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Crisis in Medicine: Have We Traded Technology for Our Six Senses?
Technology creates change, and change is moving fast and is relentless. Physicians, on the other hand, are generally slow to change. Wisely, we question change—we observe it, we study it, and we try to ensure our patients will benefit from it over time. Maybe as a result of this or as a consequence of our often myopic view of the world, we mistakenly let others lead the way and dictate how we must change and what our practices must absorb. We must turn this around and be the agents of change for our profession so we can appropriately use the available technology and create systems for managing the demands of a society that expects instant answers with fewer doctor resources devoted to the answer. The insurance industry is encouraging a wholesale dismantling of the classic patient visit to be replaced by nonphysician interactions, virtual diagnostics, and electronic medical records. We must not allow this and must ensure that we safeguard our profession by employing traditional skills, utilizing our 5 senses, and incorporating technology as a tool for better diagnosis and treatment but not as a substitute for the same.
Great doctors are often described as having a sixth sense—an intuition that guides them in diagnosing and treating patients. It is assumed, therefore, that the good doctor will have the benefit of 5 senses: sight, sound, touch, smell, and taste. Sound: What does the patient tell or neglect to tell the doctor? What sounds does a joint produce when it moves? Sight: How does the patient present? Are they weary from pain or chronic disease? Touch: What does the joint feel like? How does it move? What is the patient’s response to stabilization of a joint? Smell: Is there an odor that helps detect the presence of infection or decay? Is the patient coming into contact with a substance causing harm or preventing healing?
A good doctor must employ these senses first to understand the patient’s needs and then to treat the patient. The sixth sense is a gift, one that comes from years of experience, an attention to detail, and a commitment to the craft of medicine. A recent trend toward virtual medicine is a dangerous path that must be walked with care and discretion so that the 6 senses are maintained and nurtured. Technology must be used to enhance and not limit these senses. The patient cannot be reduced to a 2-dimensional version of his/herself so that the doctor’s powers of diagnosis and healing are similarly limited.
Change in the office has occurred with mandates for electronic medical records and work-hour restrictions for residents. Data do not support that either change has resulted in a net benefit to patients. We are mandated to invest scarce capital to support new technology, resulting in increased pressure to recoup investment. Where there is a cap on revenue, the only way to increase net profit is to increase volume and decrease services. Physician time is the variable and can be streamlined by performing video conferences or smartphone consultations. Change may bring higher order, as the English philosopher John Locke said, but it is time for all of us as physicians to step back and question that this type of change is the path we must take. An office with a schedule of 80 patients seen at 5-minute intervals by physician assistants has no place in medicine. The pressure imposed by the insurance industry or hospital administrators to meet quotas has gotten out of hand and the time is now to say with a strong but fair voice a resounding NO!
The office visit with a history and physical examination is the most exciting and effective time to meet, console, and relate to our patients. The use of the 5 senses is critical. We must not let technological advancements (eg, smartphones, the Internet, and electronic medical records) destroy what was created and taught to us all through our training. The reward that is accomplished by placing one’s hand on a patient’s knee to understand its warmth and swelling, the tactile feeling of a fluid wave, or performing carefully with compassion a provocative maneuver that gives by sight a grimace of discomfort can tell so much more than a status update on the phone. We must not allow ourselves to be replaced by ancillary services for so-called efficiency and cost saving. Rather, we must be innovative and sharp. We must find the way to use the wonders of the virtual world without giving up the human consult.
Imagine that you are able to travel to Iguazu Falls, South America, to see one of the wonders of our world. You sit in that life raft moving upstream to feel the heat from the water as it crushes the rocks below, and you feel the mist on your face. You see the majesty and hear the screams and breadth of excitement of those around you, while you listen to the deafening sounds created by this waterfall. Now imagine you are required to report on this same experience through a video or some form of technology that the world has convinced us is the best and far cheaper substitute. This is our electronic medical record. A tool we are forced to use, and while it has a purpose, it is a sterile tool that fails to provide information that will give clues to awaken the sixth sense. It is a checklist that could allow for completion of a task—like how to fix a leaky faucet.
How then do we accomplish walking the fine line of working with nonphysicians and technology and yet delivering pinnacle care? The answer isn’t simple but it must include education and a commitment to the profession. We must make the public aware that we are one of the few professions that dedicate our lives to others by promoting health and advancing research. My colleagues, the pendulum has swung too far; it is time to take back our great profession through education of ourselves and the public. While technology may help the world connect, it has a limited role unless we first use our 6 senses to help our patients. We must not submit to a compassionless and callous approach that is the inevitable outcome of virtual medicine done with speed. We must maintain our dignity and let the public understand how many years of sacrifice has taken place to earn a sixth sense and not allow a third party to take it away. We are the only source of protection for our patients and we need each one of our senses to perform this task.
Advancing research has been a cornerstone for the orthopedic surgeon. Position statements through meta-analyses and systematic reviews of the literature have recently been utilized with increasing frequency. Combining data of potentially flawed studies can often lead to erroneous conclusions and may stray away from best practices. Is this where we want evidence-based medicine to go? The end result is that decisions are made by insurance companies who rely on these flawed studies to force clinical decisions on the physician, as was most recently seen by the investigation of viscosupplementation for knee osteoarthritis.1
In a 2007 study published in JAMA (The Journal of the American Medical Association), only 62% of residents could appropriately interpret a P value.2 How can we expect young clinicians to evaluate, interpret, and apply the multitude of evidence in the literature to everyday practice? We must marry the use of best evidence with our expertise to make the most informed decision while managing the expectations of our patients. In order to achieve that balance, we must rely on our intuition, our sixth sense. There is too much patient individuality and complexity surrounding each individual’s situation for a one-size-fits-all approach and for wholesale reliance on research to address each unique situation.
If Nathan Davis in 1845 was able to convince the New York Medical Society to establish a nationwide professional association to assist in regulating the practice of medicine, then it is time for all of us to stand up and insist on a code of ethics that is unrelenting and uncompromising. Our wise leaders of the American Orthopaedic Association (AOA) who founded the formation of orthopedics in America knew guidelines were needed to “foster advances in the care of patients, improve the teaching of orthopaedic surgery in medical schools and formal orthopaedic training, and to promote orthopaedic surgery as a surgical discipline worldwide.”3 It is now our turn to renew the guidelines and encourage our leaders to help educate ourselves and patients as we work with technology and administrators, nurses and physician assistants to deliver pinnacle care. We must reform medical education and the practice of medicine so that technology is used as a companion but not a substitute for our 6 senses.
The next time a patient comes into the exam room, sit down, look the patient in the eye, listen, touch, console anxiety, make a human connection, and form a lasting relationship. By all means apologize to your patients as you fill out the electronic medical record and insurance forms. Discuss how we are in the same crisis together and ask for their help as they have come to you for yours.
1. Jevsevar DS. Treatment of osteoarthritis of the knee: evidence-based guideline, 2nd edition. J Am Acad Orthop Surg. 2013;21(9):571-576.
2. Windish DM, Huot SJ, Green ML. Medicine residents’ understanding of the biostatistics and results in the medical literature. JAMA. 2007;298(9):1010-1022.
3. DeRosa GP. 75 Years of Doing the Right Thing: A History of the American Board of Orthopaedic Surgery. American Board of Orthopaedic Surgery; 2009.
Technology creates change, and change is moving fast and is relentless. Physicians, on the other hand, are generally slow to change. Wisely, we question change—we observe it, we study it, and we try to ensure our patients will benefit from it over time. Maybe as a result of this or as a consequence of our often myopic view of the world, we mistakenly let others lead the way and dictate how we must change and what our practices must absorb. We must turn this around and be the agents of change for our profession so we can appropriately use the available technology and create systems for managing the demands of a society that expects instant answers with fewer doctor resources devoted to the answer. The insurance industry is encouraging a wholesale dismantling of the classic patient visit to be replaced by nonphysician interactions, virtual diagnostics, and electronic medical records. We must not allow this and must ensure that we safeguard our profession by employing traditional skills, utilizing our 5 senses, and incorporating technology as a tool for better diagnosis and treatment but not as a substitute for the same.
Great doctors are often described as having a sixth sense—an intuition that guides them in diagnosing and treating patients. It is assumed, therefore, that the good doctor will have the benefit of 5 senses: sight, sound, touch, smell, and taste. Sound: What does the patient tell or neglect to tell the doctor? What sounds does a joint produce when it moves? Sight: How does the patient present? Are they weary from pain or chronic disease? Touch: What does the joint feel like? How does it move? What is the patient’s response to stabilization of a joint? Smell: Is there an odor that helps detect the presence of infection or decay? Is the patient coming into contact with a substance causing harm or preventing healing?
A good doctor must employ these senses first to understand the patient’s needs and then to treat the patient. The sixth sense is a gift, one that comes from years of experience, an attention to detail, and a commitment to the craft of medicine. A recent trend toward virtual medicine is a dangerous path that must be walked with care and discretion so that the 6 senses are maintained and nurtured. Technology must be used to enhance and not limit these senses. The patient cannot be reduced to a 2-dimensional version of his/herself so that the doctor’s powers of diagnosis and healing are similarly limited.
Change in the office has occurred with mandates for electronic medical records and work-hour restrictions for residents. Data do not support that either change has resulted in a net benefit to patients. We are mandated to invest scarce capital to support new technology, resulting in increased pressure to recoup investment. Where there is a cap on revenue, the only way to increase net profit is to increase volume and decrease services. Physician time is the variable and can be streamlined by performing video conferences or smartphone consultations. Change may bring higher order, as the English philosopher John Locke said, but it is time for all of us as physicians to step back and question that this type of change is the path we must take. An office with a schedule of 80 patients seen at 5-minute intervals by physician assistants has no place in medicine. The pressure imposed by the insurance industry or hospital administrators to meet quotas has gotten out of hand and the time is now to say with a strong but fair voice a resounding NO!
The office visit with a history and physical examination is the most exciting and effective time to meet, console, and relate to our patients. The use of the 5 senses is critical. We must not let technological advancements (eg, smartphones, the Internet, and electronic medical records) destroy what was created and taught to us all through our training. The reward that is accomplished by placing one’s hand on a patient’s knee to understand its warmth and swelling, the tactile feeling of a fluid wave, or performing carefully with compassion a provocative maneuver that gives by sight a grimace of discomfort can tell so much more than a status update on the phone. We must not allow ourselves to be replaced by ancillary services for so-called efficiency and cost saving. Rather, we must be innovative and sharp. We must find the way to use the wonders of the virtual world without giving up the human consult.
Imagine that you are able to travel to Iguazu Falls, South America, to see one of the wonders of our world. You sit in that life raft moving upstream to feel the heat from the water as it crushes the rocks below, and you feel the mist on your face. You see the majesty and hear the screams and breadth of excitement of those around you, while you listen to the deafening sounds created by this waterfall. Now imagine you are required to report on this same experience through a video or some form of technology that the world has convinced us is the best and far cheaper substitute. This is our electronic medical record. A tool we are forced to use, and while it has a purpose, it is a sterile tool that fails to provide information that will give clues to awaken the sixth sense. It is a checklist that could allow for completion of a task—like how to fix a leaky faucet.
How then do we accomplish walking the fine line of working with nonphysicians and technology and yet delivering pinnacle care? The answer isn’t simple but it must include education and a commitment to the profession. We must make the public aware that we are one of the few professions that dedicate our lives to others by promoting health and advancing research. My colleagues, the pendulum has swung too far; it is time to take back our great profession through education of ourselves and the public. While technology may help the world connect, it has a limited role unless we first use our 6 senses to help our patients. We must not submit to a compassionless and callous approach that is the inevitable outcome of virtual medicine done with speed. We must maintain our dignity and let the public understand how many years of sacrifice has taken place to earn a sixth sense and not allow a third party to take it away. We are the only source of protection for our patients and we need each one of our senses to perform this task.
Advancing research has been a cornerstone for the orthopedic surgeon. Position statements through meta-analyses and systematic reviews of the literature have recently been utilized with increasing frequency. Combining data of potentially flawed studies can often lead to erroneous conclusions and may stray away from best practices. Is this where we want evidence-based medicine to go? The end result is that decisions are made by insurance companies who rely on these flawed studies to force clinical decisions on the physician, as was most recently seen by the investigation of viscosupplementation for knee osteoarthritis.1
In a 2007 study published in JAMA (The Journal of the American Medical Association), only 62% of residents could appropriately interpret a P value.2 How can we expect young clinicians to evaluate, interpret, and apply the multitude of evidence in the literature to everyday practice? We must marry the use of best evidence with our expertise to make the most informed decision while managing the expectations of our patients. In order to achieve that balance, we must rely on our intuition, our sixth sense. There is too much patient individuality and complexity surrounding each individual’s situation for a one-size-fits-all approach and for wholesale reliance on research to address each unique situation.
If Nathan Davis in 1845 was able to convince the New York Medical Society to establish a nationwide professional association to assist in regulating the practice of medicine, then it is time for all of us to stand up and insist on a code of ethics that is unrelenting and uncompromising. Our wise leaders of the American Orthopaedic Association (AOA) who founded the formation of orthopedics in America knew guidelines were needed to “foster advances in the care of patients, improve the teaching of orthopaedic surgery in medical schools and formal orthopaedic training, and to promote orthopaedic surgery as a surgical discipline worldwide.”3 It is now our turn to renew the guidelines and encourage our leaders to help educate ourselves and patients as we work with technology and administrators, nurses and physician assistants to deliver pinnacle care. We must reform medical education and the practice of medicine so that technology is used as a companion but not a substitute for our 6 senses.
The next time a patient comes into the exam room, sit down, look the patient in the eye, listen, touch, console anxiety, make a human connection, and form a lasting relationship. By all means apologize to your patients as you fill out the electronic medical record and insurance forms. Discuss how we are in the same crisis together and ask for their help as they have come to you for yours.
Technology creates change, and change is moving fast and is relentless. Physicians, on the other hand, are generally slow to change. Wisely, we question change—we observe it, we study it, and we try to ensure our patients will benefit from it over time. Maybe as a result of this or as a consequence of our often myopic view of the world, we mistakenly let others lead the way and dictate how we must change and what our practices must absorb. We must turn this around and be the agents of change for our profession so we can appropriately use the available technology and create systems for managing the demands of a society that expects instant answers with fewer doctor resources devoted to the answer. The insurance industry is encouraging a wholesale dismantling of the classic patient visit to be replaced by nonphysician interactions, virtual diagnostics, and electronic medical records. We must not allow this and must ensure that we safeguard our profession by employing traditional skills, utilizing our 5 senses, and incorporating technology as a tool for better diagnosis and treatment but not as a substitute for the same.
Great doctors are often described as having a sixth sense—an intuition that guides them in diagnosing and treating patients. It is assumed, therefore, that the good doctor will have the benefit of 5 senses: sight, sound, touch, smell, and taste. Sound: What does the patient tell or neglect to tell the doctor? What sounds does a joint produce when it moves? Sight: How does the patient present? Are they weary from pain or chronic disease? Touch: What does the joint feel like? How does it move? What is the patient’s response to stabilization of a joint? Smell: Is there an odor that helps detect the presence of infection or decay? Is the patient coming into contact with a substance causing harm or preventing healing?
A good doctor must employ these senses first to understand the patient’s needs and then to treat the patient. The sixth sense is a gift, one that comes from years of experience, an attention to detail, and a commitment to the craft of medicine. A recent trend toward virtual medicine is a dangerous path that must be walked with care and discretion so that the 6 senses are maintained and nurtured. Technology must be used to enhance and not limit these senses. The patient cannot be reduced to a 2-dimensional version of his/herself so that the doctor’s powers of diagnosis and healing are similarly limited.
Change in the office has occurred with mandates for electronic medical records and work-hour restrictions for residents. Data do not support that either change has resulted in a net benefit to patients. We are mandated to invest scarce capital to support new technology, resulting in increased pressure to recoup investment. Where there is a cap on revenue, the only way to increase net profit is to increase volume and decrease services. Physician time is the variable and can be streamlined by performing video conferences or smartphone consultations. Change may bring higher order, as the English philosopher John Locke said, but it is time for all of us as physicians to step back and question that this type of change is the path we must take. An office with a schedule of 80 patients seen at 5-minute intervals by physician assistants has no place in medicine. The pressure imposed by the insurance industry or hospital administrators to meet quotas has gotten out of hand and the time is now to say with a strong but fair voice a resounding NO!
The office visit with a history and physical examination is the most exciting and effective time to meet, console, and relate to our patients. The use of the 5 senses is critical. We must not let technological advancements (eg, smartphones, the Internet, and electronic medical records) destroy what was created and taught to us all through our training. The reward that is accomplished by placing one’s hand on a patient’s knee to understand its warmth and swelling, the tactile feeling of a fluid wave, or performing carefully with compassion a provocative maneuver that gives by sight a grimace of discomfort can tell so much more than a status update on the phone. We must not allow ourselves to be replaced by ancillary services for so-called efficiency and cost saving. Rather, we must be innovative and sharp. We must find the way to use the wonders of the virtual world without giving up the human consult.
Imagine that you are able to travel to Iguazu Falls, South America, to see one of the wonders of our world. You sit in that life raft moving upstream to feel the heat from the water as it crushes the rocks below, and you feel the mist on your face. You see the majesty and hear the screams and breadth of excitement of those around you, while you listen to the deafening sounds created by this waterfall. Now imagine you are required to report on this same experience through a video or some form of technology that the world has convinced us is the best and far cheaper substitute. This is our electronic medical record. A tool we are forced to use, and while it has a purpose, it is a sterile tool that fails to provide information that will give clues to awaken the sixth sense. It is a checklist that could allow for completion of a task—like how to fix a leaky faucet.
How then do we accomplish walking the fine line of working with nonphysicians and technology and yet delivering pinnacle care? The answer isn’t simple but it must include education and a commitment to the profession. We must make the public aware that we are one of the few professions that dedicate our lives to others by promoting health and advancing research. My colleagues, the pendulum has swung too far; it is time to take back our great profession through education of ourselves and the public. While technology may help the world connect, it has a limited role unless we first use our 6 senses to help our patients. We must not submit to a compassionless and callous approach that is the inevitable outcome of virtual medicine done with speed. We must maintain our dignity and let the public understand how many years of sacrifice has taken place to earn a sixth sense and not allow a third party to take it away. We are the only source of protection for our patients and we need each one of our senses to perform this task.
Advancing research has been a cornerstone for the orthopedic surgeon. Position statements through meta-analyses and systematic reviews of the literature have recently been utilized with increasing frequency. Combining data of potentially flawed studies can often lead to erroneous conclusions and may stray away from best practices. Is this where we want evidence-based medicine to go? The end result is that decisions are made by insurance companies who rely on these flawed studies to force clinical decisions on the physician, as was most recently seen by the investigation of viscosupplementation for knee osteoarthritis.1
In a 2007 study published in JAMA (The Journal of the American Medical Association), only 62% of residents could appropriately interpret a P value.2 How can we expect young clinicians to evaluate, interpret, and apply the multitude of evidence in the literature to everyday practice? We must marry the use of best evidence with our expertise to make the most informed decision while managing the expectations of our patients. In order to achieve that balance, we must rely on our intuition, our sixth sense. There is too much patient individuality and complexity surrounding each individual’s situation for a one-size-fits-all approach and for wholesale reliance on research to address each unique situation.
If Nathan Davis in 1845 was able to convince the New York Medical Society to establish a nationwide professional association to assist in regulating the practice of medicine, then it is time for all of us to stand up and insist on a code of ethics that is unrelenting and uncompromising. Our wise leaders of the American Orthopaedic Association (AOA) who founded the formation of orthopedics in America knew guidelines were needed to “foster advances in the care of patients, improve the teaching of orthopaedic surgery in medical schools and formal orthopaedic training, and to promote orthopaedic surgery as a surgical discipline worldwide.”3 It is now our turn to renew the guidelines and encourage our leaders to help educate ourselves and patients as we work with technology and administrators, nurses and physician assistants to deliver pinnacle care. We must reform medical education and the practice of medicine so that technology is used as a companion but not a substitute for our 6 senses.
The next time a patient comes into the exam room, sit down, look the patient in the eye, listen, touch, console anxiety, make a human connection, and form a lasting relationship. By all means apologize to your patients as you fill out the electronic medical record and insurance forms. Discuss how we are in the same crisis together and ask for their help as they have come to you for yours.
1. Jevsevar DS. Treatment of osteoarthritis of the knee: evidence-based guideline, 2nd edition. J Am Acad Orthop Surg. 2013;21(9):571-576.
2. Windish DM, Huot SJ, Green ML. Medicine residents’ understanding of the biostatistics and results in the medical literature. JAMA. 2007;298(9):1010-1022.
3. DeRosa GP. 75 Years of Doing the Right Thing: A History of the American Board of Orthopaedic Surgery. American Board of Orthopaedic Surgery; 2009.
1. Jevsevar DS. Treatment of osteoarthritis of the knee: evidence-based guideline, 2nd edition. J Am Acad Orthop Surg. 2013;21(9):571-576.
2. Windish DM, Huot SJ, Green ML. Medicine residents’ understanding of the biostatistics and results in the medical literature. JAMA. 2007;298(9):1010-1022.
3. DeRosa GP. 75 Years of Doing the Right Thing: A History of the American Board of Orthopaedic Surgery. American Board of Orthopaedic Surgery; 2009.
Timing of lifestyle interventions for obesity
Obesity has become so pervasive that it is now considered a major health concern during pregnancy. Almost 56% of women aged 20-39 years in the United States are overweight or obese, based on the World Health Organization’s criteria for body mass index (BMI) and data from the 2009-2010 National Health and Nutrition Examination Survey (NHANES). Moreover, 7.5% of women in this age group are morbidly obese, with a body mass index (BMI) greater than 40 kg/m2 (JAMA 2012;307:491-7).
Obesity in pregnancy not only increases the risk of spontaneous abortions and congenital anomalies, it also increases the risk of gestational diabetes (GDM), hypertensive disorders, and other metabolic complications that affect both the mother and fetus.
Of much concern is the increased risk of fetal overgrowth and long-term health consequences for children of obese mothers. Obesity in early pregnancy has been shown to more than double the risk of obesity in the offspring, which in turn puts these children at risk for developing the metabolic syndrome – and, as Dr. Thomas Moore pointed out in September’s Master Class – appears to program these offspring for downstream cardiovascular risk in adulthood.
Mean term birth weights have risen in the United States during the past several decades. In Cleveland, we have seen a significant 116 g increase in mean term birth weight since 1975; this increase encompasses weights from the 5th to the 95th percentiles. Even more concerning is our finding that the ponderal index in our neonatal population has increased because of decreased fetal length over the last decade.
Some recent studies have suggested that the increase in birth weight in the United States has reached a plateau, but our analyses of national trends suggest that such change is secondary to factors such as earlier gestational age of delivery. Concurrently, an alarming number of children and adolescents – 17% of those aged 2-19 years, according to the 2009-2010 NHANES data – are overweight or obese (JAMA 2012;307:483-90).
How to best treat obesity for improved maternal and fetal health has thus become a focus of research. Studies on lifestyle interventions for obese women during pregnancy have aimed to prevent excessive gestational weight gain and decrease adverse perinatal outcomes – mainly macrosomia, GDM, and hypertensive disorders.
However, the results of this recent body of research have been disappointing. Lifestyle interventions initiated during pregnancy have had only limited success in improving perinatal outcomes. The research tells us that while we may be able to reduce excessive gestational weight gain, it is unlikely that we will be successful in reducing fetal overgrowth, GDM, or preeclampsia in obese women.
Moreover, other studies show that it is a high pregravid BMI – not excessive gestational weight gain or the development of GDM – that plays the biggest role in fetal overgrowth and fetal adiposity.
A paradigm shift is in order. We must think about lifestyle intervention and weight loss before pregnancy, when the woman’s metabolic condition can be improved in time to minimize adverse perinatal metabolic outcomes and to maximize metabolic benefits relating to fetal body composition and metabolism.
Role of prepregnancy BMI
In 2008, the Institute of Medicine (IOM) and National Research Council reexamined 1990 guidelines for gestational weight gain. They concluded that excessive weight gain in pregnancy was a primary contributor to the development of obesity in women. In fact, according to the 2009 IOM report, “Weight Gain During Pregnancy: Reexamining the Guidelines” (Washington: National Academy Press, 2009), 38% of normal weight, 63% of overweight, and 46% of obese women had gained weight in excess of the earlier guidelines.
Helping our patients to gain within the guidelines is important. Excessive gestational weight gain is a primary risk factor for maternal postpartum weight retention, which increases the risk for maternal obesity in a subsequent pregnancy. It also has been associated with a modest increased risk of preterm birth and development of type 2 diabetes.
Interestingly, however, high gestational weight gain has not been related to an increased risk of fetal overgrowth or macrosomia in many obese women. Increased gestational weight gain is a greater risk for fetal overgrowth in women who are of normal weight prior to pregnancy (J. Clin. Endocrinol. Metab. 2012;97:3648-54).
Our research has found that in overweight and obese women, it is maternal pregravid BMI – and not gestational weight gain – that presents the greatest risk for fetal macrosomia, and more specifically, the greatest risk for fetal obesity. Even when glucose tolerance levels are normal, overweight and obese women have neonates who are heavier and who have significant increases in the percentage of body fat and fat mass (Am. J. Obstet. Gynecol. 2006;195:1100-3).
In an 8-year prospective study of the perinatal risk factors associated with childhood obesity, we similarly found that maternal pregravid BMI – independent of maternal glucose status or gestational weight gain – was the strongest predictor of childhood obesity and metabolic dysfunction (Am. J. Clin. Nutr. 2009;90:1303-13).
Other studies have teased apart the roles of maternal obesity and GDM in long-term health of offspring. This work has found that maternal obesity during pregnancy is associated with metabolic syndrome in the offspring and an increased risk of type 2 diabetes in youth, independent of maternal diabetes during pregnancy. A recent meta-analysis also reported that, although maternal diabetes is associated with an increased BMI z score, this was no longer significant after adjustments were made for prepregnancy BMI (Diabetologia 2011;54:1957-66).
Maternal pregravid obesity, therefore, is not only a risk factor for neonatal adiposity at birth, but also for the longer-term risk of obesity and metabolic dysfunction in the offspring – independent of maternal GDM or excessive gestational weight gain.
Interventions in Pregnancy
Numerous prospective trials have examined lifestyle interventions for obese women during pregnancy. One randomized controlled study of a low glycemic index diet in pregnancy (coined the ROLO study) involved 800 women in Ireland who had previously delivered an infant weighting greater than 4,000 g. Women were randomized to receive the restricted diet or no intervention at 13 weeks. Despite a decrease in gestational weight gain in the intervention group, there were no differences in birth weight, birth weight percentile, ponderal index, or macrosomia between the two groups (BMJ 2012;345:e5605).
Another randomized controlled trial reported by a Danish group involved an intervention that consisted of dietary guidance, free membership in a fitness center, and personal coaching initiated between 10 and 14 weeks of gestation. There was a decrease in gestational weight gain in the intervention group, but paradoxically, the infants in the intervention group also had significantly higher birth weight, compared with controls (Diabetes Care 2011;34:2502-7).
Additionally, there have been at least five meta-analyses published in the past 2 years looking at lifestyle interventions during pregnancy. All have concluded that interventions initiated during pregnancy have limited success in reducing excessive gestational weight gain but not necessarily to within the IOM guidelines. The literature contains scant evidence to support further benefits for infant or maternal health (in other words, fetal overgrowth, GDM, or hypertensive disorders).
A recent Cochrane review also concluded that the results of several randomized controlled trials suggest no significant difference in GDM incidence between women receiving exercise intervention versus routine care.
Just this year, three additional randomized controlled trials of lifestyle interventions during pregnancy were published. Only one, the Treatment of Obese Pregnant Women (TOP) study, showed a modest effect in decreasing gestational weight gain. None found a reduction in GDM or fetal overgrowth.
Focus on prepregnancy
Obesity is an inflammatory condition that increases the risk of insulin resistance, impaired beta-cell function, and abnormal adiponectin concentrations. In pregnancy, maternal obesity and hyperinsulinemia can affect placental growth and gene expression.
We have studied lean and obese women recruited prior to a planned pregnancy, as well as lean and obese women scheduled for elective pregnancy termination in the first trimester. Our research, some of which we reported recently in the American Journal of Physiology , has shown increased expression of lipogenic and inflammatory genes in maternal adipose tissue and in the placenta of obese women in the early first trimester, before any phenotypic change becomes apparent (Am. J. Physiol. Endocrinol. Metab. 2012;303:e832-40).
Specifically, hyperinsulinemia and/or defective insulin action in obese women appears to affect the placental programming of genes relating to adipokine expression and lipid metabolism, as well as mitrochondrial function. Altered inflammatory and lipid pathways affect the availability of nutrients for the fetus and, consequently, the size and body composition of the fetus. Fetal overgrowth and neonatal adiposity can result.
In addition, our research has shown that obese women have decreased insulin suppression of lipolysis in white adipose tissue, which during pregnancy results in improved lipid availability for fetal fat accretion and lipotoxicity.
When interventions aimed at weight loss and improved insulin sensitivity are undertaken before pregnancy or in the period between pregnancies, we have the opportunity to increase fat oxidation and reduce oxidative stress in early pregnancy. We also may be able to limit placental inflammation and favorably affect placental growth and gene expression. By the second trimester, our research suggests, gene expression in the placenta and early molecular changes in the white adipose tissue have already been programmed and cannot be reversed (Am. J. Physiol. Endocrinol. Metab. 2012;303:e832-40).
In studies by our group and others of interpregnancy weight loss or gain, interpregnancy weight loss has been associated with a lower risk of large-for-gestational-age (LGA) infants, whereas interpregnancy weight gain has been associated with an increased risk of LGA. Preliminary work from our group shows that the decrease in birth weight involves primarily fat and not lean mass.
The 2009 IOM guidelines support weight loss before pregnancy and state that overweight women should receive individual preconceptional counseling to improve diet quality, increase physical activity, and normalize weight. Multifaceted interventions do work: In obese nonpregnant individuals, lifestyle interventions, which include an exercise program, diet, and behavioral modification have been shown to be successful in improving insulin sensitivity, inflammation, and overall metabolic function.
According to the IOM report, preconceptional services aimed at achieving a healthy weight before conceiving will represent “a radical change to the care provided to obese women of childbearing age.” With continuing research and accumulating data, however, the concept is gaining traction as a viable paradigm for improving perinatal outcomes, with long-term benefits for both the mother and her baby.
Dr. Catalano reports that he has no disclosures relevant to this Master Class.
Obesity has become so pervasive that it is now considered a major health concern during pregnancy. Almost 56% of women aged 20-39 years in the United States are overweight or obese, based on the World Health Organization’s criteria for body mass index (BMI) and data from the 2009-2010 National Health and Nutrition Examination Survey (NHANES). Moreover, 7.5% of women in this age group are morbidly obese, with a body mass index (BMI) greater than 40 kg/m2 (JAMA 2012;307:491-7).
Obesity in pregnancy not only increases the risk of spontaneous abortions and congenital anomalies, it also increases the risk of gestational diabetes (GDM), hypertensive disorders, and other metabolic complications that affect both the mother and fetus.
Of much concern is the increased risk of fetal overgrowth and long-term health consequences for children of obese mothers. Obesity in early pregnancy has been shown to more than double the risk of obesity in the offspring, which in turn puts these children at risk for developing the metabolic syndrome – and, as Dr. Thomas Moore pointed out in September’s Master Class – appears to program these offspring for downstream cardiovascular risk in adulthood.
Mean term birth weights have risen in the United States during the past several decades. In Cleveland, we have seen a significant 116 g increase in mean term birth weight since 1975; this increase encompasses weights from the 5th to the 95th percentiles. Even more concerning is our finding that the ponderal index in our neonatal population has increased because of decreased fetal length over the last decade.
Some recent studies have suggested that the increase in birth weight in the United States has reached a plateau, but our analyses of national trends suggest that such change is secondary to factors such as earlier gestational age of delivery. Concurrently, an alarming number of children and adolescents – 17% of those aged 2-19 years, according to the 2009-2010 NHANES data – are overweight or obese (JAMA 2012;307:483-90).
How to best treat obesity for improved maternal and fetal health has thus become a focus of research. Studies on lifestyle interventions for obese women during pregnancy have aimed to prevent excessive gestational weight gain and decrease adverse perinatal outcomes – mainly macrosomia, GDM, and hypertensive disorders.
However, the results of this recent body of research have been disappointing. Lifestyle interventions initiated during pregnancy have had only limited success in improving perinatal outcomes. The research tells us that while we may be able to reduce excessive gestational weight gain, it is unlikely that we will be successful in reducing fetal overgrowth, GDM, or preeclampsia in obese women.
Moreover, other studies show that it is a high pregravid BMI – not excessive gestational weight gain or the development of GDM – that plays the biggest role in fetal overgrowth and fetal adiposity.
A paradigm shift is in order. We must think about lifestyle intervention and weight loss before pregnancy, when the woman’s metabolic condition can be improved in time to minimize adverse perinatal metabolic outcomes and to maximize metabolic benefits relating to fetal body composition and metabolism.
Role of prepregnancy BMI
In 2008, the Institute of Medicine (IOM) and National Research Council reexamined 1990 guidelines for gestational weight gain. They concluded that excessive weight gain in pregnancy was a primary contributor to the development of obesity in women. In fact, according to the 2009 IOM report, “Weight Gain During Pregnancy: Reexamining the Guidelines” (Washington: National Academy Press, 2009), 38% of normal weight, 63% of overweight, and 46% of obese women had gained weight in excess of the earlier guidelines.
Helping our patients to gain within the guidelines is important. Excessive gestational weight gain is a primary risk factor for maternal postpartum weight retention, which increases the risk for maternal obesity in a subsequent pregnancy. It also has been associated with a modest increased risk of preterm birth and development of type 2 diabetes.
Interestingly, however, high gestational weight gain has not been related to an increased risk of fetal overgrowth or macrosomia in many obese women. Increased gestational weight gain is a greater risk for fetal overgrowth in women who are of normal weight prior to pregnancy (J. Clin. Endocrinol. Metab. 2012;97:3648-54).
Our research has found that in overweight and obese women, it is maternal pregravid BMI – and not gestational weight gain – that presents the greatest risk for fetal macrosomia, and more specifically, the greatest risk for fetal obesity. Even when glucose tolerance levels are normal, overweight and obese women have neonates who are heavier and who have significant increases in the percentage of body fat and fat mass (Am. J. Obstet. Gynecol. 2006;195:1100-3).
In an 8-year prospective study of the perinatal risk factors associated with childhood obesity, we similarly found that maternal pregravid BMI – independent of maternal glucose status or gestational weight gain – was the strongest predictor of childhood obesity and metabolic dysfunction (Am. J. Clin. Nutr. 2009;90:1303-13).
Other studies have teased apart the roles of maternal obesity and GDM in long-term health of offspring. This work has found that maternal obesity during pregnancy is associated with metabolic syndrome in the offspring and an increased risk of type 2 diabetes in youth, independent of maternal diabetes during pregnancy. A recent meta-analysis also reported that, although maternal diabetes is associated with an increased BMI z score, this was no longer significant after adjustments were made for prepregnancy BMI (Diabetologia 2011;54:1957-66).
Maternal pregravid obesity, therefore, is not only a risk factor for neonatal adiposity at birth, but also for the longer-term risk of obesity and metabolic dysfunction in the offspring – independent of maternal GDM or excessive gestational weight gain.
Interventions in Pregnancy
Numerous prospective trials have examined lifestyle interventions for obese women during pregnancy. One randomized controlled study of a low glycemic index diet in pregnancy (coined the ROLO study) involved 800 women in Ireland who had previously delivered an infant weighting greater than 4,000 g. Women were randomized to receive the restricted diet or no intervention at 13 weeks. Despite a decrease in gestational weight gain in the intervention group, there were no differences in birth weight, birth weight percentile, ponderal index, or macrosomia between the two groups (BMJ 2012;345:e5605).
Another randomized controlled trial reported by a Danish group involved an intervention that consisted of dietary guidance, free membership in a fitness center, and personal coaching initiated between 10 and 14 weeks of gestation. There was a decrease in gestational weight gain in the intervention group, but paradoxically, the infants in the intervention group also had significantly higher birth weight, compared with controls (Diabetes Care 2011;34:2502-7).
Additionally, there have been at least five meta-analyses published in the past 2 years looking at lifestyle interventions during pregnancy. All have concluded that interventions initiated during pregnancy have limited success in reducing excessive gestational weight gain but not necessarily to within the IOM guidelines. The literature contains scant evidence to support further benefits for infant or maternal health (in other words, fetal overgrowth, GDM, or hypertensive disorders).
A recent Cochrane review also concluded that the results of several randomized controlled trials suggest no significant difference in GDM incidence between women receiving exercise intervention versus routine care.
Just this year, three additional randomized controlled trials of lifestyle interventions during pregnancy were published. Only one, the Treatment of Obese Pregnant Women (TOP) study, showed a modest effect in decreasing gestational weight gain. None found a reduction in GDM or fetal overgrowth.
Focus on prepregnancy
Obesity is an inflammatory condition that increases the risk of insulin resistance, impaired beta-cell function, and abnormal adiponectin concentrations. In pregnancy, maternal obesity and hyperinsulinemia can affect placental growth and gene expression.
We have studied lean and obese women recruited prior to a planned pregnancy, as well as lean and obese women scheduled for elective pregnancy termination in the first trimester. Our research, some of which we reported recently in the American Journal of Physiology , has shown increased expression of lipogenic and inflammatory genes in maternal adipose tissue and in the placenta of obese women in the early first trimester, before any phenotypic change becomes apparent (Am. J. Physiol. Endocrinol. Metab. 2012;303:e832-40).
Specifically, hyperinsulinemia and/or defective insulin action in obese women appears to affect the placental programming of genes relating to adipokine expression and lipid metabolism, as well as mitrochondrial function. Altered inflammatory and lipid pathways affect the availability of nutrients for the fetus and, consequently, the size and body composition of the fetus. Fetal overgrowth and neonatal adiposity can result.
In addition, our research has shown that obese women have decreased insulin suppression of lipolysis in white adipose tissue, which during pregnancy results in improved lipid availability for fetal fat accretion and lipotoxicity.
When interventions aimed at weight loss and improved insulin sensitivity are undertaken before pregnancy or in the period between pregnancies, we have the opportunity to increase fat oxidation and reduce oxidative stress in early pregnancy. We also may be able to limit placental inflammation and favorably affect placental growth and gene expression. By the second trimester, our research suggests, gene expression in the placenta and early molecular changes in the white adipose tissue have already been programmed and cannot be reversed (Am. J. Physiol. Endocrinol. Metab. 2012;303:e832-40).
In studies by our group and others of interpregnancy weight loss or gain, interpregnancy weight loss has been associated with a lower risk of large-for-gestational-age (LGA) infants, whereas interpregnancy weight gain has been associated with an increased risk of LGA. Preliminary work from our group shows that the decrease in birth weight involves primarily fat and not lean mass.
The 2009 IOM guidelines support weight loss before pregnancy and state that overweight women should receive individual preconceptional counseling to improve diet quality, increase physical activity, and normalize weight. Multifaceted interventions do work: In obese nonpregnant individuals, lifestyle interventions, which include an exercise program, diet, and behavioral modification have been shown to be successful in improving insulin sensitivity, inflammation, and overall metabolic function.
According to the IOM report, preconceptional services aimed at achieving a healthy weight before conceiving will represent “a radical change to the care provided to obese women of childbearing age.” With continuing research and accumulating data, however, the concept is gaining traction as a viable paradigm for improving perinatal outcomes, with long-term benefits for both the mother and her baby.
Dr. Catalano reports that he has no disclosures relevant to this Master Class.
Obesity has become so pervasive that it is now considered a major health concern during pregnancy. Almost 56% of women aged 20-39 years in the United States are overweight or obese, based on the World Health Organization’s criteria for body mass index (BMI) and data from the 2009-2010 National Health and Nutrition Examination Survey (NHANES). Moreover, 7.5% of women in this age group are morbidly obese, with a body mass index (BMI) greater than 40 kg/m2 (JAMA 2012;307:491-7).
Obesity in pregnancy not only increases the risk of spontaneous abortions and congenital anomalies, it also increases the risk of gestational diabetes (GDM), hypertensive disorders, and other metabolic complications that affect both the mother and fetus.
Of much concern is the increased risk of fetal overgrowth and long-term health consequences for children of obese mothers. Obesity in early pregnancy has been shown to more than double the risk of obesity in the offspring, which in turn puts these children at risk for developing the metabolic syndrome – and, as Dr. Thomas Moore pointed out in September’s Master Class – appears to program these offspring for downstream cardiovascular risk in adulthood.
Mean term birth weights have risen in the United States during the past several decades. In Cleveland, we have seen a significant 116 g increase in mean term birth weight since 1975; this increase encompasses weights from the 5th to the 95th percentiles. Even more concerning is our finding that the ponderal index in our neonatal population has increased because of decreased fetal length over the last decade.
Some recent studies have suggested that the increase in birth weight in the United States has reached a plateau, but our analyses of national trends suggest that such change is secondary to factors such as earlier gestational age of delivery. Concurrently, an alarming number of children and adolescents – 17% of those aged 2-19 years, according to the 2009-2010 NHANES data – are overweight or obese (JAMA 2012;307:483-90).
How to best treat obesity for improved maternal and fetal health has thus become a focus of research. Studies on lifestyle interventions for obese women during pregnancy have aimed to prevent excessive gestational weight gain and decrease adverse perinatal outcomes – mainly macrosomia, GDM, and hypertensive disorders.
However, the results of this recent body of research have been disappointing. Lifestyle interventions initiated during pregnancy have had only limited success in improving perinatal outcomes. The research tells us that while we may be able to reduce excessive gestational weight gain, it is unlikely that we will be successful in reducing fetal overgrowth, GDM, or preeclampsia in obese women.
Moreover, other studies show that it is a high pregravid BMI – not excessive gestational weight gain or the development of GDM – that plays the biggest role in fetal overgrowth and fetal adiposity.
A paradigm shift is in order. We must think about lifestyle intervention and weight loss before pregnancy, when the woman’s metabolic condition can be improved in time to minimize adverse perinatal metabolic outcomes and to maximize metabolic benefits relating to fetal body composition and metabolism.
Role of prepregnancy BMI
In 2008, the Institute of Medicine (IOM) and National Research Council reexamined 1990 guidelines for gestational weight gain. They concluded that excessive weight gain in pregnancy was a primary contributor to the development of obesity in women. In fact, according to the 2009 IOM report, “Weight Gain During Pregnancy: Reexamining the Guidelines” (Washington: National Academy Press, 2009), 38% of normal weight, 63% of overweight, and 46% of obese women had gained weight in excess of the earlier guidelines.
Helping our patients to gain within the guidelines is important. Excessive gestational weight gain is a primary risk factor for maternal postpartum weight retention, which increases the risk for maternal obesity in a subsequent pregnancy. It also has been associated with a modest increased risk of preterm birth and development of type 2 diabetes.
Interestingly, however, high gestational weight gain has not been related to an increased risk of fetal overgrowth or macrosomia in many obese women. Increased gestational weight gain is a greater risk for fetal overgrowth in women who are of normal weight prior to pregnancy (J. Clin. Endocrinol. Metab. 2012;97:3648-54).
Our research has found that in overweight and obese women, it is maternal pregravid BMI – and not gestational weight gain – that presents the greatest risk for fetal macrosomia, and more specifically, the greatest risk for fetal obesity. Even when glucose tolerance levels are normal, overweight and obese women have neonates who are heavier and who have significant increases in the percentage of body fat and fat mass (Am. J. Obstet. Gynecol. 2006;195:1100-3).
In an 8-year prospective study of the perinatal risk factors associated with childhood obesity, we similarly found that maternal pregravid BMI – independent of maternal glucose status or gestational weight gain – was the strongest predictor of childhood obesity and metabolic dysfunction (Am. J. Clin. Nutr. 2009;90:1303-13).
Other studies have teased apart the roles of maternal obesity and GDM in long-term health of offspring. This work has found that maternal obesity during pregnancy is associated with metabolic syndrome in the offspring and an increased risk of type 2 diabetes in youth, independent of maternal diabetes during pregnancy. A recent meta-analysis also reported that, although maternal diabetes is associated with an increased BMI z score, this was no longer significant after adjustments were made for prepregnancy BMI (Diabetologia 2011;54:1957-66).
Maternal pregravid obesity, therefore, is not only a risk factor for neonatal adiposity at birth, but also for the longer-term risk of obesity and metabolic dysfunction in the offspring – independent of maternal GDM or excessive gestational weight gain.
Interventions in Pregnancy
Numerous prospective trials have examined lifestyle interventions for obese women during pregnancy. One randomized controlled study of a low glycemic index diet in pregnancy (coined the ROLO study) involved 800 women in Ireland who had previously delivered an infant weighting greater than 4,000 g. Women were randomized to receive the restricted diet or no intervention at 13 weeks. Despite a decrease in gestational weight gain in the intervention group, there were no differences in birth weight, birth weight percentile, ponderal index, or macrosomia between the two groups (BMJ 2012;345:e5605).
Another randomized controlled trial reported by a Danish group involved an intervention that consisted of dietary guidance, free membership in a fitness center, and personal coaching initiated between 10 and 14 weeks of gestation. There was a decrease in gestational weight gain in the intervention group, but paradoxically, the infants in the intervention group also had significantly higher birth weight, compared with controls (Diabetes Care 2011;34:2502-7).
Additionally, there have been at least five meta-analyses published in the past 2 years looking at lifestyle interventions during pregnancy. All have concluded that interventions initiated during pregnancy have limited success in reducing excessive gestational weight gain but not necessarily to within the IOM guidelines. The literature contains scant evidence to support further benefits for infant or maternal health (in other words, fetal overgrowth, GDM, or hypertensive disorders).
A recent Cochrane review also concluded that the results of several randomized controlled trials suggest no significant difference in GDM incidence between women receiving exercise intervention versus routine care.
Just this year, three additional randomized controlled trials of lifestyle interventions during pregnancy were published. Only one, the Treatment of Obese Pregnant Women (TOP) study, showed a modest effect in decreasing gestational weight gain. None found a reduction in GDM or fetal overgrowth.
Focus on prepregnancy
Obesity is an inflammatory condition that increases the risk of insulin resistance, impaired beta-cell function, and abnormal adiponectin concentrations. In pregnancy, maternal obesity and hyperinsulinemia can affect placental growth and gene expression.
We have studied lean and obese women recruited prior to a planned pregnancy, as well as lean and obese women scheduled for elective pregnancy termination in the first trimester. Our research, some of which we reported recently in the American Journal of Physiology , has shown increased expression of lipogenic and inflammatory genes in maternal adipose tissue and in the placenta of obese women in the early first trimester, before any phenotypic change becomes apparent (Am. J. Physiol. Endocrinol. Metab. 2012;303:e832-40).
Specifically, hyperinsulinemia and/or defective insulin action in obese women appears to affect the placental programming of genes relating to adipokine expression and lipid metabolism, as well as mitrochondrial function. Altered inflammatory and lipid pathways affect the availability of nutrients for the fetus and, consequently, the size and body composition of the fetus. Fetal overgrowth and neonatal adiposity can result.
In addition, our research has shown that obese women have decreased insulin suppression of lipolysis in white adipose tissue, which during pregnancy results in improved lipid availability for fetal fat accretion and lipotoxicity.
When interventions aimed at weight loss and improved insulin sensitivity are undertaken before pregnancy or in the period between pregnancies, we have the opportunity to increase fat oxidation and reduce oxidative stress in early pregnancy. We also may be able to limit placental inflammation and favorably affect placental growth and gene expression. By the second trimester, our research suggests, gene expression in the placenta and early molecular changes in the white adipose tissue have already been programmed and cannot be reversed (Am. J. Physiol. Endocrinol. Metab. 2012;303:e832-40).
In studies by our group and others of interpregnancy weight loss or gain, interpregnancy weight loss has been associated with a lower risk of large-for-gestational-age (LGA) infants, whereas interpregnancy weight gain has been associated with an increased risk of LGA. Preliminary work from our group shows that the decrease in birth weight involves primarily fat and not lean mass.
The 2009 IOM guidelines support weight loss before pregnancy and state that overweight women should receive individual preconceptional counseling to improve diet quality, increase physical activity, and normalize weight. Multifaceted interventions do work: In obese nonpregnant individuals, lifestyle interventions, which include an exercise program, diet, and behavioral modification have been shown to be successful in improving insulin sensitivity, inflammation, and overall metabolic function.
According to the IOM report, preconceptional services aimed at achieving a healthy weight before conceiving will represent “a radical change to the care provided to obese women of childbearing age.” With continuing research and accumulating data, however, the concept is gaining traction as a viable paradigm for improving perinatal outcomes, with long-term benefits for both the mother and her baby.
Dr. Catalano reports that he has no disclosures relevant to this Master Class.
Team Dynamics
What makes some groups better to work with than others? What makes the work dynamic in some groups more optimistic?
It starts with leadership. Leaders must first know themselves. They must first know their limits and their strengths. They must work on the former while celebrating the latter. A leader must lead. At times a leader can be (and should be) an advocate for the group. But simply advocating for a group is not enough. A leader must take the group down new avenues. A leader must coach the group to better practices. A leader must be the one pioneering new ways of doing things with the intent of improving patient care and provider satisfaction.
Leaders need to be clear with their expectations for hospital medicine. This gives the group the ability to make a conscious choice as to whether or not they wish to stay within the group. If they stay, then it provides the structure for which the group functions. Examples can range from small to big: I expect that you will be at meetings on time; it’s our group’s expectation that you will greet each patient with a smile, handshake, and business card for the first meeting. With the group understanding these expectations, a leader can manage performance and hold providers accountable.
Clear expectations and objectives should be communicated early. They need to be communicated often. In certain instances goals may change. It may be institutional change or changes with Medicare. I often will communicate this change in person once; send an e-mail once and then have a follow-up communication over lunch to answer any questions regarding the change and its implementation. This trio of communication allows me to get the majority of the audience that I need to reach. It gives the audience a “hard copy” in the form of an e-mail to read and also gives the opportunity to answer any questions that I may have overlooked or was not clear with in the other forms of communication.
Ideally, the best time to communicate expectations and objectives is when new providers are hired. New physicians starting in practice need to be trained and adjusted into the team. They need on-boarding, mentors, career coaches, and the opportunity to practice applicable CME early on in the new job. These new additions need to be challenged about their future goals and supported in attaining them. Usually new hospitalists want to get involved in education (medical students or residents), administration, and quality care, or sometimes they just want to practice at becoming better physicians. We all should strive to do the latter always, but some may only want to be clinicians. Either way, all of these goals should be nurtured.
Good training leads to physician participation as an expectation. Participation should not be the stick for which the carrot hangs. Hospitalists need to be on committees and need to have representation at all levels of hospital logistics and tasks. This is how respect and autonomy are gained. And if done properly, this autonomy will receive the support from the highest levels of hospital administration.
With each individual supporting the team (because they are expected to speak on behalf of the group and report back to the group about their findings), the bunch of individuals will start to form a team. What does that mean? An individual hospitalist has her own set of beliefs and practices that makes her unique. If you take a random sampling of hospitalists from many different backgrounds and educational experiences from all over the country (which is any typical hospitalist group), you will have a bunch of individuals. Each hospitalist will come equipped with their own talents and struggles. Now if you take that bunch of individuals and train them in the ways of best practices with good leadership, you can begin to build a functional team. I want to avoid sports analogies, but I think the picture is clearer now than before. See Bad News Bears or Coach Carter. Any team that has clearly stated objectives (expectations/mission statement), that also has good on-boarding and training, will be successful. When the on-boarding process involves mentoring and coaching to help individuals become better administrators, leaders, educators, quality improvers et cetera the team develops together.
One thing that I’ve left out is the logistics of having a good team. Great teams have things like salary, time off, and other benefits included as part of the package. With money and benefits taken off of the table as an issue, the group can focus on things they’ve been trained to focus on: quality patient care. It’s been my opinion that using money to motivate anyone will get the bare minimum performance needed to get the result that leads to the money. So why not take that form of motivation out of the equation? If groups invest in their members, the rewards are greater than rewarding individuals for how many widgets they can churn out of a factory.
With these tools of good leadership, team training and development, excellent communication, and a good salary with benefits, then the expectation of participation and positive feedback should be the norm. A good positive dynamic will develop, and the team will work to support itself. Eventually, a team like this one could become a work-family that could be deployed for specialty care (such as head bleeds and gunshot wounds) as the institution needs it to be deployed. This is provided that this kind of work-family already vetted its concerns and could adapt to those needs. These work-families rely less on the leader to hold everyone accountable and allows the unit to relax together and venture off into creative endeavors for the future. That article is for another time.
Dr. Bitetto is chief for the section of Hospital Medicine at Lehigh Valley Hospital, Allentown, Pa.
What makes some groups better to work with than others? What makes the work dynamic in some groups more optimistic?
It starts with leadership. Leaders must first know themselves. They must first know their limits and their strengths. They must work on the former while celebrating the latter. A leader must lead. At times a leader can be (and should be) an advocate for the group. But simply advocating for a group is not enough. A leader must take the group down new avenues. A leader must coach the group to better practices. A leader must be the one pioneering new ways of doing things with the intent of improving patient care and provider satisfaction.
Leaders need to be clear with their expectations for hospital medicine. This gives the group the ability to make a conscious choice as to whether or not they wish to stay within the group. If they stay, then it provides the structure for which the group functions. Examples can range from small to big: I expect that you will be at meetings on time; it’s our group’s expectation that you will greet each patient with a smile, handshake, and business card for the first meeting. With the group understanding these expectations, a leader can manage performance and hold providers accountable.
Clear expectations and objectives should be communicated early. They need to be communicated often. In certain instances goals may change. It may be institutional change or changes with Medicare. I often will communicate this change in person once; send an e-mail once and then have a follow-up communication over lunch to answer any questions regarding the change and its implementation. This trio of communication allows me to get the majority of the audience that I need to reach. It gives the audience a “hard copy” in the form of an e-mail to read and also gives the opportunity to answer any questions that I may have overlooked or was not clear with in the other forms of communication.
Ideally, the best time to communicate expectations and objectives is when new providers are hired. New physicians starting in practice need to be trained and adjusted into the team. They need on-boarding, mentors, career coaches, and the opportunity to practice applicable CME early on in the new job. These new additions need to be challenged about their future goals and supported in attaining them. Usually new hospitalists want to get involved in education (medical students or residents), administration, and quality care, or sometimes they just want to practice at becoming better physicians. We all should strive to do the latter always, but some may only want to be clinicians. Either way, all of these goals should be nurtured.
Good training leads to physician participation as an expectation. Participation should not be the stick for which the carrot hangs. Hospitalists need to be on committees and need to have representation at all levels of hospital logistics and tasks. This is how respect and autonomy are gained. And if done properly, this autonomy will receive the support from the highest levels of hospital administration.
With each individual supporting the team (because they are expected to speak on behalf of the group and report back to the group about their findings), the bunch of individuals will start to form a team. What does that mean? An individual hospitalist has her own set of beliefs and practices that makes her unique. If you take a random sampling of hospitalists from many different backgrounds and educational experiences from all over the country (which is any typical hospitalist group), you will have a bunch of individuals. Each hospitalist will come equipped with their own talents and struggles. Now if you take that bunch of individuals and train them in the ways of best practices with good leadership, you can begin to build a functional team. I want to avoid sports analogies, but I think the picture is clearer now than before. See Bad News Bears or Coach Carter. Any team that has clearly stated objectives (expectations/mission statement), that also has good on-boarding and training, will be successful. When the on-boarding process involves mentoring and coaching to help individuals become better administrators, leaders, educators, quality improvers et cetera the team develops together.
One thing that I’ve left out is the logistics of having a good team. Great teams have things like salary, time off, and other benefits included as part of the package. With money and benefits taken off of the table as an issue, the group can focus on things they’ve been trained to focus on: quality patient care. It’s been my opinion that using money to motivate anyone will get the bare minimum performance needed to get the result that leads to the money. So why not take that form of motivation out of the equation? If groups invest in their members, the rewards are greater than rewarding individuals for how many widgets they can churn out of a factory.
With these tools of good leadership, team training and development, excellent communication, and a good salary with benefits, then the expectation of participation and positive feedback should be the norm. A good positive dynamic will develop, and the team will work to support itself. Eventually, a team like this one could become a work-family that could be deployed for specialty care (such as head bleeds and gunshot wounds) as the institution needs it to be deployed. This is provided that this kind of work-family already vetted its concerns and could adapt to those needs. These work-families rely less on the leader to hold everyone accountable and allows the unit to relax together and venture off into creative endeavors for the future. That article is for another time.
Dr. Bitetto is chief for the section of Hospital Medicine at Lehigh Valley Hospital, Allentown, Pa.
What makes some groups better to work with than others? What makes the work dynamic in some groups more optimistic?
It starts with leadership. Leaders must first know themselves. They must first know their limits and their strengths. They must work on the former while celebrating the latter. A leader must lead. At times a leader can be (and should be) an advocate for the group. But simply advocating for a group is not enough. A leader must take the group down new avenues. A leader must coach the group to better practices. A leader must be the one pioneering new ways of doing things with the intent of improving patient care and provider satisfaction.
Leaders need to be clear with their expectations for hospital medicine. This gives the group the ability to make a conscious choice as to whether or not they wish to stay within the group. If they stay, then it provides the structure for which the group functions. Examples can range from small to big: I expect that you will be at meetings on time; it’s our group’s expectation that you will greet each patient with a smile, handshake, and business card for the first meeting. With the group understanding these expectations, a leader can manage performance and hold providers accountable.
Clear expectations and objectives should be communicated early. They need to be communicated often. In certain instances goals may change. It may be institutional change or changes with Medicare. I often will communicate this change in person once; send an e-mail once and then have a follow-up communication over lunch to answer any questions regarding the change and its implementation. This trio of communication allows me to get the majority of the audience that I need to reach. It gives the audience a “hard copy” in the form of an e-mail to read and also gives the opportunity to answer any questions that I may have overlooked or was not clear with in the other forms of communication.
Ideally, the best time to communicate expectations and objectives is when new providers are hired. New physicians starting in practice need to be trained and adjusted into the team. They need on-boarding, mentors, career coaches, and the opportunity to practice applicable CME early on in the new job. These new additions need to be challenged about their future goals and supported in attaining them. Usually new hospitalists want to get involved in education (medical students or residents), administration, and quality care, or sometimes they just want to practice at becoming better physicians. We all should strive to do the latter always, but some may only want to be clinicians. Either way, all of these goals should be nurtured.
Good training leads to physician participation as an expectation. Participation should not be the stick for which the carrot hangs. Hospitalists need to be on committees and need to have representation at all levels of hospital logistics and tasks. This is how respect and autonomy are gained. And if done properly, this autonomy will receive the support from the highest levels of hospital administration.
With each individual supporting the team (because they are expected to speak on behalf of the group and report back to the group about their findings), the bunch of individuals will start to form a team. What does that mean? An individual hospitalist has her own set of beliefs and practices that makes her unique. If you take a random sampling of hospitalists from many different backgrounds and educational experiences from all over the country (which is any typical hospitalist group), you will have a bunch of individuals. Each hospitalist will come equipped with their own talents and struggles. Now if you take that bunch of individuals and train them in the ways of best practices with good leadership, you can begin to build a functional team. I want to avoid sports analogies, but I think the picture is clearer now than before. See Bad News Bears or Coach Carter. Any team that has clearly stated objectives (expectations/mission statement), that also has good on-boarding and training, will be successful. When the on-boarding process involves mentoring and coaching to help individuals become better administrators, leaders, educators, quality improvers et cetera the team develops together.
One thing that I’ve left out is the logistics of having a good team. Great teams have things like salary, time off, and other benefits included as part of the package. With money and benefits taken off of the table as an issue, the group can focus on things they’ve been trained to focus on: quality patient care. It’s been my opinion that using money to motivate anyone will get the bare minimum performance needed to get the result that leads to the money. So why not take that form of motivation out of the equation? If groups invest in their members, the rewards are greater than rewarding individuals for how many widgets they can churn out of a factory.
With these tools of good leadership, team training and development, excellent communication, and a good salary with benefits, then the expectation of participation and positive feedback should be the norm. A good positive dynamic will develop, and the team will work to support itself. Eventually, a team like this one could become a work-family that could be deployed for specialty care (such as head bleeds and gunshot wounds) as the institution needs it to be deployed. This is provided that this kind of work-family already vetted its concerns and could adapt to those needs. These work-families rely less on the leader to hold everyone accountable and allows the unit to relax together and venture off into creative endeavors for the future. That article is for another time.
Dr. Bitetto is chief for the section of Hospital Medicine at Lehigh Valley Hospital, Allentown, Pa.
Halt the Hits
In December 2010, unsettled by the seemingly epidemic proportions of school and workplace violence, I wrote an editorial on the subject.1 Almost four years later, I find that recent behavior by well-known people compels me to write again, because I'm concerned that the problem of violence—this time, domestic—is pandemic and we as a society are so out of control that we have lost our moral compass.
In the latter part of this summer, it seemed that every television, newspaper, and radio announcement included at least one incident of a professional athlete and his abusive behavior toward a team member, a spouse, or a child. The behavior was so outrageous that just hearing about it made me nauseous. To add insult to the injuries inflicted on the victims, the coaches, bosses, and teammates of the alleged perpetrators ostensibly ignored the events.
In the National Football League (NFL) alone, dozens of players have been arrested for domestic violence (DV) in the past few years.2 Moreover, these repeated incidents of abuse occurred with little or no repercussions for the players' atrocious behavior. As the most recent incidents involving Ray Rice and Adrian Peterson were being disclosed, the unbalanced approach to applying sanctions for off-field conduct was revealed. Apparently, to the NFL, DV has been a lesser offense than substance abuse, so the number of games' suspension is fewer for DV.
Regardless of how the NFL has sanctioned off-field (mis)conduct, what do the actions of these players portray to the younger generation? In addition, what is the approach of essentially tolerating these bad behaviors teaching young men (and women) about DV? We know that the problem of DV is not isolated to professional athletes. Nevertheless, we need to know more about the problem—and more importantly, how to stop it.
I believe that the first step is to recognize that children who witness domestic violence are more likely to be abusive than children who do not.3 Second, we need to change our perception of who the victims of DV are. Data on DV tend to focus on women; however, a national survey conducted by the CDC and the US Department of Justice revealed that in 2011, more men than women were victims of intimate partner physical violence, with more than 40% of severe physical violence directed at men.4,5 In addition to recognizing the demographics of DV, we must realize the associated financial costs. In the US alone, the cost of DV exceeds $5 billion annually: $4.1 billion for direct health care services and $1.8 billion in lost productivity.3
DV is one of the most pressing issues in our society. A human problem, it includes intimate partner violence (IPV), sexual violence, child maltreatment, bullying, suicidal behavior, and elder abuse and neglect.6 On average, 20 people per minute in the US are victims of physical violence by an intimate partner.7
While reports of DV among our "rich and famous" make headlines, those incidents are just the tip of the iceberg. DV/IPV is an insidious and frequently deadly social problem that crosses economic and geographic boundaries. Globally, approximately 520,000 people die each year as a result of DV/IPV. That translates to 1,400 deaths per day, the "equivalent of three long-haul commercial aircraft crashing every single day, week in and week out, year after year."8
In recent weeks, as I brooded (and pontificated) about the Rice and Peterson incidents and listened to the NFL address their policies and programs relating to DV and sexual assault, I wondered what was being done (or could be done), and what role we have in reducing this epidemic. Searching for an answer, I discovered a program dedicated to DV/IPV prevention (although it saddens me to think we actually need a dedicated program for this).
In 2002, authorized by the Family Violence Prevention Services Act, the CDC developed the Domestic Violence Prevention Enhancements and Leadership Through Alliances (DELTA) Program (see box).9 The focus is on primary prevention to reduce the incidence of DV/IPV by stopping it before it occurs. Prevention requires understanding the circumstances and factors that influence violence. Understanding risk and protective factors is important, because comprehending the complexity of those factors can assist in violence prevention in our communities.
However, understanding is not enough—we need to advocate for more training and educational programs in our schools and sports programs that can help address the problem at its roots. We need programs and professionals to teach and promote interpersonal respect, healthy relationships, and positive role modeling. We need to develop a comprehensive, coordinated approach to reducing all DV/IPV.
Professional sports leagues and players are in the spotlight; they have the opportunity to lead by positive example and help catalyze change.10 Let's call "time out" on DV and stop tolerating any form of violence, on or off the field.
REFERENCES
1. Onieal M-E. Conduct unbecoming. Clinician Reviews. 2010;20(12):C2, 8-10.
2. NFL player arrests: arrest database. USA Today. www.usatoday.com/sports/nfl/arrests. Accessed October 19, 2014.
3. Domestic Violence Statistics. http://domes ticviolencestatistics.org/domestic-violence-statistics/. Accessed October 19, 2014.
4. Hoff BH. National study: more men than women victims of intimate partner physical violence, psychological aggression. MenWeb online Journal (ISSN: 1095‐5240). www.bat teredmen.com/NISVS.htm. Accessed October 19, 2014.
5. Hines DA, Brown J, Dunning E. Characteristics of callers to the domestic abuse helpline for men. J Fam Viol. 2007;22:63–72.
6. Wilkins N. Tsao B, Hertz M, et al. Connecting the Dots: an Overview of the Links Among Multiple Forms of Violence. 2014. Atlanta, GA: National Center for Injury Prevention and Control, CDC, and Oakland, CA: Prevention Institute.
7. CDC. The National Intimate Partner and Sexual Violence Survey. www.cdc.gov/violen ceprevention/nisvs/index.html. Accessed October 19, 2014.
8. Butchart A, Phinney A, Check P, Villaveces A. Preventing Violence: a Guide to Implementing the Recommendations of the World Report on Violence and Health. 2004. Geneva: World Health Organization.
9. CDC. Domestic Violence Prevention Enhancement and Leadership Through Alliances. www.cdc.gov/violenceprevention/delta/index.html. Accessed October 19, 2014.
10. Brisbo L. Let's call "time out" on domestic violence. Futures Without Violence blog. September 22, 2014. www.futureswithout violence.org/movements-are-made-of-momentslets-call-time-out-on-domestic-violence/. Accessed October 19, 2014.
In December 2010, unsettled by the seemingly epidemic proportions of school and workplace violence, I wrote an editorial on the subject.1 Almost four years later, I find that recent behavior by well-known people compels me to write again, because I'm concerned that the problem of violence—this time, domestic—is pandemic and we as a society are so out of control that we have lost our moral compass.
In the latter part of this summer, it seemed that every television, newspaper, and radio announcement included at least one incident of a professional athlete and his abusive behavior toward a team member, a spouse, or a child. The behavior was so outrageous that just hearing about it made me nauseous. To add insult to the injuries inflicted on the victims, the coaches, bosses, and teammates of the alleged perpetrators ostensibly ignored the events.
In the National Football League (NFL) alone, dozens of players have been arrested for domestic violence (DV) in the past few years.2 Moreover, these repeated incidents of abuse occurred with little or no repercussions for the players' atrocious behavior. As the most recent incidents involving Ray Rice and Adrian Peterson were being disclosed, the unbalanced approach to applying sanctions for off-field conduct was revealed. Apparently, to the NFL, DV has been a lesser offense than substance abuse, so the number of games' suspension is fewer for DV.
Regardless of how the NFL has sanctioned off-field (mis)conduct, what do the actions of these players portray to the younger generation? In addition, what is the approach of essentially tolerating these bad behaviors teaching young men (and women) about DV? We know that the problem of DV is not isolated to professional athletes. Nevertheless, we need to know more about the problem—and more importantly, how to stop it.
I believe that the first step is to recognize that children who witness domestic violence are more likely to be abusive than children who do not.3 Second, we need to change our perception of who the victims of DV are. Data on DV tend to focus on women; however, a national survey conducted by the CDC and the US Department of Justice revealed that in 2011, more men than women were victims of intimate partner physical violence, with more than 40% of severe physical violence directed at men.4,5 In addition to recognizing the demographics of DV, we must realize the associated financial costs. In the US alone, the cost of DV exceeds $5 billion annually: $4.1 billion for direct health care services and $1.8 billion in lost productivity.3
DV is one of the most pressing issues in our society. A human problem, it includes intimate partner violence (IPV), sexual violence, child maltreatment, bullying, suicidal behavior, and elder abuse and neglect.6 On average, 20 people per minute in the US are victims of physical violence by an intimate partner.7
While reports of DV among our "rich and famous" make headlines, those incidents are just the tip of the iceberg. DV/IPV is an insidious and frequently deadly social problem that crosses economic and geographic boundaries. Globally, approximately 520,000 people die each year as a result of DV/IPV. That translates to 1,400 deaths per day, the "equivalent of three long-haul commercial aircraft crashing every single day, week in and week out, year after year."8
In recent weeks, as I brooded (and pontificated) about the Rice and Peterson incidents and listened to the NFL address their policies and programs relating to DV and sexual assault, I wondered what was being done (or could be done), and what role we have in reducing this epidemic. Searching for an answer, I discovered a program dedicated to DV/IPV prevention (although it saddens me to think we actually need a dedicated program for this).
In 2002, authorized by the Family Violence Prevention Services Act, the CDC developed the Domestic Violence Prevention Enhancements and Leadership Through Alliances (DELTA) Program (see box).9 The focus is on primary prevention to reduce the incidence of DV/IPV by stopping it before it occurs. Prevention requires understanding the circumstances and factors that influence violence. Understanding risk and protective factors is important, because comprehending the complexity of those factors can assist in violence prevention in our communities.
However, understanding is not enough—we need to advocate for more training and educational programs in our schools and sports programs that can help address the problem at its roots. We need programs and professionals to teach and promote interpersonal respect, healthy relationships, and positive role modeling. We need to develop a comprehensive, coordinated approach to reducing all DV/IPV.
Professional sports leagues and players are in the spotlight; they have the opportunity to lead by positive example and help catalyze change.10 Let's call "time out" on DV and stop tolerating any form of violence, on or off the field.
REFERENCES
1. Onieal M-E. Conduct unbecoming. Clinician Reviews. 2010;20(12):C2, 8-10.
2. NFL player arrests: arrest database. USA Today. www.usatoday.com/sports/nfl/arrests. Accessed October 19, 2014.
3. Domestic Violence Statistics. http://domes ticviolencestatistics.org/domestic-violence-statistics/. Accessed October 19, 2014.
4. Hoff BH. National study: more men than women victims of intimate partner physical violence, psychological aggression. MenWeb online Journal (ISSN: 1095‐5240). www.bat teredmen.com/NISVS.htm. Accessed October 19, 2014.
5. Hines DA, Brown J, Dunning E. Characteristics of callers to the domestic abuse helpline for men. J Fam Viol. 2007;22:63–72.
6. Wilkins N. Tsao B, Hertz M, et al. Connecting the Dots: an Overview of the Links Among Multiple Forms of Violence. 2014. Atlanta, GA: National Center for Injury Prevention and Control, CDC, and Oakland, CA: Prevention Institute.
7. CDC. The National Intimate Partner and Sexual Violence Survey. www.cdc.gov/violen ceprevention/nisvs/index.html. Accessed October 19, 2014.
8. Butchart A, Phinney A, Check P, Villaveces A. Preventing Violence: a Guide to Implementing the Recommendations of the World Report on Violence and Health. 2004. Geneva: World Health Organization.
9. CDC. Domestic Violence Prevention Enhancement and Leadership Through Alliances. www.cdc.gov/violenceprevention/delta/index.html. Accessed October 19, 2014.
10. Brisbo L. Let's call "time out" on domestic violence. Futures Without Violence blog. September 22, 2014. www.futureswithout violence.org/movements-are-made-of-momentslets-call-time-out-on-domestic-violence/. Accessed October 19, 2014.
In December 2010, unsettled by the seemingly epidemic proportions of school and workplace violence, I wrote an editorial on the subject.1 Almost four years later, I find that recent behavior by well-known people compels me to write again, because I'm concerned that the problem of violence—this time, domestic—is pandemic and we as a society are so out of control that we have lost our moral compass.
In the latter part of this summer, it seemed that every television, newspaper, and radio announcement included at least one incident of a professional athlete and his abusive behavior toward a team member, a spouse, or a child. The behavior was so outrageous that just hearing about it made me nauseous. To add insult to the injuries inflicted on the victims, the coaches, bosses, and teammates of the alleged perpetrators ostensibly ignored the events.
In the National Football League (NFL) alone, dozens of players have been arrested for domestic violence (DV) in the past few years.2 Moreover, these repeated incidents of abuse occurred with little or no repercussions for the players' atrocious behavior. As the most recent incidents involving Ray Rice and Adrian Peterson were being disclosed, the unbalanced approach to applying sanctions for off-field conduct was revealed. Apparently, to the NFL, DV has been a lesser offense than substance abuse, so the number of games' suspension is fewer for DV.
Regardless of how the NFL has sanctioned off-field (mis)conduct, what do the actions of these players portray to the younger generation? In addition, what is the approach of essentially tolerating these bad behaviors teaching young men (and women) about DV? We know that the problem of DV is not isolated to professional athletes. Nevertheless, we need to know more about the problem—and more importantly, how to stop it.
I believe that the first step is to recognize that children who witness domestic violence are more likely to be abusive than children who do not.3 Second, we need to change our perception of who the victims of DV are. Data on DV tend to focus on women; however, a national survey conducted by the CDC and the US Department of Justice revealed that in 2011, more men than women were victims of intimate partner physical violence, with more than 40% of severe physical violence directed at men.4,5 In addition to recognizing the demographics of DV, we must realize the associated financial costs. In the US alone, the cost of DV exceeds $5 billion annually: $4.1 billion for direct health care services and $1.8 billion in lost productivity.3
DV is one of the most pressing issues in our society. A human problem, it includes intimate partner violence (IPV), sexual violence, child maltreatment, bullying, suicidal behavior, and elder abuse and neglect.6 On average, 20 people per minute in the US are victims of physical violence by an intimate partner.7
While reports of DV among our "rich and famous" make headlines, those incidents are just the tip of the iceberg. DV/IPV is an insidious and frequently deadly social problem that crosses economic and geographic boundaries. Globally, approximately 520,000 people die each year as a result of DV/IPV. That translates to 1,400 deaths per day, the "equivalent of three long-haul commercial aircraft crashing every single day, week in and week out, year after year."8
In recent weeks, as I brooded (and pontificated) about the Rice and Peterson incidents and listened to the NFL address their policies and programs relating to DV and sexual assault, I wondered what was being done (or could be done), and what role we have in reducing this epidemic. Searching for an answer, I discovered a program dedicated to DV/IPV prevention (although it saddens me to think we actually need a dedicated program for this).
In 2002, authorized by the Family Violence Prevention Services Act, the CDC developed the Domestic Violence Prevention Enhancements and Leadership Through Alliances (DELTA) Program (see box).9 The focus is on primary prevention to reduce the incidence of DV/IPV by stopping it before it occurs. Prevention requires understanding the circumstances and factors that influence violence. Understanding risk and protective factors is important, because comprehending the complexity of those factors can assist in violence prevention in our communities.
However, understanding is not enough—we need to advocate for more training and educational programs in our schools and sports programs that can help address the problem at its roots. We need programs and professionals to teach and promote interpersonal respect, healthy relationships, and positive role modeling. We need to develop a comprehensive, coordinated approach to reducing all DV/IPV.
Professional sports leagues and players are in the spotlight; they have the opportunity to lead by positive example and help catalyze change.10 Let's call "time out" on DV and stop tolerating any form of violence, on or off the field.
REFERENCES
1. Onieal M-E. Conduct unbecoming. Clinician Reviews. 2010;20(12):C2, 8-10.
2. NFL player arrests: arrest database. USA Today. www.usatoday.com/sports/nfl/arrests. Accessed October 19, 2014.
3. Domestic Violence Statistics. http://domes ticviolencestatistics.org/domestic-violence-statistics/. Accessed October 19, 2014.
4. Hoff BH. National study: more men than women victims of intimate partner physical violence, psychological aggression. MenWeb online Journal (ISSN: 1095‐5240). www.bat teredmen.com/NISVS.htm. Accessed October 19, 2014.
5. Hines DA, Brown J, Dunning E. Characteristics of callers to the domestic abuse helpline for men. J Fam Viol. 2007;22:63–72.
6. Wilkins N. Tsao B, Hertz M, et al. Connecting the Dots: an Overview of the Links Among Multiple Forms of Violence. 2014. Atlanta, GA: National Center for Injury Prevention and Control, CDC, and Oakland, CA: Prevention Institute.
7. CDC. The National Intimate Partner and Sexual Violence Survey. www.cdc.gov/violen ceprevention/nisvs/index.html. Accessed October 19, 2014.
8. Butchart A, Phinney A, Check P, Villaveces A. Preventing Violence: a Guide to Implementing the Recommendations of the World Report on Violence and Health. 2004. Geneva: World Health Organization.
9. CDC. Domestic Violence Prevention Enhancement and Leadership Through Alliances. www.cdc.gov/violenceprevention/delta/index.html. Accessed October 19, 2014.
10. Brisbo L. Let's call "time out" on domestic violence. Futures Without Violence blog. September 22, 2014. www.futureswithout violence.org/movements-are-made-of-momentslets-call-time-out-on-domestic-violence/. Accessed October 19, 2014.
Drugs, Pregnancy, and Lactation: Herbs
Herbs are commonly consumed by pregnant and breast-feeding women, possibly because they believe that “natural products” are safer than drugs. However, even though some have been available for hundreds or thousands of years, little is known about their effects on the embryo, fetus, newborn, or nursing infant. Moreover, as unregulated products, the concentration, contents, and presence of contaminants cannot be easily determined. Detailed reviews of the 22 most commonly used herbs discussed here can be found in “Drugs in Pregnancy and Lactation,” Briggs GG, Freeman RK, 10th ed., Philadelphia: Wolters Kluwer Health, 2014).
In the following discussions, dose, one of the two key factors that determine the risk of developmental toxicity (abnormal growth, structural anomalies, functional and/or neurobehavioral deficits, or death), is rarely reported. In addition, all herbs contain multiple chemical compounds, few of which have been studied during pregnancy or lactation. Thus, with few exceptions, a woman who takes an herb in pregnancy should be informed that the risk to her developing baby is unknown.
Six herbs are considered contraindicated in pregnancy: arnica, black seed /kalanji, blue cohosh, feverfew, salvia divinorum, and valerian.
• Arnica. The dried flowers, and sometimes the roots and rhizomes, are the parts of this perennial plant that are used topically for their anti-inflammatory and analgesic effects. There is no clinical evidence to support this use. Occasional topical use probably represents a low risk, but absorption may occur when it is applied to broken skin. The Food and Drug Administration has classified arnica as an unsafe herb and, when used orally, it is considered a poison. It is a uterine stimulant and an abortifacient. Nevertheless, in homeopathic formulations, it has been promoted for use before and during labor for internal and external bruising of the mother and newborn. In Italy, it is one of the top 10 herbs taken by women (Pharmacoepidemiol. Drug Saf. 2006;15:354-9).
• Black seed/kalanji. This herb has been used for thousands of year as a medicine, food, or spice. Because of this, it is unlikely that it causes teratogenesis. Nevertheless, its use to stimulate menstruation and its potential contraceptive properties suggest that it is contraindicated in pregnancy.
• Blue cohosh. Some of the components of this herb have been shown to be teratogenic and toxic in various animal species, so it should be avoided in the first trimester. The herb has uterine stimulant properties that are used by nurse-midwives to stimulate labor. Blue cohosh was the most frequently used herbal preparation for this purpose. However, some sources believe that the potential fetal and newborn toxicity may outweigh any medical benefit (“PDR for Herbal Medicine,” 2nd ed., Montvale, N.J.: Medical Economics, 2000:109-10; “The Review of Natural Products,” St. Louis, MO: Facts and Comparisons, 2000).
• Feverfew. This herb has been used for labor, menstrual disorders, potential miscarriage, and morning sickness; as an abortifacient; and for several other indications. Because of its antipyretic properties, it has been known as “medieval aspirin.” The doses used for these indications have not been quantified. Because of its emmenagogic (capable of provoking menstruation) activity, the herb should not be used in pregnancy.
• Salvia divinorum. This herb has hallucinogenic effects and is used in certain regions of Mexico for healing and divinatory rituals. It is also thought to have antidiarrheal properties. The herb is either smoked or chewed, or its juices are ingested. When taken orally, systemic effects are dependent upon absorption across the oral mucosa as the active ingredient is destroyed in the GI tract. Persistent psychosis has been observed in people who smoked the herb, so it is contraindicated in pregnancy.
• Valerian. A large number of preparations containing valerian are available. It has been used as a sedative and hypnotic for anxiety, restlessness, and sleep disturbances, as well as several other pharmacologic claims. Because of the risk of cytotoxicity in the fetus and hepatotoxicity in the mother, the herb should be avoided during gestation.
For the remaining 16 herbs, small, infrequent doses probably cause no harm to the mother, embryo, fetus, or newborn. Nevertheless, as noted below, some of these herbs are best avoided during pregnancy.
• Chamomile. Excessive use of this herb should be avoided because it is thought to have uterine stimulant, emmenagogic, and abortifacient properties. Although controversial, some nurse-midwives prescribe chamomile teas for the treatment of morning sickness. Because the plant sources of the herb contain coumarin compounds, ingesting chamomile by pregnant women with coagulation disorders is a concern. However, the herb has been used for thousands of years, so the risk of harm, at least from occasional use, must be very rare.
• Echinacea. This herb is used topically to enhance wound healing and systemically as an immunostimulant. An IV formulation is used in Germany but is not available in the United States. It also has been recommended to assist in the prevention or treatment of viral upper respiratory tract infections. Its use in pregnancy is limited to one small study.
• Evening primrose oil. The oil contains two essential fatty acids: cis-linoleic and gamma-linolenic acid. In a national survey of nurse-midwives, it was the most frequently used herbal preparation for the induction of labor. No adverse effects have been reported in the fetus or newborn from this use. The doses used varied widely and included both oral and vaginal routes of administration. In addition, the oil has been used for rheumatoid arthritis and diabetic neuropathy, but there are no reports of these uses in pregnancy.
• Garlic. Garlic has been used for food flavoring since ancient times and appears to be safe during pregnancy. Some components cross the placenta, as shown by garlic odor in the amniotic fluid and on the newborn’s breath. Very high doses have the potential to induce menstruation or uterine contractions, but apparently these effects have not been reported.
• Ginger. No reports of ginger-induced developmental toxicity have been located. Ginger has been used as antiemetic for nausea and vomiting of pregnancy.
• Ginseng. The root is the most important part of this plant that is found throughout the world and has been used in medicine for more than 2,000 years. The herb has been promoted for multiple pharmacologic effects, including adaptogenic, CNS, cardiovascular, endocrine, ergogenic, antineoplastic, and immunomodulatory effects.
Hypertension and hypoglycemia have been reported in nonpregnant patients, but not in the limited human pregnancy data. A brief 1991 study compared 88 women who took the herb during pregnancy with 88 controls. No differences between the groups were found with regard to the mode of delivery, birth weight, low birth weight (< 2,500 ), preterm delivery (< 37 weeks), low Apgar score (< 7), stillbirths, neonatal deaths, or maternal complications (Asia Oceania J. Obstet. Gynaecol. 1991;17:379-80).
• Ginkgo biloba. The limited animal reproduction data suggest low risk, but there is no reported human pregnancy experience. Nevertheless, it is an ancient herbal preparation that is commonly used for organic brain syndrome, circulatory disorders, asthma, vertigo, and tinnitus. Because of its widespread use, it is doubtful that a major teratogenic effect would have escaped notice, but more subtle or low-incidence toxic effects may not have been detected.
• Kudzu. No human or animal data regarding pregnancy have been located. The herb has been used for more than 2,500 years for the treatment of alcohol hangover, drunkenness, alcoholism, muscle pain, and measles. Many of its chemical constituents can be found in foods. Nevertheless, high, frequent doses should be avoided.
• Nutmeg. This is a commonly used spice but, as with any herb, high doses can produce toxicity. The toxicity is caused by a chemical in the seeds, myristicin, which has anticholinergic properties. A woman at 30 weeks’ gestation misread a recipe and used a whole grated nutmeg rather than 1/8 teaspoon when making cookies. When she ate a cookie, she experienced sinus tachycardia, hypertension, and a sensation of impending doom. The fetus had tachycardia, and atropine-like poisoning was diagnosed. After about 12 hours, both mother and fetus made an uneventful recovery and a healthy infant was born at term.
• Passion flower. The name of this herb may refer to about 400 species of the genus Passiflora. It is available in both oral and topical forms and is used for nervousness, neuralgia, insomnia, pain, asthma, seizures, burns, hemorrhoids, and menopausal complaints. As with many herbs, it contains a large number of chemicals, none of which have undergone reproductive testing. No reports describing the use of this herb in human pregnancy have been located. However, because it has uterine stimulant properties, the oral formulation is best avoided in pregnancy.
• Peppermint. This popular flavoring appears to be harmless for the mother and developing baby when low, recommended doses are ingested. Peppermint oil is available in numerous topical and oral formulations. High oral doses, however, can cause significant toxicity, including death. During pregnancy, ingestion of more than the recommended doses is unsafe because of possible emmenagogic and abortifacient properties.
• Pumpkin seed. This herb, when used as a food, appears to be harmless for the mother and embryo-fetus, but no reports describing its use in pregnancy have been located. High doses, such as those used in traditional medicine or in eating disorders, should be avoided because of the potential for toxic effects from the many chemicals these seeds contain.
• Raspberry leaf. Raspberry leaf tea is commonly used by pregnant women. Nurse-midwives often prescribe the tea to treat nausea and vomiting and as a uterine tonic to shorten labor. A double-blind, randomized, placebo-controlled study evaluated the effect of raspberry leaf tablets (2 tablets/day) on pregnancy outcomes. Compared with controls, no differences were found for length of labor or stages of labor, mode of delivery, admission to the neonatal intensive care unit, Apgar score, and birth weight (J. Midwifery Womens Health 2001;46:51-9).
• Safflower. Safflower oil is commonly used in cooking and has been given for its laxative action. There are no reports describing the use of the herb in pregnancy. It is doubtful if such use would have any adverse effect on a pregnancy. Although abortifacient and emmenagogic effects have been suggested, there is no evidence supporting these effects when used as a food.
• St. John’s wort. No toxicity in pregnant humans has been reported. The use of the herb is widespread and dates back thousands of years. Thus, it is doubtful that the herb is a major teratogen or causes other elements of developmental toxicity. The herb has been used for the management of anxiety, depression, insomnia, inflammation, and gastritis. It is also used as a diuretic and, topically, for the treatment of hemorrhoids and enhanced wound healing.
• Yohimbine. The use of this herb in human pregnancies has not been reported. It has been used as an aphrodisiac and for weight loss, sexual dysfunction, and the treatment of orthostatic hypotension. Although it has no Food and Drug Administration–sanctioned indications, it is also available by prescription for male erectile dysfunction. Due to the lack of data regarding pregnancy, the herb is best avoided during pregnancy.
There are few data regarding the effects of the above herbs on a breast-feeding infant. Depending upon the herb, nursing infants will be exposed to many chemical compounds. For those herbs used as food, nursing is probably safe. The safety of the other herbs during lactation is unknown. However, toxicity has been reported in a 9-day-old term infant whose mother was taking arnica (Clin. Toxicol. 2009;47:726, abstract 120). The infant presented with lethargy, decreased milk intake, anemia, and jaundice but recovered with treatment. After the mother stopped the herb and resumed nursing, no further problems were noted in the infant.
Mr. Briggs is a pharmacist clinical specialist at the outpatient clinics of Memorial Care Center for Women at Miller Children’s Hospital in Long Beach, Calif.; clinical professor of pharmacy at the University of California, San Francisco; and adjunct professor of pharmacy at the University of Southern California, Los Angeles, and Washington State University, Spokane. He also is coauthor of “Drugs in Pregnancy and Lactation,” and coeditor of “Diseases, Complications, and Drug Therapy in Obstetrics.” He had no relevant financial disclosures. Contact him at [email protected].
Herbs are commonly consumed by pregnant and breast-feeding women, possibly because they believe that “natural products” are safer than drugs. However, even though some have been available for hundreds or thousands of years, little is known about their effects on the embryo, fetus, newborn, or nursing infant. Moreover, as unregulated products, the concentration, contents, and presence of contaminants cannot be easily determined. Detailed reviews of the 22 most commonly used herbs discussed here can be found in “Drugs in Pregnancy and Lactation,” Briggs GG, Freeman RK, 10th ed., Philadelphia: Wolters Kluwer Health, 2014).
In the following discussions, dose, one of the two key factors that determine the risk of developmental toxicity (abnormal growth, structural anomalies, functional and/or neurobehavioral deficits, or death), is rarely reported. In addition, all herbs contain multiple chemical compounds, few of which have been studied during pregnancy or lactation. Thus, with few exceptions, a woman who takes an herb in pregnancy should be informed that the risk to her developing baby is unknown.
Six herbs are considered contraindicated in pregnancy: arnica, black seed /kalanji, blue cohosh, feverfew, salvia divinorum, and valerian.
• Arnica. The dried flowers, and sometimes the roots and rhizomes, are the parts of this perennial plant that are used topically for their anti-inflammatory and analgesic effects. There is no clinical evidence to support this use. Occasional topical use probably represents a low risk, but absorption may occur when it is applied to broken skin. The Food and Drug Administration has classified arnica as an unsafe herb and, when used orally, it is considered a poison. It is a uterine stimulant and an abortifacient. Nevertheless, in homeopathic formulations, it has been promoted for use before and during labor for internal and external bruising of the mother and newborn. In Italy, it is one of the top 10 herbs taken by women (Pharmacoepidemiol. Drug Saf. 2006;15:354-9).
• Black seed/kalanji. This herb has been used for thousands of year as a medicine, food, or spice. Because of this, it is unlikely that it causes teratogenesis. Nevertheless, its use to stimulate menstruation and its potential contraceptive properties suggest that it is contraindicated in pregnancy.
• Blue cohosh. Some of the components of this herb have been shown to be teratogenic and toxic in various animal species, so it should be avoided in the first trimester. The herb has uterine stimulant properties that are used by nurse-midwives to stimulate labor. Blue cohosh was the most frequently used herbal preparation for this purpose. However, some sources believe that the potential fetal and newborn toxicity may outweigh any medical benefit (“PDR for Herbal Medicine,” 2nd ed., Montvale, N.J.: Medical Economics, 2000:109-10; “The Review of Natural Products,” St. Louis, MO: Facts and Comparisons, 2000).
• Feverfew. This herb has been used for labor, menstrual disorders, potential miscarriage, and morning sickness; as an abortifacient; and for several other indications. Because of its antipyretic properties, it has been known as “medieval aspirin.” The doses used for these indications have not been quantified. Because of its emmenagogic (capable of provoking menstruation) activity, the herb should not be used in pregnancy.
• Salvia divinorum. This herb has hallucinogenic effects and is used in certain regions of Mexico for healing and divinatory rituals. It is also thought to have antidiarrheal properties. The herb is either smoked or chewed, or its juices are ingested. When taken orally, systemic effects are dependent upon absorption across the oral mucosa as the active ingredient is destroyed in the GI tract. Persistent psychosis has been observed in people who smoked the herb, so it is contraindicated in pregnancy.
• Valerian. A large number of preparations containing valerian are available. It has been used as a sedative and hypnotic for anxiety, restlessness, and sleep disturbances, as well as several other pharmacologic claims. Because of the risk of cytotoxicity in the fetus and hepatotoxicity in the mother, the herb should be avoided during gestation.
For the remaining 16 herbs, small, infrequent doses probably cause no harm to the mother, embryo, fetus, or newborn. Nevertheless, as noted below, some of these herbs are best avoided during pregnancy.
• Chamomile. Excessive use of this herb should be avoided because it is thought to have uterine stimulant, emmenagogic, and abortifacient properties. Although controversial, some nurse-midwives prescribe chamomile teas for the treatment of morning sickness. Because the plant sources of the herb contain coumarin compounds, ingesting chamomile by pregnant women with coagulation disorders is a concern. However, the herb has been used for thousands of years, so the risk of harm, at least from occasional use, must be very rare.
• Echinacea. This herb is used topically to enhance wound healing and systemically as an immunostimulant. An IV formulation is used in Germany but is not available in the United States. It also has been recommended to assist in the prevention or treatment of viral upper respiratory tract infections. Its use in pregnancy is limited to one small study.
• Evening primrose oil. The oil contains two essential fatty acids: cis-linoleic and gamma-linolenic acid. In a national survey of nurse-midwives, it was the most frequently used herbal preparation for the induction of labor. No adverse effects have been reported in the fetus or newborn from this use. The doses used varied widely and included both oral and vaginal routes of administration. In addition, the oil has been used for rheumatoid arthritis and diabetic neuropathy, but there are no reports of these uses in pregnancy.
• Garlic. Garlic has been used for food flavoring since ancient times and appears to be safe during pregnancy. Some components cross the placenta, as shown by garlic odor in the amniotic fluid and on the newborn’s breath. Very high doses have the potential to induce menstruation or uterine contractions, but apparently these effects have not been reported.
• Ginger. No reports of ginger-induced developmental toxicity have been located. Ginger has been used as antiemetic for nausea and vomiting of pregnancy.
• Ginseng. The root is the most important part of this plant that is found throughout the world and has been used in medicine for more than 2,000 years. The herb has been promoted for multiple pharmacologic effects, including adaptogenic, CNS, cardiovascular, endocrine, ergogenic, antineoplastic, and immunomodulatory effects.
Hypertension and hypoglycemia have been reported in nonpregnant patients, but not in the limited human pregnancy data. A brief 1991 study compared 88 women who took the herb during pregnancy with 88 controls. No differences between the groups were found with regard to the mode of delivery, birth weight, low birth weight (< 2,500 ), preterm delivery (< 37 weeks), low Apgar score (< 7), stillbirths, neonatal deaths, or maternal complications (Asia Oceania J. Obstet. Gynaecol. 1991;17:379-80).
• Ginkgo biloba. The limited animal reproduction data suggest low risk, but there is no reported human pregnancy experience. Nevertheless, it is an ancient herbal preparation that is commonly used for organic brain syndrome, circulatory disorders, asthma, vertigo, and tinnitus. Because of its widespread use, it is doubtful that a major teratogenic effect would have escaped notice, but more subtle or low-incidence toxic effects may not have been detected.
• Kudzu. No human or animal data regarding pregnancy have been located. The herb has been used for more than 2,500 years for the treatment of alcohol hangover, drunkenness, alcoholism, muscle pain, and measles. Many of its chemical constituents can be found in foods. Nevertheless, high, frequent doses should be avoided.
• Nutmeg. This is a commonly used spice but, as with any herb, high doses can produce toxicity. The toxicity is caused by a chemical in the seeds, myristicin, which has anticholinergic properties. A woman at 30 weeks’ gestation misread a recipe and used a whole grated nutmeg rather than 1/8 teaspoon when making cookies. When she ate a cookie, she experienced sinus tachycardia, hypertension, and a sensation of impending doom. The fetus had tachycardia, and atropine-like poisoning was diagnosed. After about 12 hours, both mother and fetus made an uneventful recovery and a healthy infant was born at term.
• Passion flower. The name of this herb may refer to about 400 species of the genus Passiflora. It is available in both oral and topical forms and is used for nervousness, neuralgia, insomnia, pain, asthma, seizures, burns, hemorrhoids, and menopausal complaints. As with many herbs, it contains a large number of chemicals, none of which have undergone reproductive testing. No reports describing the use of this herb in human pregnancy have been located. However, because it has uterine stimulant properties, the oral formulation is best avoided in pregnancy.
• Peppermint. This popular flavoring appears to be harmless for the mother and developing baby when low, recommended doses are ingested. Peppermint oil is available in numerous topical and oral formulations. High oral doses, however, can cause significant toxicity, including death. During pregnancy, ingestion of more than the recommended doses is unsafe because of possible emmenagogic and abortifacient properties.
• Pumpkin seed. This herb, when used as a food, appears to be harmless for the mother and embryo-fetus, but no reports describing its use in pregnancy have been located. High doses, such as those used in traditional medicine or in eating disorders, should be avoided because of the potential for toxic effects from the many chemicals these seeds contain.
• Raspberry leaf. Raspberry leaf tea is commonly used by pregnant women. Nurse-midwives often prescribe the tea to treat nausea and vomiting and as a uterine tonic to shorten labor. A double-blind, randomized, placebo-controlled study evaluated the effect of raspberry leaf tablets (2 tablets/day) on pregnancy outcomes. Compared with controls, no differences were found for length of labor or stages of labor, mode of delivery, admission to the neonatal intensive care unit, Apgar score, and birth weight (J. Midwifery Womens Health 2001;46:51-9).
• Safflower. Safflower oil is commonly used in cooking and has been given for its laxative action. There are no reports describing the use of the herb in pregnancy. It is doubtful if such use would have any adverse effect on a pregnancy. Although abortifacient and emmenagogic effects have been suggested, there is no evidence supporting these effects when used as a food.
• St. John’s wort. No toxicity in pregnant humans has been reported. The use of the herb is widespread and dates back thousands of years. Thus, it is doubtful that the herb is a major teratogen or causes other elements of developmental toxicity. The herb has been used for the management of anxiety, depression, insomnia, inflammation, and gastritis. It is also used as a diuretic and, topically, for the treatment of hemorrhoids and enhanced wound healing.
• Yohimbine. The use of this herb in human pregnancies has not been reported. It has been used as an aphrodisiac and for weight loss, sexual dysfunction, and the treatment of orthostatic hypotension. Although it has no Food and Drug Administration–sanctioned indications, it is also available by prescription for male erectile dysfunction. Due to the lack of data regarding pregnancy, the herb is best avoided during pregnancy.
There are few data regarding the effects of the above herbs on a breast-feeding infant. Depending upon the herb, nursing infants will be exposed to many chemical compounds. For those herbs used as food, nursing is probably safe. The safety of the other herbs during lactation is unknown. However, toxicity has been reported in a 9-day-old term infant whose mother was taking arnica (Clin. Toxicol. 2009;47:726, abstract 120). The infant presented with lethargy, decreased milk intake, anemia, and jaundice but recovered with treatment. After the mother stopped the herb and resumed nursing, no further problems were noted in the infant.
Mr. Briggs is a pharmacist clinical specialist at the outpatient clinics of Memorial Care Center for Women at Miller Children’s Hospital in Long Beach, Calif.; clinical professor of pharmacy at the University of California, San Francisco; and adjunct professor of pharmacy at the University of Southern California, Los Angeles, and Washington State University, Spokane. He also is coauthor of “Drugs in Pregnancy and Lactation,” and coeditor of “Diseases, Complications, and Drug Therapy in Obstetrics.” He had no relevant financial disclosures. Contact him at [email protected].
Herbs are commonly consumed by pregnant and breast-feeding women, possibly because they believe that “natural products” are safer than drugs. However, even though some have been available for hundreds or thousands of years, little is known about their effects on the embryo, fetus, newborn, or nursing infant. Moreover, as unregulated products, the concentration, contents, and presence of contaminants cannot be easily determined. Detailed reviews of the 22 most commonly used herbs discussed here can be found in “Drugs in Pregnancy and Lactation,” Briggs GG, Freeman RK, 10th ed., Philadelphia: Wolters Kluwer Health, 2014).
In the following discussions, dose, one of the two key factors that determine the risk of developmental toxicity (abnormal growth, structural anomalies, functional and/or neurobehavioral deficits, or death), is rarely reported. In addition, all herbs contain multiple chemical compounds, few of which have been studied during pregnancy or lactation. Thus, with few exceptions, a woman who takes an herb in pregnancy should be informed that the risk to her developing baby is unknown.
Six herbs are considered contraindicated in pregnancy: arnica, black seed /kalanji, blue cohosh, feverfew, salvia divinorum, and valerian.
• Arnica. The dried flowers, and sometimes the roots and rhizomes, are the parts of this perennial plant that are used topically for their anti-inflammatory and analgesic effects. There is no clinical evidence to support this use. Occasional topical use probably represents a low risk, but absorption may occur when it is applied to broken skin. The Food and Drug Administration has classified arnica as an unsafe herb and, when used orally, it is considered a poison. It is a uterine stimulant and an abortifacient. Nevertheless, in homeopathic formulations, it has been promoted for use before and during labor for internal and external bruising of the mother and newborn. In Italy, it is one of the top 10 herbs taken by women (Pharmacoepidemiol. Drug Saf. 2006;15:354-9).
• Black seed/kalanji. This herb has been used for thousands of year as a medicine, food, or spice. Because of this, it is unlikely that it causes teratogenesis. Nevertheless, its use to stimulate menstruation and its potential contraceptive properties suggest that it is contraindicated in pregnancy.
• Blue cohosh. Some of the components of this herb have been shown to be teratogenic and toxic in various animal species, so it should be avoided in the first trimester. The herb has uterine stimulant properties that are used by nurse-midwives to stimulate labor. Blue cohosh was the most frequently used herbal preparation for this purpose. However, some sources believe that the potential fetal and newborn toxicity may outweigh any medical benefit (“PDR for Herbal Medicine,” 2nd ed., Montvale, N.J.: Medical Economics, 2000:109-10; “The Review of Natural Products,” St. Louis, MO: Facts and Comparisons, 2000).
• Feverfew. This herb has been used for labor, menstrual disorders, potential miscarriage, and morning sickness; as an abortifacient; and for several other indications. Because of its antipyretic properties, it has been known as “medieval aspirin.” The doses used for these indications have not been quantified. Because of its emmenagogic (capable of provoking menstruation) activity, the herb should not be used in pregnancy.
• Salvia divinorum. This herb has hallucinogenic effects and is used in certain regions of Mexico for healing and divinatory rituals. It is also thought to have antidiarrheal properties. The herb is either smoked or chewed, or its juices are ingested. When taken orally, systemic effects are dependent upon absorption across the oral mucosa as the active ingredient is destroyed in the GI tract. Persistent psychosis has been observed in people who smoked the herb, so it is contraindicated in pregnancy.
• Valerian. A large number of preparations containing valerian are available. It has been used as a sedative and hypnotic for anxiety, restlessness, and sleep disturbances, as well as several other pharmacologic claims. Because of the risk of cytotoxicity in the fetus and hepatotoxicity in the mother, the herb should be avoided during gestation.
For the remaining 16 herbs, small, infrequent doses probably cause no harm to the mother, embryo, fetus, or newborn. Nevertheless, as noted below, some of these herbs are best avoided during pregnancy.
• Chamomile. Excessive use of this herb should be avoided because it is thought to have uterine stimulant, emmenagogic, and abortifacient properties. Although controversial, some nurse-midwives prescribe chamomile teas for the treatment of morning sickness. Because the plant sources of the herb contain coumarin compounds, ingesting chamomile by pregnant women with coagulation disorders is a concern. However, the herb has been used for thousands of years, so the risk of harm, at least from occasional use, must be very rare.
• Echinacea. This herb is used topically to enhance wound healing and systemically as an immunostimulant. An IV formulation is used in Germany but is not available in the United States. It also has been recommended to assist in the prevention or treatment of viral upper respiratory tract infections. Its use in pregnancy is limited to one small study.
• Evening primrose oil. The oil contains two essential fatty acids: cis-linoleic and gamma-linolenic acid. In a national survey of nurse-midwives, it was the most frequently used herbal preparation for the induction of labor. No adverse effects have been reported in the fetus or newborn from this use. The doses used varied widely and included both oral and vaginal routes of administration. In addition, the oil has been used for rheumatoid arthritis and diabetic neuropathy, but there are no reports of these uses in pregnancy.
• Garlic. Garlic has been used for food flavoring since ancient times and appears to be safe during pregnancy. Some components cross the placenta, as shown by garlic odor in the amniotic fluid and on the newborn’s breath. Very high doses have the potential to induce menstruation or uterine contractions, but apparently these effects have not been reported.
• Ginger. No reports of ginger-induced developmental toxicity have been located. Ginger has been used as antiemetic for nausea and vomiting of pregnancy.
• Ginseng. The root is the most important part of this plant that is found throughout the world and has been used in medicine for more than 2,000 years. The herb has been promoted for multiple pharmacologic effects, including adaptogenic, CNS, cardiovascular, endocrine, ergogenic, antineoplastic, and immunomodulatory effects.
Hypertension and hypoglycemia have been reported in nonpregnant patients, but not in the limited human pregnancy data. A brief 1991 study compared 88 women who took the herb during pregnancy with 88 controls. No differences between the groups were found with regard to the mode of delivery, birth weight, low birth weight (< 2,500 ), preterm delivery (< 37 weeks), low Apgar score (< 7), stillbirths, neonatal deaths, or maternal complications (Asia Oceania J. Obstet. Gynaecol. 1991;17:379-80).
• Ginkgo biloba. The limited animal reproduction data suggest low risk, but there is no reported human pregnancy experience. Nevertheless, it is an ancient herbal preparation that is commonly used for organic brain syndrome, circulatory disorders, asthma, vertigo, and tinnitus. Because of its widespread use, it is doubtful that a major teratogenic effect would have escaped notice, but more subtle or low-incidence toxic effects may not have been detected.
• Kudzu. No human or animal data regarding pregnancy have been located. The herb has been used for more than 2,500 years for the treatment of alcohol hangover, drunkenness, alcoholism, muscle pain, and measles. Many of its chemical constituents can be found in foods. Nevertheless, high, frequent doses should be avoided.
• Nutmeg. This is a commonly used spice but, as with any herb, high doses can produce toxicity. The toxicity is caused by a chemical in the seeds, myristicin, which has anticholinergic properties. A woman at 30 weeks’ gestation misread a recipe and used a whole grated nutmeg rather than 1/8 teaspoon when making cookies. When she ate a cookie, she experienced sinus tachycardia, hypertension, and a sensation of impending doom. The fetus had tachycardia, and atropine-like poisoning was diagnosed. After about 12 hours, both mother and fetus made an uneventful recovery and a healthy infant was born at term.
• Passion flower. The name of this herb may refer to about 400 species of the genus Passiflora. It is available in both oral and topical forms and is used for nervousness, neuralgia, insomnia, pain, asthma, seizures, burns, hemorrhoids, and menopausal complaints. As with many herbs, it contains a large number of chemicals, none of which have undergone reproductive testing. No reports describing the use of this herb in human pregnancy have been located. However, because it has uterine stimulant properties, the oral formulation is best avoided in pregnancy.
• Peppermint. This popular flavoring appears to be harmless for the mother and developing baby when low, recommended doses are ingested. Peppermint oil is available in numerous topical and oral formulations. High oral doses, however, can cause significant toxicity, including death. During pregnancy, ingestion of more than the recommended doses is unsafe because of possible emmenagogic and abortifacient properties.
• Pumpkin seed. This herb, when used as a food, appears to be harmless for the mother and embryo-fetus, but no reports describing its use in pregnancy have been located. High doses, such as those used in traditional medicine or in eating disorders, should be avoided because of the potential for toxic effects from the many chemicals these seeds contain.
• Raspberry leaf. Raspberry leaf tea is commonly used by pregnant women. Nurse-midwives often prescribe the tea to treat nausea and vomiting and as a uterine tonic to shorten labor. A double-blind, randomized, placebo-controlled study evaluated the effect of raspberry leaf tablets (2 tablets/day) on pregnancy outcomes. Compared with controls, no differences were found for length of labor or stages of labor, mode of delivery, admission to the neonatal intensive care unit, Apgar score, and birth weight (J. Midwifery Womens Health 2001;46:51-9).
• Safflower. Safflower oil is commonly used in cooking and has been given for its laxative action. There are no reports describing the use of the herb in pregnancy. It is doubtful if such use would have any adverse effect on a pregnancy. Although abortifacient and emmenagogic effects have been suggested, there is no evidence supporting these effects when used as a food.
• St. John’s wort. No toxicity in pregnant humans has been reported. The use of the herb is widespread and dates back thousands of years. Thus, it is doubtful that the herb is a major teratogen or causes other elements of developmental toxicity. The herb has been used for the management of anxiety, depression, insomnia, inflammation, and gastritis. It is also used as a diuretic and, topically, for the treatment of hemorrhoids and enhanced wound healing.
• Yohimbine. The use of this herb in human pregnancies has not been reported. It has been used as an aphrodisiac and for weight loss, sexual dysfunction, and the treatment of orthostatic hypotension. Although it has no Food and Drug Administration–sanctioned indications, it is also available by prescription for male erectile dysfunction. Due to the lack of data regarding pregnancy, the herb is best avoided during pregnancy.
There are few data regarding the effects of the above herbs on a breast-feeding infant. Depending upon the herb, nursing infants will be exposed to many chemical compounds. For those herbs used as food, nursing is probably safe. The safety of the other herbs during lactation is unknown. However, toxicity has been reported in a 9-day-old term infant whose mother was taking arnica (Clin. Toxicol. 2009;47:726, abstract 120). The infant presented with lethargy, decreased milk intake, anemia, and jaundice but recovered with treatment. After the mother stopped the herb and resumed nursing, no further problems were noted in the infant.
Mr. Briggs is a pharmacist clinical specialist at the outpatient clinics of Memorial Care Center for Women at Miller Children’s Hospital in Long Beach, Calif.; clinical professor of pharmacy at the University of California, San Francisco; and adjunct professor of pharmacy at the University of Southern California, Los Angeles, and Washington State University, Spokane. He also is coauthor of “Drugs in Pregnancy and Lactation,” and coeditor of “Diseases, Complications, and Drug Therapy in Obstetrics.” He had no relevant financial disclosures. Contact him at [email protected].
Risk-reducing salpingectomy during surgery for benign indications
Ovarian cancer is the most deadly gynecologic malignancy in the United States, with 14,270 deaths expected in 2014 (CA Cancer J. Clin. 2014;64:9-29 ). The 5-year overall survival remains less than 50%. Difficulties in treatment arise due to its aggressive nature, coupled with vague symptomatology and no effective screening test. Advanced-stage disease at the time of diagnosis is an unfortunate hallmark.
Traditional teaching about the pathogenesis of ovarian cancers has been that a metaplastic change in the mesothelial ovarian surface leads to their de novo development. Under this paradigm, 70% of serous tumors were ovarian, 17% peritoneal, and 13% tubal in origin. However, a major change occurred when BRCA carriers began having risk-reducing bilateral salpingo-oophorectomies (BSO). Sequential histologic sections of the adnexa found occult malignancy in 30% of fallopian tubes, but similar lesions were not present within the ovary (Am. J. Surg. Pathol. 1020;34:1407-16). Could these cancers in the fallopian tube be the precursor lesion and then seed or spread to the ovarian surface?
Molecular and genetic analysis of these serous tubal intraepithelial carcinoma (STIC) cells found p53 mutations that were identical to those in concurrent “ovarian” tumors. STICs have been identified in 70% of nonhereditary forms of serous ovarian cancer. Under this paradigm of STIC as tubal in origin, only 28% of serous tumors were ovarian and 64% were of tubal origin (Am. J. Surg. Pathol. 2007;31:161-9).
This paradigm shift elicited new hypotheses about the etiology of endometrioid and clear cell types of ovarian cancer. Rather than metaplasia of the surface epithelium, endometrioid and clear cell tumors may result from retrograde menstruation, with the fallopian tube acting as a conduit for cells to gain access to the peritoneal cavity and the ovarian surface. This hypothesis provides a mechanism for the 34% reduction in ovarian cancer with bilateral tubal ligation (Hum. Reprod. Update 2011;17:55-67). Interestingly, in a large collaborative pooled analysis, the risk reduction of tubal ligation was greatest for endometrioid and clear cell subtypes (Int. J. Epidemiol. 2013;42:579-89).
Given the mounting evidence of fallopian tube involvement in the development of ovarian cancers, there are new primary prevention considerations. After 5 or more years of oral contraceptive use, a 50% reduction in the relative risk of ovarian cancer has been reported (Ann. Epidemiol. 2011;21:188-96). Bilateral salpingo-oophorectomy provides a greater than 50% risk reduction even in the highest-risk BRCA-positive population. However, results from the Nurses’ Health Study suggest that while there are fewer cancers in a low-risk population following BSO, it comes with an increase in all-cause mortality, predominately due to negative cardiovascular effects. With these issues in mind, is it time to consider incorporating prophylactic bilateral salpingectomy in benign gynecologic surgery (Obstet. Gynecol. 2013;121:709-16)?
While salpingectomy at the time of hysterectomy for benign conditions or for sterilization is becoming more common, there are concerns about premature loss of ovarian function secondary to compromise of ovarian blood supply. However, amassing data demonstrates preserved ovarian function. A retrospective study comparing total laparoscopic hysterectomy (TLH) to TLH with bilateral salpingectomy found no difference in markers of ovarian function (anti-Müllerian hormone, FSH, antral follicle count, mean ovarian diameters) up to 3 months postoperatively (Gynecol. Oncol. 2013;129:448-51). In a randomized controlled trial, 30 women were 1:1 randomized to TLH vs. TLH with salpingectomy. There was no change in anti-Müllerian hormone levels (at 3 months), operative time, or estimated blood loss (Fertil. Steril. 2013;100:1704-8). While there are concerns about the paucity of long-term follow-up data, these initial studies are encouraging. Additionally, a large retrospective study of 540 BRCA-negative patients found no difference in surgical outcomes with salpingectomy (estimated blood loss, hospital stay), and furthermore, the study found that removal of the tubes significantly reduces the risk of developing subsequent benign adnexal lesions by nearly 50% (J. Cancer Res. Clin. Oncol. 2014;140:859-65).
Though salpingectomy removes tubal re-anastomosis as an option in cases of “tubal ligation regret,” wisely choosing candidates can minimize this risk. Women less than 30 years old are at highest risk for regret, and the decision for salpingectomy in these patients should be made with caution and extensive counseling. Yet recently, emerging thought leaders in family planning have called for removal to be routinely considered (Obstet. Gynecol. 2014;124:596-9).
Surgical technique involves electrosurgery or suture ligation just inferior to the fallopian tube, ligating the fallopian branches of the ovarian and utero-ovarian arteries while avoiding unnecessary involvement of ovarian branches within the mesosalpinx. Since the fimbria are thought to be the site of origin for many serous carcinomas, removing the fimbrial portion of the tube is crucial.
Ovarian cancer remains the most deadly gynecologic malignancy. Efforts to find effective screening methods have not yet delivered. Pathologic data confirms that over half of “ovarian” cancers are actually of tubal origin, and we should consider risk-reducing salpingectomy in the low-risk population. The Society of Gynecologic Oncology in their November 2013 Clinical Practice Statement stated, “For women at average risk of ovarian cancer, risk-reducing salpingectomy should also be discussed and considered with patients at the time of abdominal or pelvic surgery, hysterectomy or in lieu of tubal ligation [once childbearing is complete].”
Dr. Pierce is a third-year resident in the department of obstetrics and gynecology at the University of North Carolina at Chapel Hill. Dr. Clarke-Pearson is the chair and the Robert A. Ross Distinguished Professor of Obstetrics and Gynecology, and a professor in the division of gynecologic oncology at the university. Dr. Pierce and Dr. Clarke-Pearson said that they had no relevant financial disclosures.
Ovarian cancer is the most deadly gynecologic malignancy in the United States, with 14,270 deaths expected in 2014 (CA Cancer J. Clin. 2014;64:9-29 ). The 5-year overall survival remains less than 50%. Difficulties in treatment arise due to its aggressive nature, coupled with vague symptomatology and no effective screening test. Advanced-stage disease at the time of diagnosis is an unfortunate hallmark.
Traditional teaching about the pathogenesis of ovarian cancers has been that a metaplastic change in the mesothelial ovarian surface leads to their de novo development. Under this paradigm, 70% of serous tumors were ovarian, 17% peritoneal, and 13% tubal in origin. However, a major change occurred when BRCA carriers began having risk-reducing bilateral salpingo-oophorectomies (BSO). Sequential histologic sections of the adnexa found occult malignancy in 30% of fallopian tubes, but similar lesions were not present within the ovary (Am. J. Surg. Pathol. 1020;34:1407-16). Could these cancers in the fallopian tube be the precursor lesion and then seed or spread to the ovarian surface?
Molecular and genetic analysis of these serous tubal intraepithelial carcinoma (STIC) cells found p53 mutations that were identical to those in concurrent “ovarian” tumors. STICs have been identified in 70% of nonhereditary forms of serous ovarian cancer. Under this paradigm of STIC as tubal in origin, only 28% of serous tumors were ovarian and 64% were of tubal origin (Am. J. Surg. Pathol. 2007;31:161-9).
This paradigm shift elicited new hypotheses about the etiology of endometrioid and clear cell types of ovarian cancer. Rather than metaplasia of the surface epithelium, endometrioid and clear cell tumors may result from retrograde menstruation, with the fallopian tube acting as a conduit for cells to gain access to the peritoneal cavity and the ovarian surface. This hypothesis provides a mechanism for the 34% reduction in ovarian cancer with bilateral tubal ligation (Hum. Reprod. Update 2011;17:55-67). Interestingly, in a large collaborative pooled analysis, the risk reduction of tubal ligation was greatest for endometrioid and clear cell subtypes (Int. J. Epidemiol. 2013;42:579-89).
Given the mounting evidence of fallopian tube involvement in the development of ovarian cancers, there are new primary prevention considerations. After 5 or more years of oral contraceptive use, a 50% reduction in the relative risk of ovarian cancer has been reported (Ann. Epidemiol. 2011;21:188-96). Bilateral salpingo-oophorectomy provides a greater than 50% risk reduction even in the highest-risk BRCA-positive population. However, results from the Nurses’ Health Study suggest that while there are fewer cancers in a low-risk population following BSO, it comes with an increase in all-cause mortality, predominately due to negative cardiovascular effects. With these issues in mind, is it time to consider incorporating prophylactic bilateral salpingectomy in benign gynecologic surgery (Obstet. Gynecol. 2013;121:709-16)?
While salpingectomy at the time of hysterectomy for benign conditions or for sterilization is becoming more common, there are concerns about premature loss of ovarian function secondary to compromise of ovarian blood supply. However, amassing data demonstrates preserved ovarian function. A retrospective study comparing total laparoscopic hysterectomy (TLH) to TLH with bilateral salpingectomy found no difference in markers of ovarian function (anti-Müllerian hormone, FSH, antral follicle count, mean ovarian diameters) up to 3 months postoperatively (Gynecol. Oncol. 2013;129:448-51). In a randomized controlled trial, 30 women were 1:1 randomized to TLH vs. TLH with salpingectomy. There was no change in anti-Müllerian hormone levels (at 3 months), operative time, or estimated blood loss (Fertil. Steril. 2013;100:1704-8). While there are concerns about the paucity of long-term follow-up data, these initial studies are encouraging. Additionally, a large retrospective study of 540 BRCA-negative patients found no difference in surgical outcomes with salpingectomy (estimated blood loss, hospital stay), and furthermore, the study found that removal of the tubes significantly reduces the risk of developing subsequent benign adnexal lesions by nearly 50% (J. Cancer Res. Clin. Oncol. 2014;140:859-65).
Though salpingectomy removes tubal re-anastomosis as an option in cases of “tubal ligation regret,” wisely choosing candidates can minimize this risk. Women less than 30 years old are at highest risk for regret, and the decision for salpingectomy in these patients should be made with caution and extensive counseling. Yet recently, emerging thought leaders in family planning have called for removal to be routinely considered (Obstet. Gynecol. 2014;124:596-9).
Surgical technique involves electrosurgery or suture ligation just inferior to the fallopian tube, ligating the fallopian branches of the ovarian and utero-ovarian arteries while avoiding unnecessary involvement of ovarian branches within the mesosalpinx. Since the fimbria are thought to be the site of origin for many serous carcinomas, removing the fimbrial portion of the tube is crucial.
Ovarian cancer remains the most deadly gynecologic malignancy. Efforts to find effective screening methods have not yet delivered. Pathologic data confirms that over half of “ovarian” cancers are actually of tubal origin, and we should consider risk-reducing salpingectomy in the low-risk population. The Society of Gynecologic Oncology in their November 2013 Clinical Practice Statement stated, “For women at average risk of ovarian cancer, risk-reducing salpingectomy should also be discussed and considered with patients at the time of abdominal or pelvic surgery, hysterectomy or in lieu of tubal ligation [once childbearing is complete].”
Dr. Pierce is a third-year resident in the department of obstetrics and gynecology at the University of North Carolina at Chapel Hill. Dr. Clarke-Pearson is the chair and the Robert A. Ross Distinguished Professor of Obstetrics and Gynecology, and a professor in the division of gynecologic oncology at the university. Dr. Pierce and Dr. Clarke-Pearson said that they had no relevant financial disclosures.
Ovarian cancer is the most deadly gynecologic malignancy in the United States, with 14,270 deaths expected in 2014 (CA Cancer J. Clin. 2014;64:9-29 ). The 5-year overall survival remains less than 50%. Difficulties in treatment arise due to its aggressive nature, coupled with vague symptomatology and no effective screening test. Advanced-stage disease at the time of diagnosis is an unfortunate hallmark.
Traditional teaching about the pathogenesis of ovarian cancers has been that a metaplastic change in the mesothelial ovarian surface leads to their de novo development. Under this paradigm, 70% of serous tumors were ovarian, 17% peritoneal, and 13% tubal in origin. However, a major change occurred when BRCA carriers began having risk-reducing bilateral salpingo-oophorectomies (BSO). Sequential histologic sections of the adnexa found occult malignancy in 30% of fallopian tubes, but similar lesions were not present within the ovary (Am. J. Surg. Pathol. 1020;34:1407-16). Could these cancers in the fallopian tube be the precursor lesion and then seed or spread to the ovarian surface?
Molecular and genetic analysis of these serous tubal intraepithelial carcinoma (STIC) cells found p53 mutations that were identical to those in concurrent “ovarian” tumors. STICs have been identified in 70% of nonhereditary forms of serous ovarian cancer. Under this paradigm of STIC as tubal in origin, only 28% of serous tumors were ovarian and 64% were of tubal origin (Am. J. Surg. Pathol. 2007;31:161-9).
This paradigm shift elicited new hypotheses about the etiology of endometrioid and clear cell types of ovarian cancer. Rather than metaplasia of the surface epithelium, endometrioid and clear cell tumors may result from retrograde menstruation, with the fallopian tube acting as a conduit for cells to gain access to the peritoneal cavity and the ovarian surface. This hypothesis provides a mechanism for the 34% reduction in ovarian cancer with bilateral tubal ligation (Hum. Reprod. Update 2011;17:55-67). Interestingly, in a large collaborative pooled analysis, the risk reduction of tubal ligation was greatest for endometrioid and clear cell subtypes (Int. J. Epidemiol. 2013;42:579-89).
Given the mounting evidence of fallopian tube involvement in the development of ovarian cancers, there are new primary prevention considerations. After 5 or more years of oral contraceptive use, a 50% reduction in the relative risk of ovarian cancer has been reported (Ann. Epidemiol. 2011;21:188-96). Bilateral salpingo-oophorectomy provides a greater than 50% risk reduction even in the highest-risk BRCA-positive population. However, results from the Nurses’ Health Study suggest that while there are fewer cancers in a low-risk population following BSO, it comes with an increase in all-cause mortality, predominately due to negative cardiovascular effects. With these issues in mind, is it time to consider incorporating prophylactic bilateral salpingectomy in benign gynecologic surgery (Obstet. Gynecol. 2013;121:709-16)?
While salpingectomy at the time of hysterectomy for benign conditions or for sterilization is becoming more common, there are concerns about premature loss of ovarian function secondary to compromise of ovarian blood supply. However, amassing data demonstrates preserved ovarian function. A retrospective study comparing total laparoscopic hysterectomy (TLH) to TLH with bilateral salpingectomy found no difference in markers of ovarian function (anti-Müllerian hormone, FSH, antral follicle count, mean ovarian diameters) up to 3 months postoperatively (Gynecol. Oncol. 2013;129:448-51). In a randomized controlled trial, 30 women were 1:1 randomized to TLH vs. TLH with salpingectomy. There was no change in anti-Müllerian hormone levels (at 3 months), operative time, or estimated blood loss (Fertil. Steril. 2013;100:1704-8). While there are concerns about the paucity of long-term follow-up data, these initial studies are encouraging. Additionally, a large retrospective study of 540 BRCA-negative patients found no difference in surgical outcomes with salpingectomy (estimated blood loss, hospital stay), and furthermore, the study found that removal of the tubes significantly reduces the risk of developing subsequent benign adnexal lesions by nearly 50% (J. Cancer Res. Clin. Oncol. 2014;140:859-65).
Though salpingectomy removes tubal re-anastomosis as an option in cases of “tubal ligation regret,” wisely choosing candidates can minimize this risk. Women less than 30 years old are at highest risk for regret, and the decision for salpingectomy in these patients should be made with caution and extensive counseling. Yet recently, emerging thought leaders in family planning have called for removal to be routinely considered (Obstet. Gynecol. 2014;124:596-9).
Surgical technique involves electrosurgery or suture ligation just inferior to the fallopian tube, ligating the fallopian branches of the ovarian and utero-ovarian arteries while avoiding unnecessary involvement of ovarian branches within the mesosalpinx. Since the fimbria are thought to be the site of origin for many serous carcinomas, removing the fimbrial portion of the tube is crucial.
Ovarian cancer remains the most deadly gynecologic malignancy. Efforts to find effective screening methods have not yet delivered. Pathologic data confirms that over half of “ovarian” cancers are actually of tubal origin, and we should consider risk-reducing salpingectomy in the low-risk population. The Society of Gynecologic Oncology in their November 2013 Clinical Practice Statement stated, “For women at average risk of ovarian cancer, risk-reducing salpingectomy should also be discussed and considered with patients at the time of abdominal or pelvic surgery, hysterectomy or in lieu of tubal ligation [once childbearing is complete].”
Dr. Pierce is a third-year resident in the department of obstetrics and gynecology at the University of North Carolina at Chapel Hill. Dr. Clarke-Pearson is the chair and the Robert A. Ross Distinguished Professor of Obstetrics and Gynecology, and a professor in the division of gynecologic oncology at the university. Dr. Pierce and Dr. Clarke-Pearson said that they had no relevant financial disclosures.
The top 10 things drug reps do to tick me off
I generally like drug reps. Some doctors don’t want to deal with them, but I don’t mind. Most are people just trying to support their families, like me. I don’t do lunches anymore, but I never mind briefly chatting and signing for samples.
I’ve fired a few, though. Obviously, I can’t get them tossed from their jobs, but I tell them to never set foot in my office again.
What sort of things really tick me off?
1. Excessive pushiness. Yes, I know you have to sell a product. But endlessly emphasizing it and asking for my support is irritating. I signed for your samples.
2. Not respecting time constraints. Most reps know that doctors only have a few seconds to sign and exchange a few words and respect that, but some will chatter on about their drug at length, even when I’m obviously trying to run to see a patient. My responsibility is to those who need my help, not to those trying to show me a slick iPad graphic.
3. Stalking me. I’ve had reps follow me over to the hospital and out to my car while still talking. Don’t make me get a restraining order.
4. Wasting my staff’s time. My awesome receptionist is very busy. She also is not the one prescribing your product. Do not interfere with her job by rambling about your drug’s dosing, mechanism of action, plan coverage, or pretty much anything. I am paying her. You aren’t. She has a patient to check out, 12 things to fax, an MRI to schedule, and two calls on hold. When you are done talking to me, you are done here. Pack up your bag and move on.
5. Overt rudeness to me and my staff. Believe it or not, I’ve had reps blatantly accuse my secretary of lying to them about such things as not scheduling lunches or not needing samples. Telling her to just “get the doctor” won’t get you anywhere. She runs the office up front, and if you cross her you won’t get to me, either. I will back her up every time.
6. Trespassing. Back before we installed a lock on the door between the lobby and office, I had a rep just walk on back without checking in with the staff. He came to my office and interrupted me with a patient. If your company encourages this, you should work somewhere else. This is a fast way to be told to get out and never come back.
7. Discuss politics. You are welcome to your viewpoints. So am I. They have no place in the interaction between a doctor and a rep. Around the 2012 election, one rep expressed viewpoints that were extreme to the point of being delusional. When she discovered that none of us agreed with her, she became quite angry and confrontational. I told her to never come back.
8. Whip out my prescribing data. Allegedly, mine is shielded, but some reps still seem to be able to access it. Quoting to me (or showing me graphs) as to how much of your product I’m writing vs. another company’s is rude. I will make my decisions based on my patients’ needs, not your sales figures.
9. Selling to my patients. They see enough direct-to-consumer advertising on TV. And magazines. And online. If they ask you questions, I have no problem with you answering them, but don’t start randomly handing them your sales brochures and telling them your drug is better than whatever I have them on.
10. Telling me that my prescribing your drug can help improve your salary or bonus. Like I don’t know that. But, again, that doesn’t and shouldn’t ever factor in to how I manage a patient. Their health, not your car payments, is my concern.
I don’t think I’m unreasonable. Like them, I have a job to do. And, at my office, the patients will always be my priority. As it should be.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
I generally like drug reps. Some doctors don’t want to deal with them, but I don’t mind. Most are people just trying to support their families, like me. I don’t do lunches anymore, but I never mind briefly chatting and signing for samples.
I’ve fired a few, though. Obviously, I can’t get them tossed from their jobs, but I tell them to never set foot in my office again.
What sort of things really tick me off?
1. Excessive pushiness. Yes, I know you have to sell a product. But endlessly emphasizing it and asking for my support is irritating. I signed for your samples.
2. Not respecting time constraints. Most reps know that doctors only have a few seconds to sign and exchange a few words and respect that, but some will chatter on about their drug at length, even when I’m obviously trying to run to see a patient. My responsibility is to those who need my help, not to those trying to show me a slick iPad graphic.
3. Stalking me. I’ve had reps follow me over to the hospital and out to my car while still talking. Don’t make me get a restraining order.
4. Wasting my staff’s time. My awesome receptionist is very busy. She also is not the one prescribing your product. Do not interfere with her job by rambling about your drug’s dosing, mechanism of action, plan coverage, or pretty much anything. I am paying her. You aren’t. She has a patient to check out, 12 things to fax, an MRI to schedule, and two calls on hold. When you are done talking to me, you are done here. Pack up your bag and move on.
5. Overt rudeness to me and my staff. Believe it or not, I’ve had reps blatantly accuse my secretary of lying to them about such things as not scheduling lunches or not needing samples. Telling her to just “get the doctor” won’t get you anywhere. She runs the office up front, and if you cross her you won’t get to me, either. I will back her up every time.
6. Trespassing. Back before we installed a lock on the door between the lobby and office, I had a rep just walk on back without checking in with the staff. He came to my office and interrupted me with a patient. If your company encourages this, you should work somewhere else. This is a fast way to be told to get out and never come back.
7. Discuss politics. You are welcome to your viewpoints. So am I. They have no place in the interaction between a doctor and a rep. Around the 2012 election, one rep expressed viewpoints that were extreme to the point of being delusional. When she discovered that none of us agreed with her, she became quite angry and confrontational. I told her to never come back.
8. Whip out my prescribing data. Allegedly, mine is shielded, but some reps still seem to be able to access it. Quoting to me (or showing me graphs) as to how much of your product I’m writing vs. another company’s is rude. I will make my decisions based on my patients’ needs, not your sales figures.
9. Selling to my patients. They see enough direct-to-consumer advertising on TV. And magazines. And online. If they ask you questions, I have no problem with you answering them, but don’t start randomly handing them your sales brochures and telling them your drug is better than whatever I have them on.
10. Telling me that my prescribing your drug can help improve your salary or bonus. Like I don’t know that. But, again, that doesn’t and shouldn’t ever factor in to how I manage a patient. Their health, not your car payments, is my concern.
I don’t think I’m unreasonable. Like them, I have a job to do. And, at my office, the patients will always be my priority. As it should be.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
I generally like drug reps. Some doctors don’t want to deal with them, but I don’t mind. Most are people just trying to support their families, like me. I don’t do lunches anymore, but I never mind briefly chatting and signing for samples.
I’ve fired a few, though. Obviously, I can’t get them tossed from their jobs, but I tell them to never set foot in my office again.
What sort of things really tick me off?
1. Excessive pushiness. Yes, I know you have to sell a product. But endlessly emphasizing it and asking for my support is irritating. I signed for your samples.
2. Not respecting time constraints. Most reps know that doctors only have a few seconds to sign and exchange a few words and respect that, but some will chatter on about their drug at length, even when I’m obviously trying to run to see a patient. My responsibility is to those who need my help, not to those trying to show me a slick iPad graphic.
3. Stalking me. I’ve had reps follow me over to the hospital and out to my car while still talking. Don’t make me get a restraining order.
4. Wasting my staff’s time. My awesome receptionist is very busy. She also is not the one prescribing your product. Do not interfere with her job by rambling about your drug’s dosing, mechanism of action, plan coverage, or pretty much anything. I am paying her. You aren’t. She has a patient to check out, 12 things to fax, an MRI to schedule, and two calls on hold. When you are done talking to me, you are done here. Pack up your bag and move on.
5. Overt rudeness to me and my staff. Believe it or not, I’ve had reps blatantly accuse my secretary of lying to them about such things as not scheduling lunches or not needing samples. Telling her to just “get the doctor” won’t get you anywhere. She runs the office up front, and if you cross her you won’t get to me, either. I will back her up every time.
6. Trespassing. Back before we installed a lock on the door between the lobby and office, I had a rep just walk on back without checking in with the staff. He came to my office and interrupted me with a patient. If your company encourages this, you should work somewhere else. This is a fast way to be told to get out and never come back.
7. Discuss politics. You are welcome to your viewpoints. So am I. They have no place in the interaction between a doctor and a rep. Around the 2012 election, one rep expressed viewpoints that were extreme to the point of being delusional. When she discovered that none of us agreed with her, she became quite angry and confrontational. I told her to never come back.
8. Whip out my prescribing data. Allegedly, mine is shielded, but some reps still seem to be able to access it. Quoting to me (or showing me graphs) as to how much of your product I’m writing vs. another company’s is rude. I will make my decisions based on my patients’ needs, not your sales figures.
9. Selling to my patients. They see enough direct-to-consumer advertising on TV. And magazines. And online. If they ask you questions, I have no problem with you answering them, but don’t start randomly handing them your sales brochures and telling them your drug is better than whatever I have them on.
10. Telling me that my prescribing your drug can help improve your salary or bonus. Like I don’t know that. But, again, that doesn’t and shouldn’t ever factor in to how I manage a patient. Their health, not your car payments, is my concern.
I don’t think I’m unreasonable. Like them, I have a job to do. And, at my office, the patients will always be my priority. As it should be.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
ID CONSULT: Influenza virus and pneumococci dance together
Most practitioners know that the flu vaccine has been proven to reduce the frequency of middle ear infections, sinusitis, and pneumonia. However, how that happens is not as clear. My group has been studying the details of the interaction between flu virus and pneumococci to unravel the steps in the dance between the flu virus and the pneumococcus in the nasopharynx that results in significant respiratory diseases. Pneumococci live in the posterior part of the nose and upper pharynx as commensal bacteria in all of us, harmlessly present in relatively low numbers. The bacteria are so common that studies to detect pneumococci in the nasopharynx discover their presence in up to 80% of infants and young children, and about 20% of adults at any one time. The bacteria are harmless in patients that have a competent immune system unless an intercurrent viral upper respiratory infection (URI) occurs.
The trigger in pathogenesis of pneumococcal infections is a viral URI, and particularly influenza infection. The combination of pneumococci and flu in the nose can cause compromise in all four aspects of host defense: 1) structural change, 2) physiologic change, 3) innate immunity change, and 4) adaptive immunity change. Structural change is swelling of the nasal passageways, Eustachian tube, osteomeatal sinus pathway, and tracheobronchial tree. Physiologic change is increased mucus production and reduced cilia beat, resulting in stasis of thickened mucus in the respiratory tree. Thus the stage is set for compromise in the immune response.
Innate immunity basically translates to the response of neutrophils, macrophages, and lymphocytes that are resident in the respiratory pathways or migrate there in response to signals from the site of infection that a problem is brewing. To start the process of innate immunity, chemicals are released from resident epithelial cells, lymphocytes, and neutrophils/macrophages. The chemicals are called cytokines and chemokines. The viruses enter the epithelial cells of the nasopharynx and tracheobronchial tree, and leave a change on the surface of the epithelial cells that alerts lymphocytes to kill and destroy those cells harboring virus. Neutrophils and macrophages ingest the bacteria by recognizing surface proteins on the bacteria that are foreign. Sometimes that is all that is needed, and the host clears the infection. But sometimes the innate response is not enough.
The innate response is good and bad. The bad part is that the release of the cytokines and chemokines and the migration of immune cells to the site of infection results in the release of even more cytokines and chemokines that cause increased inflammation. Microbes love inflammation. The inflammation caused by the virus, such as flu virus, creates a very favorable environment for the pneumococci. So the pneumococci start to reproduce in abundance. Then when the secretions of the nose are swept into the Eustachian tube and middle ear or the sinus drainage pathways and then to the sinuses or into the trachea and bronchi and then the lungs, we see the clinical manifestations of acute otitis media, sinusitis, or pneumonia. The innate response failed.
The adaptive response – as the word implies – is when the immune cells recognize and adapt to the presence of foreign microbes by recognizing their presence, migrating to lymph nodes and spleen, communicating with each other, and consequently multiplying into great numbers. The interaction between the immune cells – T cells and B cells – in the lymph node and migration back to the site of infection takes a few days to occur (3-5 days) if the host has prior immunity from prior infections or vaccination. If there is no prior immunity and no vaccination, then it takes 10-14 days for the adaptive immunity response to kick in and clear the infection. During that extra time, the pneumococci are gaining in numbers, causing more inflammation, and we see those clinical signs of fever, redness, and swelling at the site of infection, and pain.
So influenza can cause all of the events above by itself, but when the virus dances with the pneumococci, and the pneumococci benefit from the partnership, that is the most frequent cause of acute otitis media, sinusitis, and pneumonia. And all of that could have been prevented in most of our patients if they only got their annual flu vaccine.
Dr. Pichichero, a specialist in pediatric infectious diseases, is director of the Research Institute, Rochester (N.Y.) General Hospital. He is also a pediatrician at Legacy Pediatrics in Rochester. The study was supported by a National Institutes of Health grant. Dr. Pichichero said he had no relevant financial disclosures. Email him at [email protected].
Most practitioners know that the flu vaccine has been proven to reduce the frequency of middle ear infections, sinusitis, and pneumonia. However, how that happens is not as clear. My group has been studying the details of the interaction between flu virus and pneumococci to unravel the steps in the dance between the flu virus and the pneumococcus in the nasopharynx that results in significant respiratory diseases. Pneumococci live in the posterior part of the nose and upper pharynx as commensal bacteria in all of us, harmlessly present in relatively low numbers. The bacteria are so common that studies to detect pneumococci in the nasopharynx discover their presence in up to 80% of infants and young children, and about 20% of adults at any one time. The bacteria are harmless in patients that have a competent immune system unless an intercurrent viral upper respiratory infection (URI) occurs.
The trigger in pathogenesis of pneumococcal infections is a viral URI, and particularly influenza infection. The combination of pneumococci and flu in the nose can cause compromise in all four aspects of host defense: 1) structural change, 2) physiologic change, 3) innate immunity change, and 4) adaptive immunity change. Structural change is swelling of the nasal passageways, Eustachian tube, osteomeatal sinus pathway, and tracheobronchial tree. Physiologic change is increased mucus production and reduced cilia beat, resulting in stasis of thickened mucus in the respiratory tree. Thus the stage is set for compromise in the immune response.
Innate immunity basically translates to the response of neutrophils, macrophages, and lymphocytes that are resident in the respiratory pathways or migrate there in response to signals from the site of infection that a problem is brewing. To start the process of innate immunity, chemicals are released from resident epithelial cells, lymphocytes, and neutrophils/macrophages. The chemicals are called cytokines and chemokines. The viruses enter the epithelial cells of the nasopharynx and tracheobronchial tree, and leave a change on the surface of the epithelial cells that alerts lymphocytes to kill and destroy those cells harboring virus. Neutrophils and macrophages ingest the bacteria by recognizing surface proteins on the bacteria that are foreign. Sometimes that is all that is needed, and the host clears the infection. But sometimes the innate response is not enough.
The innate response is good and bad. The bad part is that the release of the cytokines and chemokines and the migration of immune cells to the site of infection results in the release of even more cytokines and chemokines that cause increased inflammation. Microbes love inflammation. The inflammation caused by the virus, such as flu virus, creates a very favorable environment for the pneumococci. So the pneumococci start to reproduce in abundance. Then when the secretions of the nose are swept into the Eustachian tube and middle ear or the sinus drainage pathways and then to the sinuses or into the trachea and bronchi and then the lungs, we see the clinical manifestations of acute otitis media, sinusitis, or pneumonia. The innate response failed.
The adaptive response – as the word implies – is when the immune cells recognize and adapt to the presence of foreign microbes by recognizing their presence, migrating to lymph nodes and spleen, communicating with each other, and consequently multiplying into great numbers. The interaction between the immune cells – T cells and B cells – in the lymph node and migration back to the site of infection takes a few days to occur (3-5 days) if the host has prior immunity from prior infections or vaccination. If there is no prior immunity and no vaccination, then it takes 10-14 days for the adaptive immunity response to kick in and clear the infection. During that extra time, the pneumococci are gaining in numbers, causing more inflammation, and we see those clinical signs of fever, redness, and swelling at the site of infection, and pain.
So influenza can cause all of the events above by itself, but when the virus dances with the pneumococci, and the pneumococci benefit from the partnership, that is the most frequent cause of acute otitis media, sinusitis, and pneumonia. And all of that could have been prevented in most of our patients if they only got their annual flu vaccine.
Dr. Pichichero, a specialist in pediatric infectious diseases, is director of the Research Institute, Rochester (N.Y.) General Hospital. He is also a pediatrician at Legacy Pediatrics in Rochester. The study was supported by a National Institutes of Health grant. Dr. Pichichero said he had no relevant financial disclosures. Email him at [email protected].
Most practitioners know that the flu vaccine has been proven to reduce the frequency of middle ear infections, sinusitis, and pneumonia. However, how that happens is not as clear. My group has been studying the details of the interaction between flu virus and pneumococci to unravel the steps in the dance between the flu virus and the pneumococcus in the nasopharynx that results in significant respiratory diseases. Pneumococci live in the posterior part of the nose and upper pharynx as commensal bacteria in all of us, harmlessly present in relatively low numbers. The bacteria are so common that studies to detect pneumococci in the nasopharynx discover their presence in up to 80% of infants and young children, and about 20% of adults at any one time. The bacteria are harmless in patients that have a competent immune system unless an intercurrent viral upper respiratory infection (URI) occurs.
The trigger in pathogenesis of pneumococcal infections is a viral URI, and particularly influenza infection. The combination of pneumococci and flu in the nose can cause compromise in all four aspects of host defense: 1) structural change, 2) physiologic change, 3) innate immunity change, and 4) adaptive immunity change. Structural change is swelling of the nasal passageways, Eustachian tube, osteomeatal sinus pathway, and tracheobronchial tree. Physiologic change is increased mucus production and reduced cilia beat, resulting in stasis of thickened mucus in the respiratory tree. Thus the stage is set for compromise in the immune response.
Innate immunity basically translates to the response of neutrophils, macrophages, and lymphocytes that are resident in the respiratory pathways or migrate there in response to signals from the site of infection that a problem is brewing. To start the process of innate immunity, chemicals are released from resident epithelial cells, lymphocytes, and neutrophils/macrophages. The chemicals are called cytokines and chemokines. The viruses enter the epithelial cells of the nasopharynx and tracheobronchial tree, and leave a change on the surface of the epithelial cells that alerts lymphocytes to kill and destroy those cells harboring virus. Neutrophils and macrophages ingest the bacteria by recognizing surface proteins on the bacteria that are foreign. Sometimes that is all that is needed, and the host clears the infection. But sometimes the innate response is not enough.
The innate response is good and bad. The bad part is that the release of the cytokines and chemokines and the migration of immune cells to the site of infection results in the release of even more cytokines and chemokines that cause increased inflammation. Microbes love inflammation. The inflammation caused by the virus, such as flu virus, creates a very favorable environment for the pneumococci. So the pneumococci start to reproduce in abundance. Then when the secretions of the nose are swept into the Eustachian tube and middle ear or the sinus drainage pathways and then to the sinuses or into the trachea and bronchi and then the lungs, we see the clinical manifestations of acute otitis media, sinusitis, or pneumonia. The innate response failed.
The adaptive response – as the word implies – is when the immune cells recognize and adapt to the presence of foreign microbes by recognizing their presence, migrating to lymph nodes and spleen, communicating with each other, and consequently multiplying into great numbers. The interaction between the immune cells – T cells and B cells – in the lymph node and migration back to the site of infection takes a few days to occur (3-5 days) if the host has prior immunity from prior infections or vaccination. If there is no prior immunity and no vaccination, then it takes 10-14 days for the adaptive immunity response to kick in and clear the infection. During that extra time, the pneumococci are gaining in numbers, causing more inflammation, and we see those clinical signs of fever, redness, and swelling at the site of infection, and pain.
So influenza can cause all of the events above by itself, but when the virus dances with the pneumococci, and the pneumococci benefit from the partnership, that is the most frequent cause of acute otitis media, sinusitis, and pneumonia. And all of that could have been prevented in most of our patients if they only got their annual flu vaccine.
Dr. Pichichero, a specialist in pediatric infectious diseases, is director of the Research Institute, Rochester (N.Y.) General Hospital. He is also a pediatrician at Legacy Pediatrics in Rochester. The study was supported by a National Institutes of Health grant. Dr. Pichichero said he had no relevant financial disclosures. Email him at [email protected].
Why partner with clinical pharmacists?
While reading the “Opportunities to partner with clinical pharmacists in ambulatory care” (Current Psychiatry, Evidence-Based Reviews, July 2014, p. 23-29 [http://bit.ly/1s3yqmh], I became puzzled. Several times, I asked myself, “As a psychiatrist reasonably well-trained in psychopharmacology, why would I need or want to partner with a clinical pharmacist in this fashion?” Indeed, I was under the impression that this is what I trained to do. It called to mind a bumper sticker from the feminist movement of the 1960s that read, “A woman without a man is like a fish without a bicycle.” It then occurred to me that a psychiatrist without a clinical pharmacist would find himself or herself in that same lamentable position.
Scott D. Mendelson, MD, PhD
Roseburg, Oregon
While reading the “Opportunities to partner with clinical pharmacists in ambulatory care” (Current Psychiatry, Evidence-Based Reviews, July 2014, p. 23-29 [http://bit.ly/1s3yqmh], I became puzzled. Several times, I asked myself, “As a psychiatrist reasonably well-trained in psychopharmacology, why would I need or want to partner with a clinical pharmacist in this fashion?” Indeed, I was under the impression that this is what I trained to do. It called to mind a bumper sticker from the feminist movement of the 1960s that read, “A woman without a man is like a fish without a bicycle.” It then occurred to me that a psychiatrist without a clinical pharmacist would find himself or herself in that same lamentable position.
Scott D. Mendelson, MD, PhD
Roseburg, Oregon
While reading the “Opportunities to partner with clinical pharmacists in ambulatory care” (Current Psychiatry, Evidence-Based Reviews, July 2014, p. 23-29 [http://bit.ly/1s3yqmh], I became puzzled. Several times, I asked myself, “As a psychiatrist reasonably well-trained in psychopharmacology, why would I need or want to partner with a clinical pharmacist in this fashion?” Indeed, I was under the impression that this is what I trained to do. It called to mind a bumper sticker from the feminist movement of the 1960s that read, “A woman without a man is like a fish without a bicycle.” It then occurred to me that a psychiatrist without a clinical pharmacist would find himself or herself in that same lamentable position.
Scott D. Mendelson, MD, PhD
Roseburg, Oregon
The ‘decline’ of psychoanalysis
There are many interesting aspects of Dr. Nasrallah’s review of the changes in psychiatry in recent decades (Post-World War II psychiatry: 70 years of momentous change, Current Psychiatry, From the Editor, July 2014, p. 21-22, 49-50 [http://bit.ly/1m8HcdC]). There is no doubt that great strides have been made, particularly in the care of the more seriously ill, and that those accomplishments owe a good deal to the introduction of psychoactive agents.
However, his reference to the “decline” of psychoanalysis was unfortunate and a gratuitous insult to those of us who continue to practice psychoanalysis and who recognize how much psychoanalytic thinking has contributed to the psychotherapeutic practices of non-analyst psychiatrists. If by decline he means that patients who once were in analysis now are being treated with medication alone, he is correct. That might not always be in the best interest of patients, but it is a fact. If by decline he means that in all instances all patients benefit more from pills than they would from analysis, his viewpoint is derived from misinformation.
Since academic psychiatry and psychiatric publications became wholly owned subsidiaries of the pharmaceutical industry, this dismissive attitude about psychoanalysis has attained the status of established wisdom. Psychoanalysts understand that one size does not fit all, no single treatment is the best choice for all patients, and medications can be of great value. Why can’t psychopharmacologists show a similar respect for psychoanalysis?
Charles Goodstein, MD
Tenafly, New Jersey
Dr. Nasrallah responds
Thank you, Dr. Goodstein, for expressing your view about my editorial. However, it is unfair to describe the editorial as being dismissive and insulting toward psychoanalysts. I was simply stating undeniable historical facts about the evolution of psychiatry—one aspect was the reduced prevalence and influence of psychoanalysis over the past few decades, which was partially because of the advent of pharmacotherapy. The other reason was the emergence of other psychotherapies, such as cognitive-behavioral therapy, interpersonal psychotherapy, and dialectical behavior therapy, which are evidence-based, shorter in duration, and more cost effective.
Psychoanalysis remains an important component of contemporary psychiatry, albeit limited to a smaller subgroup of patients.
In my residency, I was heavily trained in psychodynamic therapy, and many of my supervisors were psychoanalysts. I developed my neuroscience skills in a post-residency fellowship at the National Institutes of Health. Nowadays, residency programs must provide both psychotherapeutic and psychopharmacologic training to psychiatric residents.
Your statement that medications have replaced psychotherapy is inaccurate. We train our residents to provide each outpatient with both pharmacotherapy (when indicated) side-by-side with psychotherapy—whether supportive, psychoeducational, psychodynamic, or cognitive-behavioral therapy, or a combination thereof. I continually warn residents about reducing psychiatric care to giving pills, which would be a travesty.
In addition, I regard psychotherapy as a neurobiological intervention because it modifies brain connectivity and neuroplasticity (see my December 2013 Editorial, “Repositioning psychotherapy as neurobiological intervention,” available at CurrentPsychiatry.com).
Last, I wish you would not insult academic psychiatry as being a “wholly owned subsidiary of the pharmaceutical industry.” Someone must develop new and better treatments for serious psychiatric brain disorders. The only entities dedicated to doing that, in the United States, are the pharmaceutical industry and the academic psychopharmacology experts. Together, they generate new ideas and develop innovative mechanisms of action and test them in controlled clinical trials to treat disabling mental disorders. It is not fair to impugn the integrity of academic psychiatrists when they are doing what they were trained to do. They have the integrity and objectivity to criticize the industry when necessary. (See page 50 of my editorial under the subheading “Pharmaceutical industry debacle.”)
Henry A. Nasrallah, MD
Professor and Chairman
Department of Neurology & Psychiatry
Saint Louis University School of Medicine
St. Louis, Missouri
There are many interesting aspects of Dr. Nasrallah’s review of the changes in psychiatry in recent decades (Post-World War II psychiatry: 70 years of momentous change, Current Psychiatry, From the Editor, July 2014, p. 21-22, 49-50 [http://bit.ly/1m8HcdC]). There is no doubt that great strides have been made, particularly in the care of the more seriously ill, and that those accomplishments owe a good deal to the introduction of psychoactive agents.
However, his reference to the “decline” of psychoanalysis was unfortunate and a gratuitous insult to those of us who continue to practice psychoanalysis and who recognize how much psychoanalytic thinking has contributed to the psychotherapeutic practices of non-analyst psychiatrists. If by decline he means that patients who once were in analysis now are being treated with medication alone, he is correct. That might not always be in the best interest of patients, but it is a fact. If by decline he means that in all instances all patients benefit more from pills than they would from analysis, his viewpoint is derived from misinformation.
Since academic psychiatry and psychiatric publications became wholly owned subsidiaries of the pharmaceutical industry, this dismissive attitude about psychoanalysis has attained the status of established wisdom. Psychoanalysts understand that one size does not fit all, no single treatment is the best choice for all patients, and medications can be of great value. Why can’t psychopharmacologists show a similar respect for psychoanalysis?
Charles Goodstein, MD
Tenafly, New Jersey
Dr. Nasrallah responds
Thank you, Dr. Goodstein, for expressing your view about my editorial. However, it is unfair to describe the editorial as being dismissive and insulting toward psychoanalysts. I was simply stating undeniable historical facts about the evolution of psychiatry—one aspect was the reduced prevalence and influence of psychoanalysis over the past few decades, which was partially because of the advent of pharmacotherapy. The other reason was the emergence of other psychotherapies, such as cognitive-behavioral therapy, interpersonal psychotherapy, and dialectical behavior therapy, which are evidence-based, shorter in duration, and more cost effective.
Psychoanalysis remains an important component of contemporary psychiatry, albeit limited to a smaller subgroup of patients.
In my residency, I was heavily trained in psychodynamic therapy, and many of my supervisors were psychoanalysts. I developed my neuroscience skills in a post-residency fellowship at the National Institutes of Health. Nowadays, residency programs must provide both psychotherapeutic and psychopharmacologic training to psychiatric residents.
Your statement that medications have replaced psychotherapy is inaccurate. We train our residents to provide each outpatient with both pharmacotherapy (when indicated) side-by-side with psychotherapy—whether supportive, psychoeducational, psychodynamic, or cognitive-behavioral therapy, or a combination thereof. I continually warn residents about reducing psychiatric care to giving pills, which would be a travesty.
In addition, I regard psychotherapy as a neurobiological intervention because it modifies brain connectivity and neuroplasticity (see my December 2013 Editorial, “Repositioning psychotherapy as neurobiological intervention,” available at CurrentPsychiatry.com).
Last, I wish you would not insult academic psychiatry as being a “wholly owned subsidiary of the pharmaceutical industry.” Someone must develop new and better treatments for serious psychiatric brain disorders. The only entities dedicated to doing that, in the United States, are the pharmaceutical industry and the academic psychopharmacology experts. Together, they generate new ideas and develop innovative mechanisms of action and test them in controlled clinical trials to treat disabling mental disorders. It is not fair to impugn the integrity of academic psychiatrists when they are doing what they were trained to do. They have the integrity and objectivity to criticize the industry when necessary. (See page 50 of my editorial under the subheading “Pharmaceutical industry debacle.”)
Henry A. Nasrallah, MD
Professor and Chairman
Department of Neurology & Psychiatry
Saint Louis University School of Medicine
St. Louis, Missouri
There are many interesting aspects of Dr. Nasrallah’s review of the changes in psychiatry in recent decades (Post-World War II psychiatry: 70 years of momentous change, Current Psychiatry, From the Editor, July 2014, p. 21-22, 49-50 [http://bit.ly/1m8HcdC]). There is no doubt that great strides have been made, particularly in the care of the more seriously ill, and that those accomplishments owe a good deal to the introduction of psychoactive agents.
However, his reference to the “decline” of psychoanalysis was unfortunate and a gratuitous insult to those of us who continue to practice psychoanalysis and who recognize how much psychoanalytic thinking has contributed to the psychotherapeutic practices of non-analyst psychiatrists. If by decline he means that patients who once were in analysis now are being treated with medication alone, he is correct. That might not always be in the best interest of patients, but it is a fact. If by decline he means that in all instances all patients benefit more from pills than they would from analysis, his viewpoint is derived from misinformation.
Since academic psychiatry and psychiatric publications became wholly owned subsidiaries of the pharmaceutical industry, this dismissive attitude about psychoanalysis has attained the status of established wisdom. Psychoanalysts understand that one size does not fit all, no single treatment is the best choice for all patients, and medications can be of great value. Why can’t psychopharmacologists show a similar respect for psychoanalysis?
Charles Goodstein, MD
Tenafly, New Jersey
Dr. Nasrallah responds
Thank you, Dr. Goodstein, for expressing your view about my editorial. However, it is unfair to describe the editorial as being dismissive and insulting toward psychoanalysts. I was simply stating undeniable historical facts about the evolution of psychiatry—one aspect was the reduced prevalence and influence of psychoanalysis over the past few decades, which was partially because of the advent of pharmacotherapy. The other reason was the emergence of other psychotherapies, such as cognitive-behavioral therapy, interpersonal psychotherapy, and dialectical behavior therapy, which are evidence-based, shorter in duration, and more cost effective.
Psychoanalysis remains an important component of contemporary psychiatry, albeit limited to a smaller subgroup of patients.
In my residency, I was heavily trained in psychodynamic therapy, and many of my supervisors were psychoanalysts. I developed my neuroscience skills in a post-residency fellowship at the National Institutes of Health. Nowadays, residency programs must provide both psychotherapeutic and psychopharmacologic training to psychiatric residents.
Your statement that medications have replaced psychotherapy is inaccurate. We train our residents to provide each outpatient with both pharmacotherapy (when indicated) side-by-side with psychotherapy—whether supportive, psychoeducational, psychodynamic, or cognitive-behavioral therapy, or a combination thereof. I continually warn residents about reducing psychiatric care to giving pills, which would be a travesty.
In addition, I regard psychotherapy as a neurobiological intervention because it modifies brain connectivity and neuroplasticity (see my December 2013 Editorial, “Repositioning psychotherapy as neurobiological intervention,” available at CurrentPsychiatry.com).
Last, I wish you would not insult academic psychiatry as being a “wholly owned subsidiary of the pharmaceutical industry.” Someone must develop new and better treatments for serious psychiatric brain disorders. The only entities dedicated to doing that, in the United States, are the pharmaceutical industry and the academic psychopharmacology experts. Together, they generate new ideas and develop innovative mechanisms of action and test them in controlled clinical trials to treat disabling mental disorders. It is not fair to impugn the integrity of academic psychiatrists when they are doing what they were trained to do. They have the integrity and objectivity to criticize the industry when necessary. (See page 50 of my editorial under the subheading “Pharmaceutical industry debacle.”)
Henry A. Nasrallah, MD
Professor and Chairman
Department of Neurology & Psychiatry
Saint Louis University School of Medicine
St. Louis, Missouri