointestinal hemorrhage).

In summary, two-thirds of women in the ibuprofen group recovered without antibiotic treatment and one-third received antibiotics for persistent or worsening symptoms. The authors concluded that ibuprofen was inferior to fosfomycin for initial symptomatic treatment. The nonstatistically higher rate of upper urinary tract infection with ibuprofen may make some clinicians nervous.

However, perhaps this is worth exploring for select patients with mild symptoms. The investigators mention data suggesting women may be aware of disadvantages of antibiotics and may be open to the idea of delaying or avoiding treatment, which opens the door to informed discussions. I am planning to discuss it with my patient who has frequent UTIs to see if we can delay intravenous antibiotics for UTI. Intravenous antibiotics for UTI make me uncomfortable for a variety of reasons.

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 financial disclosures about this article.

Urinary tract infections (UTIs) unfortunately present an abundant opportunity for us to reflexively and mindlessly contribute to filling up the globe with multidrug resistant bacteria. Many of us have patients with recurrent UTIs, who, despite our best efforts at trying to reduce recurrence through non–medication approaches, frequently call for treatment. We stand by helplessly as we watch the resistance of these organisms increase.

Is there another way?

Investigators in Germany evaluated the benefit and harms of prescribing ibuprofen in place of an antibiotic in women with symptoms of a UTI and no risk factors (BMC Med. 2010 May 26;8:30). Women aged 18-65 years were randomized to a single dose of the broad-spectrum antibiotic fosfomycin 3 g (n = 246) or ibuprofen three 400-mg doses (n = 248) for 3 days. Patients were excluded if they had any signs of upper urinary tract infection, pregnancy, urinary catheterization, gastrointestinal ulcers, or chronic conditions. Antibiotics were prescribed for persistent, worsening, or recurrent symptoms.

Women in the ibuprofen group received significantly fewer antibiotic prescriptions (283 in the fosfomycin group and 94 in the ibuprofen group; incidence rate reduction of 66.5%; 95% confidence interval, 58.8%-74.4%; P less than .001). The ibuprofen group had more symptoms that lasted a day longer. On day 4, 56% of women in the fosfomycin vs. 39% of participants in the ibuprofen group were symptom free, which increased to 82% and 70% by day 7. The ibuprofen group were more likely to develop pyelonephritis (five cases in the ibuprofen group and one in the fosfomycin group; P = .12), but all women were treated and recovered fully. Four events led to “hospital referrals,” only one of which was related to trial drug (gastrointestinal hemorrhage).

In summary, two-thirds of women in the ibuprofen group recovered without antibiotic treatment and one-third received antibiotics for persistent or worsening symptoms. The authors concluded that ibuprofen was inferior to fosfomycin for initial symptomatic treatment. The nonstatistically higher rate of upper urinary tract infection with ibuprofen may make some clinicians nervous.

However, perhaps this is worth exploring for select patients with mild symptoms. The investigators mention data suggesting women may be aware of disadvantages of antibiotics and may be open to the idea of delaying or avoiding treatment, which opens the door to informed discussions. I am planning to discuss it with my patient who has frequent UTIs to see if we can delay intravenous antibiotics for UTI. Intravenous antibiotics for UTI make me uncomfortable for a variety of reasons.

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 financial disclosures about this article.

We are in the midst of an epidemic of heroin and prescription opioid abuse. While the two do not completely explain each other, they are tragically and irrevocably linked.

From 2001 to 2013, we have observed a threefold increase in the total number of overdose deaths from opioid pain relievers (about 16,000 in 2013) and a fivefold increase in the total number of overdose deaths from heroin (about 8,000 in 2013).

Heroin initiation is almost 20 times higher among individuals reporting nonmedical prescription pain reliever use. Among opioid-treatment seekers, the majority of individuals who initiated opioid use in the 1960s were first exposed to heroin. This is in contrast to those who initiated in the 2000s, among whom the majority were exposed to prescription opioids. For young adults, the main sources of opioids are family, friends … and clinicians.

Opioids are powerfully addictive and can be snorted, swallowed, smoked, or shot. Data from the START (Starting Treatment with Agonist Replacement Therapies) trial suggest that individuals who inject opioids are less likely to remain in treatment than noninjectors. This necessarily increases the risk for injectors to inject again and be at risk for overdose.

Opioid overdose can be reversed with the use of naloxone. But naloxone has to be immediately or quickly available for it to be effective. Take-home naloxone programs are located in 30 U.S. states and the District of Columbia. Since 1996, home naloxone programs have reported more than 26,000 drug overdose reversals with naloxone.

On Nov. 18, the Food and Drug Administration announced the approval of a naloxone nasal spray. Prior to this approval, naloxone was only available in the injectable form (syringe or auto-injector), and needle management likely posed a barrier to first responders. The nasal spray can be administered easily without medical training. Naloxone nasal spray administered in one nostril delivered approximately the same levels or higher of naloxone as a single dose of an FDA-approved naloxone intramuscular injection in approximately the same time frame.

It is one thing to save a heroin addict who has just overdosed with nasal naloxone followed by appropriate medical attention. It is entirely another to engage them in an effective drug treatment program.

If naloxone revives them, it is treatment that can save them.

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 financial disclosures about this article.

We are in the midst of an epidemic of heroin and prescription opioid abuse. While the two do not completely explain each other, they are tragically and irrevocably linked.

From 2001 to 2013, we have observed a threefold increase in the total number of overdose deaths from opioid pain relievers (about 16,000 in 2013) and a fivefold increase in the total number of overdose deaths from heroin (about 8,000 in 2013).

Heroin initiation is almost 20 times higher among individuals reporting nonmedical prescription pain reliever use. Among opioid-treatment seekers, the majority of individuals who initiated opioid use in the 1960s were first exposed to heroin. This is in contrast to those who initiated in the 2000s, among whom the majority were exposed to prescription opioids. For young adults, the main sources of opioids are family, friends … and clinicians.

Opioids are powerfully addictive and can be snorted, swallowed, smoked, or shot. Data from the START (Starting Treatment with Agonist Replacement Therapies) trial suggest that individuals who inject opioids are less likely to remain in treatment than noninjectors. This necessarily increases the risk for injectors to inject again and be at risk for overdose.

Opioid overdose can be reversed with the use of naloxone. But naloxone has to be immediately or quickly available for it to be effective. Take-home naloxone programs are located in 30 U.S. states and the District of Columbia. Since 1996, home naloxone programs have reported more than 26,000 drug overdose reversals with naloxone.

On Nov. 18, the Food and Drug Administration announced the approval of a naloxone nasal spray. Prior to this approval, naloxone was only available in the injectable form (syringe or auto-injector), and needle management likely posed a barrier to first responders. The nasal spray can be administered easily without medical training. Naloxone nasal spray administered in one nostril delivered approximately the same levels or higher of naloxone as a single dose of an FDA-approved naloxone intramuscular injection in approximately the same time frame.

It is one thing to save a heroin addict who has just overdosed with nasal naloxone followed by appropriate medical attention. It is entirely another to engage them in an effective drug treatment program.

If naloxone revives them, it is treatment that can save them.

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 financial disclosures about this article.

We are in the midst of an epidemic of heroin and prescription opioid abuse. While the two do not completely explain each other, they are tragically and irrevocably linked.

From 2001 to 2013, we have observed a threefold increase in the total number of overdose deaths from opioid pain relievers (about 16,000 in 2013) and a fivefold increase in the total number of overdose deaths from heroin (about 8,000 in 2013).

Heroin initiation is almost 20 times higher among individuals reporting nonmedical prescription pain reliever use. Among opioid-treatment seekers, the majority of individuals who initiated opioid use in the 1960s were first exposed to heroin. This is in contrast to those who initiated in the 2000s, among whom the majority were exposed to prescription opioids. For young adults, the main sources of opioids are family, friends … and clinicians.

Opioids are powerfully addictive and can be snorted, swallowed, smoked, or shot. Data from the START (Starting Treatment with Agonist Replacement Therapies) trial suggest that individuals who inject opioids are less likely to remain in treatment than noninjectors. This necessarily increases the risk for injectors to inject again and be at risk for overdose.

Opioid overdose can be reversed with the use of naloxone. But naloxone has to be immediately or quickly available for it to be effective. Take-home naloxone programs are located in 30 U.S. states and the District of Columbia. Since 1996, home naloxone programs have reported more than 26,000 drug overdose reversals with naloxone.

On Nov. 18, the Food and Drug Administration announced the approval of a naloxone nasal spray. Prior to this approval, naloxone was only available in the injectable form (syringe or auto-injector), and needle management likely posed a barrier to first responders. The nasal spray can be administered easily without medical training. Naloxone nasal spray administered in one nostril delivered approximately the same levels or higher of naloxone as a single dose of an FDA-approved naloxone intramuscular injection in approximately the same time frame.

It is one thing to save a heroin addict who has just overdosed with nasal naloxone followed by appropriate medical attention. It is entirely another to engage them in an effective drug treatment program.

If naloxone revives them, it is treatment that can save them.

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 financial disclosures about this article.

One-half of my practice is taking care of employees and dependents employed by the organization for which I work. Most of these patients sit … a lot … and present to me with musculoskeletal pain and weight concerns. My patients have a high degree of health literacy and are fully aware that 6 hours of sitting might have at least something to do with these problems.

We currently seem to be on the other side of the “walk station” mania. Sanity has been restored through a combination of concerns about medical liability for work-related treadmill injuries, expense, space issues, and reports that walkers were more forgetful and less focused. The last study resulted in some personal email for my own indulgences in walking while researching.

But let us not throw out an upright posture with the treadmill. Sitters have an increased risk for elevated blood sugars, cardiovascular disease, cancer, and death. Standers have been suggested to burn 50 more calories per hour. Some experts recommend that people should stand for at least 2 hours each day, and 4 hours is even better.

Dr. Graves and colleagues conducted a randomized controlled trial to evaluate the impact of a sit-stand workstation on sitting time, vascular, metabolic, and musculoskeletal outcomes and to investigate workstation acceptability and feasibility. Forty-seven participants without any bodily symptoms were randomized to either a sit-stand workstation or no intervention for 8 weeks. The sit-stand workstation was associated with decreased sit time (80 minutes per 8-hour work day), increased standing time (73 minutes per 8-hour work day), and a decrease in total cholesterol. No increase in musculoskeletal pain was observed with a suggestion of possible benefit in the neck and upper back (BMC Public Health. 2015;15:1145. doi 10.1186/s12889-015-2469-8).

Each of the devices cost about $550 to install for a single monitor ($20 more for a dual monitor). The intervention was only 8 weeks in duration and stronger effects in musculoskeletal and cardiovascular risk markers might be seen with longer durations of study. The qualitative work in this study suggested that several factors may influence use of a sit-stand desk such as social environment (for example, other colleagues not using it may decrease use), work tasks (for example, paperwork made difficult by limited elevated work surface), and design (for example, keyboard surface bounces too much). From personal experience, the sit-stand desk is ideal if the vast majority of work is on the computer. I’d also like to say I was standing when I wrote this. But I wasn’t. And I wasn’t walking either because I can’t remember where that desk is.

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 financial disclosures about this article. Follow him on Twitter @jonebbert.

One-half of my practice is taking care of employees and dependents employed by the organization for which I work. Most of these patients sit … a lot … and present to me with musculoskeletal pain and weight concerns. My patients have a high degree of health literacy and are fully aware that 6 hours of sitting might have at least something to do with these problems.

We currently seem to be on the other side of the “walk station” mania. Sanity has been restored through a combination of concerns about medical liability for work-related treadmill injuries, expense, space issues, and reports that walkers were more forgetful and less focused. The last study resulted in some personal email for my own indulgences in walking while researching.

But let us not throw out an upright posture with the treadmill. Sitters have an increased risk for elevated blood sugars, cardiovascular disease, cancer, and death. Standers have been suggested to burn 50 more calories per hour. Some experts recommend that people should stand for at least 2 hours each day, and 4 hours is even better.

Dr. Graves and colleagues conducted a randomized controlled trial to evaluate the impact of a sit-stand workstation on sitting time, vascular, metabolic, and musculoskeletal outcomes and to investigate workstation acceptability and feasibility. Forty-seven participants without any bodily symptoms were randomized to either a sit-stand workstation or no intervention for 8 weeks. The sit-stand workstation was associated with decreased sit time (80 minutes per 8-hour work day), increased standing time (73 minutes per 8-hour work day), and a decrease in total cholesterol. No increase in musculoskeletal pain was observed with a suggestion of possible benefit in the neck and upper back (BMC Public Health. 2015;15:1145. doi 10.1186/s12889-015-2469-8).

Each of the devices cost about $550 to install for a single monitor ($20 more for a dual monitor). The intervention was only 8 weeks in duration and stronger effects in musculoskeletal and cardiovascular risk markers might be seen with longer durations of study. The qualitative work in this study suggested that several factors may influence use of a sit-stand desk such as social environment (for example, other colleagues not using it may decrease use), work tasks (for example, paperwork made difficult by limited elevated work surface), and design (for example, keyboard surface bounces too much). From personal experience, the sit-stand desk is ideal if the vast majority of work is on the computer. I’d also like to say I was standing when I wrote this. But I wasn’t. And I wasn’t walking either because I can’t remember where that desk is.

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 financial disclosures about this article. Follow him on Twitter @jonebbert.

One-half of my practice is taking care of employees and dependents employed by the organization for which I work. Most of these patients sit … a lot … and present to me with musculoskeletal pain and weight concerns. My patients have a high degree of health literacy and are fully aware that 6 hours of sitting might have at least something to do with these problems.

We currently seem to be on the other side of the “walk station” mania. Sanity has been restored through a combination of concerns about medical liability for work-related treadmill injuries, expense, space issues, and reports that walkers were more forgetful and less focused. The last study resulted in some personal email for my own indulgences in walking while researching.

But let us not throw out an upright posture with the treadmill. Sitters have an increased risk for elevated blood sugars, cardiovascular disease, cancer, and death. Standers have been suggested to burn 50 more calories per hour. Some experts recommend that people should stand for at least 2 hours each day, and 4 hours is even better.

Dr. Graves and colleagues conducted a randomized controlled trial to evaluate the impact of a sit-stand workstation on sitting time, vascular, metabolic, and musculoskeletal outcomes and to investigate workstation acceptability and feasibility. Forty-seven participants without any bodily symptoms were randomized to either a sit-stand workstation or no intervention for 8 weeks. The sit-stand workstation was associated with decreased sit time (80 minutes per 8-hour work day), increased standing time (73 minutes per 8-hour work day), and a decrease in total cholesterol. No increase in musculoskeletal pain was observed with a suggestion of possible benefit in the neck and upper back (BMC Public Health. 2015;15:1145. doi 10.1186/s12889-015-2469-8).

Each of the devices cost about $550 to install for a single monitor ($20 more for a dual monitor). The intervention was only 8 weeks in duration and stronger effects in musculoskeletal and cardiovascular risk markers might be seen with longer durations of study. The qualitative work in this study suggested that several factors may influence use of a sit-stand desk such as social environment (for example, other colleagues not using it may decrease use), work tasks (for example, paperwork made difficult by limited elevated work surface), and design (for example, keyboard surface bounces too much). From personal experience, the sit-stand desk is ideal if the vast majority of work is on the computer. I’d also like to say I was standing when I wrote this. But I wasn’t. And I wasn’t walking either because I can’t remember where that desk is.

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 financial disclosures about this article. Follow him on Twitter @jonebbert.

Is it just me? I don’t think that I have visited with a single patient this week who’s not struggling with sleep. Our heavily caffeinated, media-obsessed, melatonin-killing, computer-screen-staring, tragic work-life imbalances explain away a lot of it. Knowing that, though, patients in front of me seek immediate relief.

A prescription takes substantially less effort than does training patients on sleep hygiene or sleep restriction. The problem with “z” drugs is, of course, that tolerance can develop within 4 weeks with daily use. These drugs have been associated with mood and cognitive changes and increased mortality. Many of my patients cannot use them sparingly, because relief of insomnia is something of which they cannot get enough. Then we are either back to square one or playing the dose-escalation game.

I have always wondered how much of this is the “placebo effect” and how we could use this to our clinical advantage. This is certainly what I hear from my cynical colleagues when I recommend melatonin – which, by the way, I personally believe is an extremely effective and underutilized intervention. We should remind ourselves to be cognizant of the “if I can’t prescribe it, it can’t work that well” mentality.

Alexander Winkler and Winfried Rief of the University of Marburg, Germany, conducted a brilliant systematic review examining the effect of placebo conditions in randomized trials including polysomnography addressing primary insomnia (Sleep. 2015 Jun 1;38[6]:925-31).

The investigators identified 32 studies with almost 4,000 patients in 82 treatment conditions: The studies were published between 1992 and 2012. Of those 82 treatment conditions, 17 included hypnotic drugs.

Results suggest that 64% of drug response to medications for primary insomnia is achieved in the placebo group.

So what does this mean clinically? I think the first thing it means is that we should consider (re)launching frank discourse about the ethics surrounding the use of placebo in clinical medicine. Are we all too horrified to think that patients may get better despite us rather than because of us to dig too deeply here?

The second thing it means is that patients should be instructed to use the medications only when needed. If a minority of the drug effect for insomnia is from the drug itself, we should minimize the buildup of tolerance by using it sparingly. Studies that have alternated a hypnotic with a placebo show that this works just as well as using a hypnotic every night.

Patients should be encouraged to alternate therapy, such as trying melatonin first and resorting to a “z” drug only if sleep remains elusive. Alternating drug therapy may also enhance the efficacy of the medication.

Always try to combine pharmacotherapy with good sleep hygiene to maximize benefits.

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 financial disclosures about this article. Follow him on Twitter @jonebbert.

Is it just me? I don’t think that I have visited with a single patient this week who’s not struggling with sleep. Our heavily caffeinated, media-obsessed, melatonin-killing, computer-screen-staring, tragic work-life imbalances explain away a lot of it. Knowing that, though, patients in front of me seek immediate relief.

A prescription takes substantially less effort than does training patients on sleep hygiene or sleep restriction. The problem with “z” drugs is, of course, that tolerance can develop within 4 weeks with daily use. These drugs have been associated with mood and cognitive changes and increased mortality. Many of my patients cannot use them sparingly, because relief of insomnia is something of which they cannot get enough. Then we are either back to square one or playing the dose-escalation game.

I have always wondered how much of this is the “placebo effect” and how we could use this to our clinical advantage. This is certainly what I hear from my cynical colleagues when I recommend melatonin – which, by the way, I personally believe is an extremely effective and underutilized intervention. We should remind ourselves to be cognizant of the “if I can’t prescribe it, it can’t work that well” mentality.

Alexander Winkler and Winfried Rief of the University of Marburg, Germany, conducted a brilliant systematic review examining the effect of placebo conditions in randomized trials including polysomnography addressing primary insomnia (Sleep. 2015 Jun 1;38[6]:925-31).

The investigators identified 32 studies with almost 4,000 patients in 82 treatment conditions: The studies were published between 1992 and 2012. Of those 82 treatment conditions, 17 included hypnotic drugs.

Results suggest that 64% of drug response to medications for primary insomnia is achieved in the placebo group.

So what does this mean clinically? I think the first thing it means is that we should consider (re)launching frank discourse about the ethics surrounding the use of placebo in clinical medicine. Are we all too horrified to think that patients may get better despite us rather than because of us to dig too deeply here?

The second thing it means is that patients should be instructed to use the medications only when needed. If a minority of the drug effect for insomnia is from the drug itself, we should minimize the buildup of tolerance by using it sparingly. Studies that have alternated a hypnotic with a placebo show that this works just as well as using a hypnotic every night.

Patients should be encouraged to alternate therapy, such as trying melatonin first and resorting to a “z” drug only if sleep remains elusive. Alternating drug therapy may also enhance the efficacy of the medication.

Always try to combine pharmacotherapy with good sleep hygiene to maximize benefits.

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 financial disclosures about this article. Follow him on Twitter @jonebbert.

Is it just me? I don’t think that I have visited with a single patient this week who’s not struggling with sleep. Our heavily caffeinated, media-obsessed, melatonin-killing, computer-screen-staring, tragic work-life imbalances explain away a lot of it. Knowing that, though, patients in front of me seek immediate relief.

A prescription takes substantially less effort than does training patients on sleep hygiene or sleep restriction. The problem with “z” drugs is, of course, that tolerance can develop within 4 weeks with daily use. These drugs have been associated with mood and cognitive changes and increased mortality. Many of my patients cannot use them sparingly, because relief of insomnia is something of which they cannot get enough. Then we are either back to square one or playing the dose-escalation game.

I have always wondered how much of this is the “placebo effect” and how we could use this to our clinical advantage. This is certainly what I hear from my cynical colleagues when I recommend melatonin – which, by the way, I personally believe is an extremely effective and underutilized intervention. We should remind ourselves to be cognizant of the “if I can’t prescribe it, it can’t work that well” mentality.

Alexander Winkler and Winfried Rief of the University of Marburg, Germany, conducted a brilliant systematic review examining the effect of placebo conditions in randomized trials including polysomnography addressing primary insomnia (Sleep. 2015 Jun 1;38[6]:925-31).

The investigators identified 32 studies with almost 4,000 patients in 82 treatment conditions: The studies were published between 1992 and 2012. Of those 82 treatment conditions, 17 included hypnotic drugs.

Results suggest that 64% of drug response to medications for primary insomnia is achieved in the placebo group.

So what does this mean clinically? I think the first thing it means is that we should consider (re)launching frank discourse about the ethics surrounding the use of placebo in clinical medicine. Are we all too horrified to think that patients may get better despite us rather than because of us to dig too deeply here?

The second thing it means is that patients should be instructed to use the medications only when needed. If a minority of the drug effect for insomnia is from the drug itself, we should minimize the buildup of tolerance by using it sparingly. Studies that have alternated a hypnotic with a placebo show that this works just as well as using a hypnotic every night.

Patients should be encouraged to alternate therapy, such as trying melatonin first and resorting to a “z” drug only if sleep remains elusive. Alternating drug therapy may also enhance the efficacy of the medication.

Always try to combine pharmacotherapy with good sleep hygiene to maximize benefits.

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 financial disclosures about this article. Follow him on Twitter @jonebbert.

Functional, a.k.a. “nonulcer,” dyspepsia is a challenging diagnosis and likely afflicts many more patients than we have identified in our practices. Functional dyspepsia (FD) is defined by the presence of postprandial fullness, early satiety, epigastric pain or burning, and no evidence of structural disease. These are the patients who do not get better with proton pump inhibitors or feel better after a bowel movement.

After a negative upper endoscopy and Helicobacter pylori stool antigen test, the task turns to symptom control. But what’s the best treatment?

Dr. Nicholas J. Talley of the University of Newcastle in Callaghan, Australia, and colleagues conducted a multicenter, randomized trial evaluating the comparative efficacy of amitriptyline or escitalopram for symptom control, gastric emptying, and meal-induced satiety in patients with FD (Gastroenterology. 2015;149(2):340-9.e2).

Participants were enrolled if they met Rome II criteria for FD requiring that folks in the preceding 12 months have at least 12 weeks of dyspepsia, absence of organic disease, and no relationship to defecation. Patients were randomized to placebo, amitriptyline 50 mg (titrated), or escitalopram 10 mg. Medication was given for 10 weeks. The primary endpoint was adequate relief of symptoms for at least 5 weeks.

A total of 292 patients (most of whom [75%] were female) with an average age of 44 years were randomized. Seventy percent had dysmotility-like FD and 30% had ulcer-like FD.

Patients with ulcer-like FD receiving amitriptyline were more likely to report adequate relief (odds ratio, 3.1; 95% confidence interval, 1.1-9.0). Neither medication affected gastric emptying or meal-induced satiety. Both medications improved overall quality of life.

The data support the use of amitriptyline for ulcer-like FD. Some of these patients may have comorbid psychiatric illness that may be improved with escitalopram. Perhaps this is what is impacting the quality-of-life metric that taps into dimensions above and beyond relief of symptoms (such as sleep disturbance or work/study).

Proton pump inhibitors tend to be overused, and many of our patients take them indefinitely without trying to see how they do off of them. Some patients for whom we have not considered a diagnosis of FD may be on PPIs because we have had nothing else to offer them. Maybe they felt better because of a PPI placebo effect and we have continued them.

If we can, we should review the diagnosis of dyspepsia, consider FD as a possibility etiology for gastrointestinal distress, stop the PPIs, and try amitriptyline.

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 financial disclosures about this article. Follow him on Twitter @jonebbert.

Functional, a.k.a. “nonulcer,” dyspepsia is a challenging diagnosis and likely afflicts many more patients than we have identified in our practices. Functional dyspepsia (FD) is defined by the presence of postprandial fullness, early satiety, epigastric pain or burning, and no evidence of structural disease. These are the patients who do not get better with proton pump inhibitors or feel better after a bowel movement.

After a negative upper endoscopy and Helicobacter pylori stool antigen test, the task turns to symptom control. But what’s the best treatment?

Dr. Nicholas J. Talley of the University of Newcastle in Callaghan, Australia, and colleagues conducted a multicenter, randomized trial evaluating the comparative efficacy of amitriptyline or escitalopram for symptom control, gastric emptying, and meal-induced satiety in patients with FD (Gastroenterology. 2015;149(2):340-9.e2).

Participants were enrolled if they met Rome II criteria for FD requiring that folks in the preceding 12 months have at least 12 weeks of dyspepsia, absence of organic disease, and no relationship to defecation. Patients were randomized to placebo, amitriptyline 50 mg (titrated), or escitalopram 10 mg. Medication was given for 10 weeks. The primary endpoint was adequate relief of symptoms for at least 5 weeks.

A total of 292 patients (most of whom [75%] were female) with an average age of 44 years were randomized. Seventy percent had dysmotility-like FD and 30% had ulcer-like FD.

Patients with ulcer-like FD receiving amitriptyline were more likely to report adequate relief (odds ratio, 3.1; 95% confidence interval, 1.1-9.0). Neither medication affected gastric emptying or meal-induced satiety. Both medications improved overall quality of life.

The data support the use of amitriptyline for ulcer-like FD. Some of these patients may have comorbid psychiatric illness that may be improved with escitalopram. Perhaps this is what is impacting the quality-of-life metric that taps into dimensions above and beyond relief of symptoms (such as sleep disturbance or work/study).

Proton pump inhibitors tend to be overused, and many of our patients take them indefinitely without trying to see how they do off of them. Some patients for whom we have not considered a diagnosis of FD may be on PPIs because we have had nothing else to offer them. Maybe they felt better because of a PPI placebo effect and we have continued them.

If we can, we should review the diagnosis of dyspepsia, consider FD as a possibility etiology for gastrointestinal distress, stop the PPIs, and try amitriptyline.

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 financial disclosures about this article. Follow him on Twitter @jonebbert.

Functional, a.k.a. “nonulcer,” dyspepsia is a challenging diagnosis and likely afflicts many more patients than we have identified in our practices. Functional dyspepsia (FD) is defined by the presence of postprandial fullness, early satiety, epigastric pain or burning, and no evidence of structural disease. These are the patients who do not get better with proton pump inhibitors or feel better after a bowel movement.

After a negative upper endoscopy and Helicobacter pylori stool antigen test, the task turns to symptom control. But what’s the best treatment?

Dr. Nicholas J. Talley of the University of Newcastle in Callaghan, Australia, and colleagues conducted a multicenter, randomized trial evaluating the comparative efficacy of amitriptyline or escitalopram for symptom control, gastric emptying, and meal-induced satiety in patients with FD (Gastroenterology. 2015;149(2):340-9.e2).

Participants were enrolled if they met Rome II criteria for FD requiring that folks in the preceding 12 months have at least 12 weeks of dyspepsia, absence of organic disease, and no relationship to defecation. Patients were randomized to placebo, amitriptyline 50 mg (titrated), or escitalopram 10 mg. Medication was given for 10 weeks. The primary endpoint was adequate relief of symptoms for at least 5 weeks.

A total of 292 patients (most of whom [75%] were female) with an average age of 44 years were randomized. Seventy percent had dysmotility-like FD and 30% had ulcer-like FD.

Patients with ulcer-like FD receiving amitriptyline were more likely to report adequate relief (odds ratio, 3.1; 95% confidence interval, 1.1-9.0). Neither medication affected gastric emptying or meal-induced satiety. Both medications improved overall quality of life.

The data support the use of amitriptyline for ulcer-like FD. Some of these patients may have comorbid psychiatric illness that may be improved with escitalopram. Perhaps this is what is impacting the quality-of-life metric that taps into dimensions above and beyond relief of symptoms (such as sleep disturbance or work/study).

Proton pump inhibitors tend to be overused, and many of our patients take them indefinitely without trying to see how they do off of them. Some patients for whom we have not considered a diagnosis of FD may be on PPIs because we have had nothing else to offer them. Maybe they felt better because of a PPI placebo effect and we have continued them.

If we can, we should review the diagnosis of dyspepsia, consider FD as a possibility etiology for gastrointestinal distress, stop the PPIs, and try amitriptyline.

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 financial disclosures about this article. Follow him on Twitter @jonebbert.