Commentary

YES: Immediate and safe patient access

Pharmacist-prescribed contraception laws are an opportunity to safely and easily improve access to contraception for women. While over-the-counter access remains an important goal, there are many practical considerations that must be addressed prior to implementation.

For example, in order to change the status of a medication to OTC, each product’s manufacturer needs to apply to the Food and Drug Administration for the change. This application includes studies that demonstrate their product can be safely used by the general public, without guidance from a health professional. The American College of Obstetricians and Gynecologists has already weighed in on the overall safety of oral contraceptives, and some studies have been done that show women can accurately complete a health questionnaire related to their OC eligibility. While these are good steps toward demonstrating safe use, they do not satisfy FDA requirements for OTC status. These initial studies never went to the next step of having women interpret the questions in an “actual use study,” an FDA requirement.

On the other hand, there have been studies demonstrating that pharmacists can safely provide hormonal contraception (J Am Pharm Assoc. 2008 Mar-Apr;48[2]:212-21). State laws can’t overrule the FDA and make hormonal contraception OTC, but they can change the scope of what pharmacists are permitted to do. In Oregon and California, specific laws allowing pharmacists to prescribe hormonal contraception have already been implemented. Speaking from our experience in Oregon, this change has solved many concerns that have been raised about hormonal contraception going OTC.

Maintaining insurance coverage

Since pharmacists are able to write prescriptions, they can bill insurance plans for the product in the same way as for any other prescription. The majority of OTC medications are not covered by insurance and if a future law required insurance to cover contraception obtained OTC, pharmacists would still be involved in billing.

Patients will continue to get counseling

Pharmacists need to undergo training/certification in order to prescribe hormonal contraception. In Oregon, the certification was developed by pharmacists and physicians with input from the Oregon Health Authority and the Oregon Board of Pharmacy. Having a trained health care professional involved in counseling means that accurate and important information is still conveyed, including ensuring women are aware that hormonal contraception is not going to protect against sexually transmitted infections, and teaching women about the importance of adherence, but also how to deal with missed pills and problems. The importance of accessing other preventive health services can also be stressed.

Patients will be appropriately screened for their eligibility

Women who are unable to safely use hormonal contraceptives will be referred for more appropriate methods.

We have the opportunity to act now to prevent unintended pregnancy through pharmacist-prescribed hormonal contraceptives. In addition, allowing pharmacists to directly prescribe hormonal contraceptives provides the opportunity to evaluate the safety, efficacy, and acceptability of the practice. This evidence can then be used to look at the feasibility and possible mechanisms that could be undertaken to safely move hormonal contraceptives to OTC, which helps the OTC movement rather than distracting from it.

Dr. Anderson is an instructor at the Oregon State University College of Pharmacy in Corvallis. Dr. Rodriguez is an assistant professor of ob.gyn. at Oregon Health & Science University in Portland. Dr. Edelman is a professor of ob.gyn. and director of the Oregon Family Planning Fellowship at OHSU. They reported having no relevant financial disclosures.

NO: Exchanging one barrier for another

Birth control is an essential part of women’s health care and the value of contraception has been proven time and again. Not only do oral contraceptives provide women with the ability to choose if, and when, they want to become pregnant, they allow women to have more control over their lives by timing pregnancy around education, careers, and other life goals. Nearly 90% of women in the United States between the ages of 15 and 44 will use a highly effective, reversible method of contraception, such as oral contraceptives, injected contraceptives, cervical rings, contraceptive implants, or intrauterine devices.

Ob.gyns. know from evidence and experience that oral contraceptives are safe enough for OTC access. In fact, oral contraceptives are safer than many other medications that are already available OTC, such as acetaminophen. Of note, thromboembolism, the most common serious risk associated with oral contraceptives, is not only exceedingly low but is also much lower than the risk for thromboembolism during pregnancy and the postpartum period. After all, no diagnosis is required to prescribe oral contraceptives. Of course, ob.gyns. and other women’s health care providers do screen for easily recognizable risk factors, such as smoking. However, research shows that women are very adept at self-screening for any potential risks.

For these reasons, ACOG has long been a public supporter of OTC access to oral contraceptives, as it already is in many countries around the world. ACOG supports efforts to increase affordable, reliable access for American women to the contraceptives they need, when they need them.

However, the pharmacist-prescribing laws do not go far enough in expanding access to contraception. A pharmacist’s prescription simply exchanges one barrier – a physician’s prescription – for another.

Women still need to arrange a consultation with a pharmacist during pharmacy hours and any potential cost associated with that consultation would add out-of-pocket expenses. This will not allow us to reach women who remain underserved by the current prescribing requirements. For example, this may prevent women who are uninsured or underinsured from accessing contraception. For some, the need to visit a health care provider prevents access to contraception.

ACOG continues to stand by full, no-copay coverage of all FDA-approved methods of birth control, under the Affordable Care Act, as we recognize that OTC access to birth control is not a blanket solution. We also continue to strongly advocate for access to long-acting reversible contraceptive methods, the most effective method of preventing pregnancy.

Pharmacists and ob.gyns. alike share a commitment to quality patient care. However, if our shared goal is increasing access to safe, effective contraception, women should be trusted to control their reproductive lives and should be able to do so without barriers.

Dr. DeFrancesco is an ob.gyn. in Cheshire, Conn., and the president of the American College of Obstetricians and Gynecologists. He reported having no relevant financial disclosures.

YES: Immediate and safe patient access

Pharmacist-prescribed contraception laws are an opportunity to safely and easily improve access to contraception for women. While over-the-counter access remains an important goal, there are many practical considerations that must be addressed prior to implementation.

For example, in order to change the status of a medication to OTC, each product’s manufacturer needs to apply to the Food and Drug Administration for the change. This application includes studies that demonstrate their product can be safely used by the general public, without guidance from a health professional. The American College of Obstetricians and Gynecologists has already weighed in on the overall safety of oral contraceptives, and some studies have been done that show women can accurately complete a health questionnaire related to their OC eligibility. While these are good steps toward demonstrating safe use, they do not satisfy FDA requirements for OTC status. These initial studies never went to the next step of having women interpret the questions in an “actual use study,” an FDA requirement.

On the other hand, there have been studies demonstrating that pharmacists can safely provide hormonal contraception (J Am Pharm Assoc. 2008 Mar-Apr;48[2]:212-21). State laws can’t overrule the FDA and make hormonal contraception OTC, but they can change the scope of what pharmacists are permitted to do. In Oregon and California, specific laws allowing pharmacists to prescribe hormonal contraception have already been implemented. Speaking from our experience in Oregon, this change has solved many concerns that have been raised about hormonal contraception going OTC.

Maintaining insurance coverage

Since pharmacists are able to write prescriptions, they can bill insurance plans for the product in the same way as for any other prescription. The majority of OTC medications are not covered by insurance and if a future law required insurance to cover contraception obtained OTC, pharmacists would still be involved in billing.

Patients will continue to get counseling

Pharmacists need to undergo training/certification in order to prescribe hormonal contraception. In Oregon, the certification was developed by pharmacists and physicians with input from the Oregon Health Authority and the Oregon Board of Pharmacy. Having a trained health care professional involved in counseling means that accurate and important information is still conveyed, including ensuring women are aware that hormonal contraception is not going to protect against sexually transmitted infections, and teaching women about the importance of adherence, but also how to deal with missed pills and problems. The importance of accessing other preventive health services can also be stressed.

Patients will be appropriately screened for their eligibility

Women who are unable to safely use hormonal contraceptives will be referred for more appropriate methods.

We have the opportunity to act now to prevent unintended pregnancy through pharmacist-prescribed hormonal contraceptives. In addition, allowing pharmacists to directly prescribe hormonal contraceptives provides the opportunity to evaluate the safety, efficacy, and acceptability of the practice. This evidence can then be used to look at the feasibility and possible mechanisms that could be undertaken to safely move hormonal contraceptives to OTC, which helps the OTC movement rather than distracting from it.

Dr. Anderson is an instructor at the Oregon State University College of Pharmacy in Corvallis. Dr. Rodriguez is an assistant professor of ob.gyn. at Oregon Health & Science University in Portland. Dr. Edelman is a professor of ob.gyn. and director of the Oregon Family Planning Fellowship at OHSU. They reported having no relevant financial disclosures.

NO: Exchanging one barrier for another

Birth control is an essential part of women’s health care and the value of contraception has been proven time and again. Not only do oral contraceptives provide women with the ability to choose if, and when, they want to become pregnant, they allow women to have more control over their lives by timing pregnancy around education, careers, and other life goals. Nearly 90% of women in the United States between the ages of 15 and 44 will use a highly effective, reversible method of contraception, such as oral contraceptives, injected contraceptives, cervical rings, contraceptive implants, or intrauterine devices.

Ob.gyns. know from evidence and experience that oral contraceptives are safe enough for OTC access. In fact, oral contraceptives are safer than many other medications that are already available OTC, such as acetaminophen. Of note, thromboembolism, the most common serious risk associated with oral contraceptives, is not only exceedingly low but is also much lower than the risk for thromboembolism during pregnancy and the postpartum period. After all, no diagnosis is required to prescribe oral contraceptives. Of course, ob.gyns. and other women’s health care providers do screen for easily recognizable risk factors, such as smoking. However, research shows that women are very adept at self-screening for any potential risks.

For these reasons, ACOG has long been a public supporter of OTC access to oral contraceptives, as it already is in many countries around the world. ACOG supports efforts to increase affordable, reliable access for American women to the contraceptives they need, when they need them.

However, the pharmacist-prescribing laws do not go far enough in expanding access to contraception. A pharmacist’s prescription simply exchanges one barrier – a physician’s prescription – for another.

Women still need to arrange a consultation with a pharmacist during pharmacy hours and any potential cost associated with that consultation would add out-of-pocket expenses. This will not allow us to reach women who remain underserved by the current prescribing requirements. For example, this may prevent women who are uninsured or underinsured from accessing contraception. For some, the need to visit a health care provider prevents access to contraception.

ACOG continues to stand by full, no-copay coverage of all FDA-approved methods of birth control, under the Affordable Care Act, as we recognize that OTC access to birth control is not a blanket solution. We also continue to strongly advocate for access to long-acting reversible contraceptive methods, the most effective method of preventing pregnancy.

Pharmacists and ob.gyns. alike share a commitment to quality patient care. However, if our shared goal is increasing access to safe, effective contraception, women should be trusted to control their reproductive lives and should be able to do so without barriers.

Dr. DeFrancesco is an ob.gyn. in Cheshire, Conn., and the president of the American College of Obstetricians and Gynecologists. He reported having no relevant financial disclosures.

YES: Immediate and safe patient access

Pharmacist-prescribed contraception laws are an opportunity to safely and easily improve access to contraception for women. While over-the-counter access remains an important goal, there are many practical considerations that must be addressed prior to implementation.

For example, in order to change the status of a medication to OTC, each product’s manufacturer needs to apply to the Food and Drug Administration for the change. This application includes studies that demonstrate their product can be safely used by the general public, without guidance from a health professional. The American College of Obstetricians and Gynecologists has already weighed in on the overall safety of oral contraceptives, and some studies have been done that show women can accurately complete a health questionnaire related to their OC eligibility. While these are good steps toward demonstrating safe use, they do not satisfy FDA requirements for OTC status. These initial studies never went to the next step of having women interpret the questions in an “actual use study,” an FDA requirement.

On the other hand, there have been studies demonstrating that pharmacists can safely provide hormonal contraception (J Am Pharm Assoc. 2008 Mar-Apr;48[2]:212-21). State laws can’t overrule the FDA and make hormonal contraception OTC, but they can change the scope of what pharmacists are permitted to do. In Oregon and California, specific laws allowing pharmacists to prescribe hormonal contraception have already been implemented. Speaking from our experience in Oregon, this change has solved many concerns that have been raised about hormonal contraception going OTC.

Maintaining insurance coverage

Since pharmacists are able to write prescriptions, they can bill insurance plans for the product in the same way as for any other prescription. The majority of OTC medications are not covered by insurance and if a future law required insurance to cover contraception obtained OTC, pharmacists would still be involved in billing.

Patients will continue to get counseling

Pharmacists need to undergo training/certification in order to prescribe hormonal contraception. In Oregon, the certification was developed by pharmacists and physicians with input from the Oregon Health Authority and the Oregon Board of Pharmacy. Having a trained health care professional involved in counseling means that accurate and important information is still conveyed, including ensuring women are aware that hormonal contraception is not going to protect against sexually transmitted infections, and teaching women about the importance of adherence, but also how to deal with missed pills and problems. The importance of accessing other preventive health services can also be stressed.

Patients will be appropriately screened for their eligibility

Women who are unable to safely use hormonal contraceptives will be referred for more appropriate methods.

We have the opportunity to act now to prevent unintended pregnancy through pharmacist-prescribed hormonal contraceptives. In addition, allowing pharmacists to directly prescribe hormonal contraceptives provides the opportunity to evaluate the safety, efficacy, and acceptability of the practice. This evidence can then be used to look at the feasibility and possible mechanisms that could be undertaken to safely move hormonal contraceptives to OTC, which helps the OTC movement rather than distracting from it.

Dr. Anderson is an instructor at the Oregon State University College of Pharmacy in Corvallis. Dr. Rodriguez is an assistant professor of ob.gyn. at Oregon Health & Science University in Portland. Dr. Edelman is a professor of ob.gyn. and director of the Oregon Family Planning Fellowship at OHSU. They reported having no relevant financial disclosures.

NO: Exchanging one barrier for another

Birth control is an essential part of women’s health care and the value of contraception has been proven time and again. Not only do oral contraceptives provide women with the ability to choose if, and when, they want to become pregnant, they allow women to have more control over their lives by timing pregnancy around education, careers, and other life goals. Nearly 90% of women in the United States between the ages of 15 and 44 will use a highly effective, reversible method of contraception, such as oral contraceptives, injected contraceptives, cervical rings, contraceptive implants, or intrauterine devices.

Ob.gyns. know from evidence and experience that oral contraceptives are safe enough for OTC access. In fact, oral contraceptives are safer than many other medications that are already available OTC, such as acetaminophen. Of note, thromboembolism, the most common serious risk associated with oral contraceptives, is not only exceedingly low but is also much lower than the risk for thromboembolism during pregnancy and the postpartum period. After all, no diagnosis is required to prescribe oral contraceptives. Of course, ob.gyns. and other women’s health care providers do screen for easily recognizable risk factors, such as smoking. However, research shows that women are very adept at self-screening for any potential risks.

For these reasons, ACOG has long been a public supporter of OTC access to oral contraceptives, as it already is in many countries around the world. ACOG supports efforts to increase affordable, reliable access for American women to the contraceptives they need, when they need them.

However, the pharmacist-prescribing laws do not go far enough in expanding access to contraception. A pharmacist’s prescription simply exchanges one barrier – a physician’s prescription – for another.

Women still need to arrange a consultation with a pharmacist during pharmacy hours and any potential cost associated with that consultation would add out-of-pocket expenses. This will not allow us to reach women who remain underserved by the current prescribing requirements. For example, this may prevent women who are uninsured or underinsured from accessing contraception. For some, the need to visit a health care provider prevents access to contraception.

ACOG continues to stand by full, no-copay coverage of all FDA-approved methods of birth control, under the Affordable Care Act, as we recognize that OTC access to birth control is not a blanket solution. We also continue to strongly advocate for access to long-acting reversible contraceptive methods, the most effective method of preventing pregnancy.

Pharmacists and ob.gyns. alike share a commitment to quality patient care. However, if our shared goal is increasing access to safe, effective contraception, women should be trusted to control their reproductive lives and should be able to do so without barriers.

Dr. DeFrancesco is an ob.gyn. in Cheshire, Conn., and the president of the American College of Obstetricians and Gynecologists. He reported having no relevant financial disclosures.

Voice recognition software has come a long way. I tried it 15 years ago, but gave up in frustration. Recently, I took another look and found that technology has advanced a lot. Although I can now dictate fast and see the words pour out with impressive accuracy, there are still plenty of errors – some of them quite … interesting. Below is a case summary made up of examples from my growing collection of things the computer seems to have thought I said.

The moral: If you dictate with voice recognition software, proofread!

Chief Complaint

This 43-year-old woman presents with chief complaints of “facial and skin issues.”

Past Medical History

She reports that he has been engaged in a prolonged bottle with acne. It has lasted 18 months, urinary half. A previous physician prescribed an oral antibiotic, either doxycycline or minor cycling. She reports recurrent tachycardia on the forehead and cheeks. Although her outbreaks are not always hormonal, she sometimes gets worse around her. I said around her.! Her menstrual.!! Oh, never mind. It’s good that her name isn’t Cohen, because the computer hears that as :

She has scalp itch and here loss, and is convinced she has pediculosis capitis because of head Lausten chief found. There is a remote history of localized baldness, but not of alopecia universe Alice.

Though free of eczema in recent years, she recalls ataxic childhood.

She was recently exposed to chicken pox but did not contract Maricella. Her history of viral illnesses includes Molested contagiosum.

When she goes in the sun, she is not able to get a 10. She takes no narcotic analgesics, especially Oxyclean.

Occasional scaly rashes have been treated with both antifungal and antibiotic East creams, and sometimes with topical spheroids.

The patient has undergone various medical anesthetic procedures.

Personal and social history

The last 4 digits of her Social Security number are 1/6/09.

She is Director of Marketing for an appetizing agency. Her uncle is a scientist who won the No Bell Prize.

Hobbies: Skiing in Aspirin, Colorado. Competitive barbecue in dialysis, Texas.

Physical Examination

Eyes: There is a cystic lesion on the right I. This is a she’ll lazy on.

Face: Her breakouts are popular. The facial lesions are robbed because of Washington with vigor. Several are just above the nose on the club Ella. There is also sun damage: She has to saltwater keratoses on the 4 head.

Neck: Shotty notes. There is dark thickening typical of a cantholysis Neighbor can’t. There are firm lesions on the occipital scalp consistent with folliculitis Keloid Dallas. The redness on both sides of her neck represents Poikilokderma of survived.

Hands: Xerosis, aggravated by frequent hand washing with puerile. Nails demonstrate the partial separation of cholelithiasis.

Torso: There is a lichenoid rash that sometimes loses. This rash is all over and is very expensive. It is lichenoid and shows a violent color. She has many demented lesions. All are B9.

Upper extremities: There are four systolic keratoses on the vulvar forearm.

Lower extremities: There is a bleeding red lesion of recent onset on the left thigh. It is a high and Janet granuloma.

Groin: Her penile wart is not visible.

Assessment and plan

I will desiccate her high and Janet granuloma.

Will treat her losing rash with Burro solution soaks, followed by topical spheroids.

She was worried that she has precancerous cemented lesions, but I see no indication that she dies.

She will clean her hands less often, otherwise he will have Cirrhosis from Washington. She will moisturize with Aqua 4.

While outdoors, she will protect herself from the son.

For acne, recommended isotretinoin, enrolled patient in iPledge program. She cannot have a fasting blood test today, as she 8 this morning. He will obtain a pregnancy test, and I will confirm patient’s cuddling.

My staph will send a report of today’s visit to the patient’s Coronary Physician.

Dr. Rockoff practices dermatology in Brookline, Mass. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years.

Voice recognition software has come a long way. I tried it 15 years ago, but gave up in frustration. Recently, I took another look and found that technology has advanced a lot. Although I can now dictate fast and see the words pour out with impressive accuracy, there are still plenty of errors – some of them quite … interesting. Below is a case summary made up of examples from my growing collection of things the computer seems to have thought I said.

The moral: If you dictate with voice recognition software, proofread!

Chief Complaint

This 43-year-old woman presents with chief complaints of “facial and skin issues.”

Past Medical History

She reports that he has been engaged in a prolonged bottle with acne. It has lasted 18 months, urinary half. A previous physician prescribed an oral antibiotic, either doxycycline or minor cycling. She reports recurrent tachycardia on the forehead and cheeks. Although her outbreaks are not always hormonal, she sometimes gets worse around her. I said around her.! Her menstrual.!! Oh, never mind. It’s good that her name isn’t Cohen, because the computer hears that as :

She has scalp itch and here loss, and is convinced she has pediculosis capitis because of head Lausten chief found. There is a remote history of localized baldness, but not of alopecia universe Alice.

Though free of eczema in recent years, she recalls ataxic childhood.

She was recently exposed to chicken pox but did not contract Maricella. Her history of viral illnesses includes Molested contagiosum.

When she goes in the sun, she is not able to get a 10. She takes no narcotic analgesics, especially Oxyclean.

Occasional scaly rashes have been treated with both antifungal and antibiotic East creams, and sometimes with topical spheroids.

The patient has undergone various medical anesthetic procedures.

Personal and social history

The last 4 digits of her Social Security number are 1/6/09.

She is Director of Marketing for an appetizing agency. Her uncle is a scientist who won the No Bell Prize.

Hobbies: Skiing in Aspirin, Colorado. Competitive barbecue in dialysis, Texas.

Physical Examination

Eyes: There is a cystic lesion on the right I. This is a she’ll lazy on.

Face: Her breakouts are popular. The facial lesions are robbed because of Washington with vigor. Several are just above the nose on the club Ella. There is also sun damage: She has to saltwater keratoses on the 4 head.

Neck: Shotty notes. There is dark thickening typical of a cantholysis Neighbor can’t. There are firm lesions on the occipital scalp consistent with folliculitis Keloid Dallas. The redness on both sides of her neck represents Poikilokderma of survived.

Hands: Xerosis, aggravated by frequent hand washing with puerile. Nails demonstrate the partial separation of cholelithiasis.

Torso: There is a lichenoid rash that sometimes loses. This rash is all over and is very expensive. It is lichenoid and shows a violent color. She has many demented lesions. All are B9.

Upper extremities: There are four systolic keratoses on the vulvar forearm.

Lower extremities: There is a bleeding red lesion of recent onset on the left thigh. It is a high and Janet granuloma.

Groin: Her penile wart is not visible.

Assessment and plan

I will desiccate her high and Janet granuloma.

Will treat her losing rash with Burro solution soaks, followed by topical spheroids.

She was worried that she has precancerous cemented lesions, but I see no indication that she dies.

She will clean her hands less often, otherwise he will have Cirrhosis from Washington. She will moisturize with Aqua 4.

While outdoors, she will protect herself from the son.

For acne, recommended isotretinoin, enrolled patient in iPledge program. She cannot have a fasting blood test today, as she 8 this morning. He will obtain a pregnancy test, and I will confirm patient’s cuddling.

My staph will send a report of today’s visit to the patient’s Coronary Physician.

Dr. Rockoff practices dermatology in Brookline, Mass. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years.

Voice recognition software has come a long way. I tried it 15 years ago, but gave up in frustration. Recently, I took another look and found that technology has advanced a lot. Although I can now dictate fast and see the words pour out with impressive accuracy, there are still plenty of errors – some of them quite … interesting. Below is a case summary made up of examples from my growing collection of things the computer seems to have thought I said.

The moral: If you dictate with voice recognition software, proofread!

Chief Complaint

This 43-year-old woman presents with chief complaints of “facial and skin issues.”

Past Medical History

She reports that he has been engaged in a prolonged bottle with acne. It has lasted 18 months, urinary half. A previous physician prescribed an oral antibiotic, either doxycycline or minor cycling. She reports recurrent tachycardia on the forehead and cheeks. Although her outbreaks are not always hormonal, she sometimes gets worse around her. I said around her.! Her menstrual.!! Oh, never mind. It’s good that her name isn’t Cohen, because the computer hears that as :

She has scalp itch and here loss, and is convinced she has pediculosis capitis because of head Lausten chief found. There is a remote history of localized baldness, but not of alopecia universe Alice.

Though free of eczema in recent years, she recalls ataxic childhood.

She was recently exposed to chicken pox but did not contract Maricella. Her history of viral illnesses includes Molested contagiosum.

When she goes in the sun, she is not able to get a 10. She takes no narcotic analgesics, especially Oxyclean.

Occasional scaly rashes have been treated with both antifungal and antibiotic East creams, and sometimes with topical spheroids.

The patient has undergone various medical anesthetic procedures.

Personal and social history

The last 4 digits of her Social Security number are 1/6/09.

She is Director of Marketing for an appetizing agency. Her uncle is a scientist who won the No Bell Prize.

Hobbies: Skiing in Aspirin, Colorado. Competitive barbecue in dialysis, Texas.

Physical Examination

Eyes: There is a cystic lesion on the right I. This is a she’ll lazy on.

Face: Her breakouts are popular. The facial lesions are robbed because of Washington with vigor. Several are just above the nose on the club Ella. There is also sun damage: She has to saltwater keratoses on the 4 head.

Neck: Shotty notes. There is dark thickening typical of a cantholysis Neighbor can’t. There are firm lesions on the occipital scalp consistent with folliculitis Keloid Dallas. The redness on both sides of her neck represents Poikilokderma of survived.

Hands: Xerosis, aggravated by frequent hand washing with puerile. Nails demonstrate the partial separation of cholelithiasis.

Torso: There is a lichenoid rash that sometimes loses. This rash is all over and is very expensive. It is lichenoid and shows a violent color. She has many demented lesions. All are B9.

Upper extremities: There are four systolic keratoses on the vulvar forearm.

Lower extremities: There is a bleeding red lesion of recent onset on the left thigh. It is a high and Janet granuloma.

Groin: Her penile wart is not visible.

Assessment and plan

I will desiccate her high and Janet granuloma.

Will treat her losing rash with Burro solution soaks, followed by topical spheroids.

She was worried that she has precancerous cemented lesions, but I see no indication that she dies.

She will clean her hands less often, otherwise he will have Cirrhosis from Washington. She will moisturize with Aqua 4.

While outdoors, she will protect herself from the son.

For acne, recommended isotretinoin, enrolled patient in iPledge program. She cannot have a fasting blood test today, as she 8 this morning. He will obtain a pregnancy test, and I will confirm patient’s cuddling.

My staph will send a report of today’s visit to the patient’s Coronary Physician.

Dr. Rockoff practices dermatology in Brookline, Mass. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years.

Editor’s Note: This is the fifth and final installment of a five-part monthly series that will discuss the biologic, genomic, and health system factors that contribute to the racial survival disparity in breast cancer. The series was adapted from an article that originally appeared in CA: A Cancer Journal for Clinicians,¹ a journal of the American Cancer Society.

As discussed in the last installment of this series, multifaceted interventions that address all stakeholders are needed to close the racial disparity gap in breast cancer. The Patient Protection and Affordable Care Act (PPACA) emphasizes delivery system reform with a focus on the triple aim of better health, better health care, and lower costs.² One component of this reform will be accountable care organizations (ACOs). ACOs potentially could assist in closing the racial mortality gap, because provider groups will take responsibility for improving the health of a defined population and will be held accountable for the quality of care delivered.

In the ACO model, an integrated network of providers, led by primary care practitioners, will evaluate the necessity, quality, value, and accountable delivery of specialty diagnostic and therapeutic procedures, including cancer care.³ ACOs will also collect extensive patient data through the meaningful use of medical records.³ These detailed data can then be used to shape locoregional protocols for clinical decision making in oncology and evaluate physician performance. Intermountain Healthcare is an example of an organization that has had success with instituting these clinical protocols to highlight best practices and improve the quality of care.⁴ In breast cancer, oncologists will need to be prepared to develop and follow protocols tailored for their communities, which will lead to standardized, improved care for minority populations.

The oncology medical home is one example of an ACO delivery system reform that has the potential to reduce the racial mortality gap. The oncology medical home replaces episodic care with long-term coordinated care and replaces the fee-for-service model with a performance and outcomes-based system. A key trait of the oncology medical home is care that is continuously improved by measurement against quality standards.⁵ The model oncology home accomplishes this by incorporating software to extract clinical data as well as provider compliance with locoregional guidelines to give oncologists feedback regarding the quality of care that they are providing.⁶ Through this system reform, oncologists will be held accountable for the care they deliver, and it is hoped that this will eliminate the delays, misuse, and underuse of treatment. This could be especially important for optimizing use of hormone therapy for estrogen receptor-positive breast cancer. Trial oncology medical homes in North Carolina and Michigan have yielded promising results regarding improved care (fewer emergency department visits and inpatient admissions) and high adherence to national and practice-selected guidelines.^7,8

PPACA also increases funding for community health centers and provides grants to support community health workers; this highlights again the importance of place in racial health care disparities.⁹ Encouraging collaboration between community health centers and academic institutions, this funding could build bridges between minority communities and high-quality health care institutions while also improving patient communication and education.⁹ As this series has discussed, a failure to provide culturally appropriate clinical information can lead to issues with follow-up and adjuvant treatment compliance and further widen the breast cancer racial mortality gap.

Frontline Medical News

Delivery system reform has the potential to help close the disparity gap by improving the quality of care delivered to minority breast cancer patients. As Chin et al¹⁰ describe in their analysis of effective strategies for reducing health disparities, successful interventions are “culturally tailored to meet patients’ needs, employ multidisciplinary teams of care providers, and target multiple leverage points along a patient’s pathway of care.” ACOs have the financial incentive to meet these features of a successful intervention and improve quality across the continuum of breast cancer care. In addition, the PPACA “incentivized experimentation” with health care delivery, such as the oncology medical home and novel telemedicine interventions, to provide higher quality care outside of hospital settings, which could impact the disparity gap.¹¹

In the face of this new era of organizational structures focused on coordinated, population-based care, oncology providers put themselves at financial risk if they do not position themselves for policy and reimbursement changes that reduce disparities.¹⁰ However, ongoing research will be needed to ensure that as these changes are implemented, the racial mortality gap in breast cancer decreases, and that no vulnerable patient populations are left out.

Precision medicine for all

In addition, as discussed earlier in this series, there are differences in the tumor biology and genomics of breast cancer in African American patients. Beyond quality interventions, initiatives to reduce the mortality gap should focus on precision medicine for all. These initiatives should allow researchers to better understand biologic and genomic differences among breast cancer patients and tailor treatments accordingly. The PPACA has taken steps in this direction and is the first federal law to require group health plans and state-licensed health insurance companies to cover standard-of-care costs associated with participation in clinical trials as well as genetic testing for prevention.¹²

The clinical trial regulations also expressly require plans to show that administrative burdens are not used to create barriers to cancer care for anyone who might benefit from participation in a clinical trial.⁹ The overarching goal of this push to eliminate financial and administrative barriers is to increase the enrollment of minority patients, especially those who do not live close to academic medical centers. In his April 2016 address at the annual meeting of the American Association for Cancer Research, Vice President Joseph Biden identified increased clinical trial participation as a key component of the administration’s cancer “moonshot” as well. Community medical oncologists will be called upon to facilitate and encourage clinical trial participation by their minority patients and should be supported in this endeavor by academic medical centers. With greater minority patient involvement, however, there also should be further research on how trial designs can better lead to clinically significant findings for minority patients. As Polite et al¹³ argue, at a bare minimum, basic sociodemographic and detailed comorbidity information should be prospectively collected and integrated with tumor and host biology data to better examine racial differences in cancer outcomes.

Initiatives also are needed to address the gap in referrals to cancer risk clinics so that more data are available on African American genetic variants, allowing the creation of more robust risk assessment models. Risk assessment relies on predictive statistical models to estimate an individual’s risk of developing cancer, and without accurate estimates of mutation prevalence in minority subgroups, these models’ reliability is compromised.¹⁴ As shown in a recent study at the University of Chicago’s Comprehensive Cancer Risk and Prevention Clinic using targeted genomic capture and next-generation sequencing, nearly one in four African American breast cancer patients referred to the clinic had inherited at least one damaging mutation that increased their risk for the most aggressive type of breast cancer.¹⁵

To identify damaging mutations only after a diagnosis of incurable breast cancer is a failure of prevention. As has been documented in Ashkenazi Jewish populations, there is evidence of high rates of inherited mutations in genes that increase the risk for aggressive breast cancers in populations of African ancestry. This is a fertile area for further research to better understand how these mutations affect the clinical course of breast cancer, what targeted interventions will increase the proportion of breast cancer diagnosed at stage 1, and what molecularly targeted treatments will produce a response in these tumors. Churpek et al¹⁵ also demonstrated the need for continued technological innovation to reduce the disparity gap, because next-generation sequencing is a faster and more cost-efficient way to evaluate multiple variants in many genes. This approach is particularly valuable for African Americans, who tend to have greater genetic diversity.¹⁶ The current administration is also heralding this approach to cancer care. In his 2015 State of the Union address, President Obama announced a precision medicine initiative, including a request for $70 million for the National Cancer Institute to investigate genes that may contribute to the risk of developing cancer.¹⁷ African American women should no longer be left behind in the push for personalized medicine that caters to a patient’s tumor biology and genetic profile. As Subbiah and Kurzrock state, universal genomic testing is not necessarily cost prohibitive, as the cost to obtain a “complete diagnosis and to select appropriate therapy may be miniscule compared with the money wasted on ill-chosen therapies.”¹⁸ 

In conclusion, there is an opportunity in the current climate of health care reform ushered in by the Affordable Care Act to address many of the discussed elements leading to the persistent racial mortality gap in breast cancer. We have argued that two substantial factors lead to this eroding gap. One is differences in tumor biology and genomics, and the second is a quality difference in patterns of care. In describing the perfect storm, Sebastian Junger¹⁹ wrote of the collision of two forces – a hurricane’s warm-air, low-pressure system and an anticyclone’s cool-air, high-pressure system – that combined to create a more powerful and devastating meteorological force. Similarly, we argue that it is the collision of these two factors – tumor biology and genomics with patterns of care – that leads to the breast cancer mortality gap. The delays, misuse, and underuse of treatment that we have underscored are of increased significance when patients present with more aggressive forms of breast cancer. Interventions to close this gap will take leaders at the patient, provider, payer, and community levels to drive system change.

1. Daly B, Olopade OI: A perfect storm: How tumor biology, genomics, and health care delivery patterns collide to create a racial survival disparity in breast cancer and proposed interventions for change. CA Cancer J Clin. 2015 Apr;65:221-38.

2. Fox J: Lessons from an oncology medical home collaborative. Am J Manag Care. 2013; 19:SP5-9.

3. Mehta AJ, Macklis RM: Overview of accountable care organizations for oncology specialists. J Oncol Pract. 2013 Jul; 9(4):216-21.

4. Daly B, Mort EA: A decade after to Err is Human: what should health care leaders be doing? Physician Exec. 2014 May-Jun; 40(3):50-2, 54.

5. Dangi-Garimella S: Oncology medical home: improved quality and cost of care. Am J Manag Care. 2014 Sep.

6. McAneny BL: The future of oncology? COME HOME, the oncology medical home. Am J Manag Care. 2013 Feb.

7. Goyal RK, Wheeler SB, Kohler RE, et al: Health care utilization from chemotherapy-related adverse events among low-income breast cancer patients: effect of enrollment in a medical home program. N C Med J. 2014 Jul-Aug;75(4):231-8.

8. Kuntz G, Tozer JM, Snegosky J, et al: Michigan Oncology Medical Home Demonstration Project: first-year results. J Oncol Pract. 2014 Sep. 10:294-7.

9. Moy B, Polite BN, Halpern MT, et al: American Society of Clinical Oncology policy statement: opportunities in the patient protection and affordable care act to reduce cancer care disparities. J Clin Oncol. 2011 Oct;29(28):3816-24.

10. Chin MH, Clarke AR, Nocon RS, et al: A roadmap and best practices for organizations to reduce racial and ethnic disparities in health care. J Gen Intern Med. 2012 Aug; 27(8):992-1000.

11. Emanuel EJ: How Well Is the Affordable Care Act Doing?: Reasons for Optimism. JAMA 315:1331-2, 2016.

12. Zhang SQ, Polite BN: Achieving a deeper understanding of the implemented provisions of the Affordable Care Act. Am Soc Clin Oncol Educ Book. 2014:e472-7.

13. Polite BN, Sylvester BE, Olopade OI: Race and subset analyses in clinical trials: time to get serious about data integration. J Natl Cancer Inst. 2011 Oct. 103(20):1486-8.

14. Hall MJ, Olopade OI: Disparities in genetic testing: thinking outside the BRCA box. J Clin Oncol. 2006 May; 24(14):2197-203.

15. Churpek JE, Walsh T, Zheng Y, et al: Inherited predisposition to breast cancer among African American women. Breast Cancer Res Treat. 2015 Jan;149(1):31-9.

16. Easton J: Genetic mutations more common among African American women with breast cancer: early testing could protect patients and their relatives. news.uchicago.edu/article/2013/06/03/genetic-mutations-more-common-among-african-american-women-breast-cancer. Published June 3, 2013. Accessed April 20, 2016.

17. Pear R: U.S. to collect genetic data to hone care. New York Times. January 30, 2015.

18. Subbiah V, Kurzrock R: Universal Genomic Testing Needed to Win the War Against Cancer: Genomics IS the Diagnosis. JAMA Oncol, 2016.

19. Junger S: The Perfect Storm. New York, NY: WW Norton and Co; 2009.

Bobby Daly, MD, MBA, is the chief fellow in the section of hematology/oncology at the University of Chicago Medicine. His clinical focus is breast and thoracic oncology, and his research focus is health services. Specifically, Dr. Daly researches disparities in oncology care delivery, oncology health care utilization, aggressive end-of-life oncology care, and oncology payment models. He received his MD and MBA from Harvard Medical School and Harvard Business School, both in Boston, and a BA in Economics and History from Stanford (Calif.) University. He was the recipient of the Dean’s Award at Harvard Medical and Business Schools.

Olufunmilayo Olopade, MD, FACP, OON, is the Walter L. Palmer Distinguished Service Professor of Medicine and Human Genetics, and director, Center for Global Health at the University of Chicago. She is adopting emerging high throughput genomic and informatics strategies to identify genetic and nongenetic risk factors for breast cancer in order to implement precision health care in diverse populations. This innovative approach has the potential to improve the quality of care and reduce costs while saving more lives.

Disclosures: Dr. Olopade serves on the Medical Advisory Board for CancerIQ. Dr. Daly serves as a director of Quadrant Holdings Corporation and receives compensation from this entity. Frontline Medical Communications is a subsidiary of Quadrant Holdings Corporation.

Published in conjunction with Susan G. Komen®.

Editor’s Note: This is the fifth and final installment of a five-part monthly series that will discuss the biologic, genomic, and health system factors that contribute to the racial survival disparity in breast cancer. The series was adapted from an article that originally appeared in CA: A Cancer Journal for Clinicians,¹ a journal of the American Cancer Society.

As discussed in the last installment of this series, multifaceted interventions that address all stakeholders are needed to close the racial disparity gap in breast cancer. The Patient Protection and Affordable Care Act (PPACA) emphasizes delivery system reform with a focus on the triple aim of better health, better health care, and lower costs.² One component of this reform will be accountable care organizations (ACOs). ACOs potentially could assist in closing the racial mortality gap, because provider groups will take responsibility for improving the health of a defined population and will be held accountable for the quality of care delivered.

In the ACO model, an integrated network of providers, led by primary care practitioners, will evaluate the necessity, quality, value, and accountable delivery of specialty diagnostic and therapeutic procedures, including cancer care.³ ACOs will also collect extensive patient data through the meaningful use of medical records.³ These detailed data can then be used to shape locoregional protocols for clinical decision making in oncology and evaluate physician performance. Intermountain Healthcare is an example of an organization that has had success with instituting these clinical protocols to highlight best practices and improve the quality of care.⁴ In breast cancer, oncologists will need to be prepared to develop and follow protocols tailored for their communities, which will lead to standardized, improved care for minority populations.

The oncology medical home is one example of an ACO delivery system reform that has the potential to reduce the racial mortality gap. The oncology medical home replaces episodic care with long-term coordinated care and replaces the fee-for-service model with a performance and outcomes-based system. A key trait of the oncology medical home is care that is continuously improved by measurement against quality standards.⁵ The model oncology home accomplishes this by incorporating software to extract clinical data as well as provider compliance with locoregional guidelines to give oncologists feedback regarding the quality of care that they are providing.⁶ Through this system reform, oncologists will be held accountable for the care they deliver, and it is hoped that this will eliminate the delays, misuse, and underuse of treatment. This could be especially important for optimizing use of hormone therapy for estrogen receptor-positive breast cancer. Trial oncology medical homes in North Carolina and Michigan have yielded promising results regarding improved care (fewer emergency department visits and inpatient admissions) and high adherence to national and practice-selected guidelines.^7,8

PPACA also increases funding for community health centers and provides grants to support community health workers; this highlights again the importance of place in racial health care disparities.⁹ Encouraging collaboration between community health centers and academic institutions, this funding could build bridges between minority communities and high-quality health care institutions while also improving patient communication and education.⁹ As this series has discussed, a failure to provide culturally appropriate clinical information can lead to issues with follow-up and adjuvant treatment compliance and further widen the breast cancer racial mortality gap.

Frontline Medical News

Delivery system reform has the potential to help close the disparity gap by improving the quality of care delivered to minority breast cancer patients. As Chin et al¹⁰ describe in their analysis of effective strategies for reducing health disparities, successful interventions are “culturally tailored to meet patients’ needs, employ multidisciplinary teams of care providers, and target multiple leverage points along a patient’s pathway of care.” ACOs have the financial incentive to meet these features of a successful intervention and improve quality across the continuum of breast cancer care. In addition, the PPACA “incentivized experimentation” with health care delivery, such as the oncology medical home and novel telemedicine interventions, to provide higher quality care outside of hospital settings, which could impact the disparity gap.¹¹

In the face of this new era of organizational structures focused on coordinated, population-based care, oncology providers put themselves at financial risk if they do not position themselves for policy and reimbursement changes that reduce disparities.¹⁰ However, ongoing research will be needed to ensure that as these changes are implemented, the racial mortality gap in breast cancer decreases, and that no vulnerable patient populations are left out.

Precision medicine for all

In addition, as discussed earlier in this series, there are differences in the tumor biology and genomics of breast cancer in African American patients. Beyond quality interventions, initiatives to reduce the mortality gap should focus on precision medicine for all. These initiatives should allow researchers to better understand biologic and genomic differences among breast cancer patients and tailor treatments accordingly. The PPACA has taken steps in this direction and is the first federal law to require group health plans and state-licensed health insurance companies to cover standard-of-care costs associated with participation in clinical trials as well as genetic testing for prevention.¹²

The clinical trial regulations also expressly require plans to show that administrative burdens are not used to create barriers to cancer care for anyone who might benefit from participation in a clinical trial.⁹ The overarching goal of this push to eliminate financial and administrative barriers is to increase the enrollment of minority patients, especially those who do not live close to academic medical centers. In his April 2016 address at the annual meeting of the American Association for Cancer Research, Vice President Joseph Biden identified increased clinical trial participation as a key component of the administration’s cancer “moonshot” as well. Community medical oncologists will be called upon to facilitate and encourage clinical trial participation by their minority patients and should be supported in this endeavor by academic medical centers. With greater minority patient involvement, however, there also should be further research on how trial designs can better lead to clinically significant findings for minority patients. As Polite et al¹³ argue, at a bare minimum, basic sociodemographic and detailed comorbidity information should be prospectively collected and integrated with tumor and host biology data to better examine racial differences in cancer outcomes.

Initiatives also are needed to address the gap in referrals to cancer risk clinics so that more data are available on African American genetic variants, allowing the creation of more robust risk assessment models. Risk assessment relies on predictive statistical models to estimate an individual’s risk of developing cancer, and without accurate estimates of mutation prevalence in minority subgroups, these models’ reliability is compromised.¹⁴ As shown in a recent study at the University of Chicago’s Comprehensive Cancer Risk and Prevention Clinic using targeted genomic capture and next-generation sequencing, nearly one in four African American breast cancer patients referred to the clinic had inherited at least one damaging mutation that increased their risk for the most aggressive type of breast cancer.¹⁵

To identify damaging mutations only after a diagnosis of incurable breast cancer is a failure of prevention. As has been documented in Ashkenazi Jewish populations, there is evidence of high rates of inherited mutations in genes that increase the risk for aggressive breast cancers in populations of African ancestry. This is a fertile area for further research to better understand how these mutations affect the clinical course of breast cancer, what targeted interventions will increase the proportion of breast cancer diagnosed at stage 1, and what molecularly targeted treatments will produce a response in these tumors. Churpek et al¹⁵ also demonstrated the need for continued technological innovation to reduce the disparity gap, because next-generation sequencing is a faster and more cost-efficient way to evaluate multiple variants in many genes. This approach is particularly valuable for African Americans, who tend to have greater genetic diversity.¹⁶ The current administration is also heralding this approach to cancer care. In his 2015 State of the Union address, President Obama announced a precision medicine initiative, including a request for $70 million for the National Cancer Institute to investigate genes that may contribute to the risk of developing cancer.¹⁷ African American women should no longer be left behind in the push for personalized medicine that caters to a patient’s tumor biology and genetic profile. As Subbiah and Kurzrock state, universal genomic testing is not necessarily cost prohibitive, as the cost to obtain a “complete diagnosis and to select appropriate therapy may be miniscule compared with the money wasted on ill-chosen therapies.”¹⁸ 

In conclusion, there is an opportunity in the current climate of health care reform ushered in by the Affordable Care Act to address many of the discussed elements leading to the persistent racial mortality gap in breast cancer. We have argued that two substantial factors lead to this eroding gap. One is differences in tumor biology and genomics, and the second is a quality difference in patterns of care. In describing the perfect storm, Sebastian Junger¹⁹ wrote of the collision of two forces – a hurricane’s warm-air, low-pressure system and an anticyclone’s cool-air, high-pressure system – that combined to create a more powerful and devastating meteorological force. Similarly, we argue that it is the collision of these two factors – tumor biology and genomics with patterns of care – that leads to the breast cancer mortality gap. The delays, misuse, and underuse of treatment that we have underscored are of increased significance when patients present with more aggressive forms of breast cancer. Interventions to close this gap will take leaders at the patient, provider, payer, and community levels to drive system change.

1. Daly B, Olopade OI: A perfect storm: How tumor biology, genomics, and health care delivery patterns collide to create a racial survival disparity in breast cancer and proposed interventions for change. CA Cancer J Clin. 2015 Apr;65:221-38.

2. Fox J: Lessons from an oncology medical home collaborative. Am J Manag Care. 2013; 19:SP5-9.

3. Mehta AJ, Macklis RM: Overview of accountable care organizations for oncology specialists. J Oncol Pract. 2013 Jul; 9(4):216-21.

4. Daly B, Mort EA: A decade after to Err is Human: what should health care leaders be doing? Physician Exec. 2014 May-Jun; 40(3):50-2, 54.

5. Dangi-Garimella S: Oncology medical home: improved quality and cost of care. Am J Manag Care. 2014 Sep.

6. McAneny BL: The future of oncology? COME HOME, the oncology medical home. Am J Manag Care. 2013 Feb.

7. Goyal RK, Wheeler SB, Kohler RE, et al: Health care utilization from chemotherapy-related adverse events among low-income breast cancer patients: effect of enrollment in a medical home program. N C Med J. 2014 Jul-Aug;75(4):231-8.

8. Kuntz G, Tozer JM, Snegosky J, et al: Michigan Oncology Medical Home Demonstration Project: first-year results. J Oncol Pract. 2014 Sep. 10:294-7.

9. Moy B, Polite BN, Halpern MT, et al: American Society of Clinical Oncology policy statement: opportunities in the patient protection and affordable care act to reduce cancer care disparities. J Clin Oncol. 2011 Oct;29(28):3816-24.

10. Chin MH, Clarke AR, Nocon RS, et al: A roadmap and best practices for organizations to reduce racial and ethnic disparities in health care. J Gen Intern Med. 2012 Aug; 27(8):992-1000.

11. Emanuel EJ: How Well Is the Affordable Care Act Doing?: Reasons for Optimism. JAMA 315:1331-2, 2016.

12. Zhang SQ, Polite BN: Achieving a deeper understanding of the implemented provisions of the Affordable Care Act. Am Soc Clin Oncol Educ Book. 2014:e472-7.

13. Polite BN, Sylvester BE, Olopade OI: Race and subset analyses in clinical trials: time to get serious about data integration. J Natl Cancer Inst. 2011 Oct. 103(20):1486-8.

14. Hall MJ, Olopade OI: Disparities in genetic testing: thinking outside the BRCA box. J Clin Oncol. 2006 May; 24(14):2197-203.

15. Churpek JE, Walsh T, Zheng Y, et al: Inherited predisposition to breast cancer among African American women. Breast Cancer Res Treat. 2015 Jan;149(1):31-9.

16. Easton J: Genetic mutations more common among African American women with breast cancer: early testing could protect patients and their relatives. news.uchicago.edu/article/2013/06/03/genetic-mutations-more-common-among-african-american-women-breast-cancer. Published June 3, 2013. Accessed April 20, 2016.

17. Pear R: U.S. to collect genetic data to hone care. New York Times. January 30, 2015.

18. Subbiah V, Kurzrock R: Universal Genomic Testing Needed to Win the War Against Cancer: Genomics IS the Diagnosis. JAMA Oncol, 2016.

19. Junger S: The Perfect Storm. New York, NY: WW Norton and Co; 2009.

Bobby Daly, MD, MBA, is the chief fellow in the section of hematology/oncology at the University of Chicago Medicine. His clinical focus is breast and thoracic oncology, and his research focus is health services. Specifically, Dr. Daly researches disparities in oncology care delivery, oncology health care utilization, aggressive end-of-life oncology care, and oncology payment models. He received his MD and MBA from Harvard Medical School and Harvard Business School, both in Boston, and a BA in Economics and History from Stanford (Calif.) University. He was the recipient of the Dean’s Award at Harvard Medical and Business Schools.

Olufunmilayo Olopade, MD, FACP, OON, is the Walter L. Palmer Distinguished Service Professor of Medicine and Human Genetics, and director, Center for Global Health at the University of Chicago. She is adopting emerging high throughput genomic and informatics strategies to identify genetic and nongenetic risk factors for breast cancer in order to implement precision health care in diverse populations. This innovative approach has the potential to improve the quality of care and reduce costs while saving more lives.

Disclosures: Dr. Olopade serves on the Medical Advisory Board for CancerIQ. Dr. Daly serves as a director of Quadrant Holdings Corporation and receives compensation from this entity. Frontline Medical Communications is a subsidiary of Quadrant Holdings Corporation.

Published in conjunction with Susan G. Komen®.

Editor’s Note: This is the fifth and final installment of a five-part monthly series that will discuss the biologic, genomic, and health system factors that contribute to the racial survival disparity in breast cancer. The series was adapted from an article that originally appeared in CA: A Cancer Journal for Clinicians,¹ a journal of the American Cancer Society.

As discussed in the last installment of this series, multifaceted interventions that address all stakeholders are needed to close the racial disparity gap in breast cancer. The Patient Protection and Affordable Care Act (PPACA) emphasizes delivery system reform with a focus on the triple aim of better health, better health care, and lower costs.² One component of this reform will be accountable care organizations (ACOs). ACOs potentially could assist in closing the racial mortality gap, because provider groups will take responsibility for improving the health of a defined population and will be held accountable for the quality of care delivered.

In the ACO model, an integrated network of providers, led by primary care practitioners, will evaluate the necessity, quality, value, and accountable delivery of specialty diagnostic and therapeutic procedures, including cancer care.³ ACOs will also collect extensive patient data through the meaningful use of medical records.³ These detailed data can then be used to shape locoregional protocols for clinical decision making in oncology and evaluate physician performance. Intermountain Healthcare is an example of an organization that has had success with instituting these clinical protocols to highlight best practices and improve the quality of care.⁴ In breast cancer, oncologists will need to be prepared to develop and follow protocols tailored for their communities, which will lead to standardized, improved care for minority populations.

The oncology medical home is one example of an ACO delivery system reform that has the potential to reduce the racial mortality gap. The oncology medical home replaces episodic care with long-term coordinated care and replaces the fee-for-service model with a performance and outcomes-based system. A key trait of the oncology medical home is care that is continuously improved by measurement against quality standards.⁵ The model oncology home accomplishes this by incorporating software to extract clinical data as well as provider compliance with locoregional guidelines to give oncologists feedback regarding the quality of care that they are providing.⁶ Through this system reform, oncologists will be held accountable for the care they deliver, and it is hoped that this will eliminate the delays, misuse, and underuse of treatment. This could be especially important for optimizing use of hormone therapy for estrogen receptor-positive breast cancer. Trial oncology medical homes in North Carolina and Michigan have yielded promising results regarding improved care (fewer emergency department visits and inpatient admissions) and high adherence to national and practice-selected guidelines.^7,8

PPACA also increases funding for community health centers and provides grants to support community health workers; this highlights again the importance of place in racial health care disparities.⁹ Encouraging collaboration between community health centers and academic institutions, this funding could build bridges between minority communities and high-quality health care institutions while also improving patient communication and education.⁹ As this series has discussed, a failure to provide culturally appropriate clinical information can lead to issues with follow-up and adjuvant treatment compliance and further widen the breast cancer racial mortality gap.

Frontline Medical News

Delivery system reform has the potential to help close the disparity gap by improving the quality of care delivered to minority breast cancer patients. As Chin et al¹⁰ describe in their analysis of effective strategies for reducing health disparities, successful interventions are “culturally tailored to meet patients’ needs, employ multidisciplinary teams of care providers, and target multiple leverage points along a patient’s pathway of care.” ACOs have the financial incentive to meet these features of a successful intervention and improve quality across the continuum of breast cancer care. In addition, the PPACA “incentivized experimentation” with health care delivery, such as the oncology medical home and novel telemedicine interventions, to provide higher quality care outside of hospital settings, which could impact the disparity gap.¹¹

In the face of this new era of organizational structures focused on coordinated, population-based care, oncology providers put themselves at financial risk if they do not position themselves for policy and reimbursement changes that reduce disparities.¹⁰ However, ongoing research will be needed to ensure that as these changes are implemented, the racial mortality gap in breast cancer decreases, and that no vulnerable patient populations are left out.

Precision medicine for all

In addition, as discussed earlier in this series, there are differences in the tumor biology and genomics of breast cancer in African American patients. Beyond quality interventions, initiatives to reduce the mortality gap should focus on precision medicine for all. These initiatives should allow researchers to better understand biologic and genomic differences among breast cancer patients and tailor treatments accordingly. The PPACA has taken steps in this direction and is the first federal law to require group health plans and state-licensed health insurance companies to cover standard-of-care costs associated with participation in clinical trials as well as genetic testing for prevention.¹²

The clinical trial regulations also expressly require plans to show that administrative burdens are not used to create barriers to cancer care for anyone who might benefit from participation in a clinical trial.⁹ The overarching goal of this push to eliminate financial and administrative barriers is to increase the enrollment of minority patients, especially those who do not live close to academic medical centers. In his April 2016 address at the annual meeting of the American Association for Cancer Research, Vice President Joseph Biden identified increased clinical trial participation as a key component of the administration’s cancer “moonshot” as well. Community medical oncologists will be called upon to facilitate and encourage clinical trial participation by their minority patients and should be supported in this endeavor by academic medical centers. With greater minority patient involvement, however, there also should be further research on how trial designs can better lead to clinically significant findings for minority patients. As Polite et al¹³ argue, at a bare minimum, basic sociodemographic and detailed comorbidity information should be prospectively collected and integrated with tumor and host biology data to better examine racial differences in cancer outcomes.

Initiatives also are needed to address the gap in referrals to cancer risk clinics so that more data are available on African American genetic variants, allowing the creation of more robust risk assessment models. Risk assessment relies on predictive statistical models to estimate an individual’s risk of developing cancer, and without accurate estimates of mutation prevalence in minority subgroups, these models’ reliability is compromised.¹⁴ As shown in a recent study at the University of Chicago’s Comprehensive Cancer Risk and Prevention Clinic using targeted genomic capture and next-generation sequencing, nearly one in four African American breast cancer patients referred to the clinic had inherited at least one damaging mutation that increased their risk for the most aggressive type of breast cancer.¹⁵

To identify damaging mutations only after a diagnosis of incurable breast cancer is a failure of prevention. As has been documented in Ashkenazi Jewish populations, there is evidence of high rates of inherited mutations in genes that increase the risk for aggressive breast cancers in populations of African ancestry. This is a fertile area for further research to better understand how these mutations affect the clinical course of breast cancer, what targeted interventions will increase the proportion of breast cancer diagnosed at stage 1, and what molecularly targeted treatments will produce a response in these tumors. Churpek et al¹⁵ also demonstrated the need for continued technological innovation to reduce the disparity gap, because next-generation sequencing is a faster and more cost-efficient way to evaluate multiple variants in many genes. This approach is particularly valuable for African Americans, who tend to have greater genetic diversity.¹⁶ The current administration is also heralding this approach to cancer care. In his 2015 State of the Union address, President Obama announced a precision medicine initiative, including a request for $70 million for the National Cancer Institute to investigate genes that may contribute to the risk of developing cancer.¹⁷ African American women should no longer be left behind in the push for personalized medicine that caters to a patient’s tumor biology and genetic profile. As Subbiah and Kurzrock state, universal genomic testing is not necessarily cost prohibitive, as the cost to obtain a “complete diagnosis and to select appropriate therapy may be miniscule compared with the money wasted on ill-chosen therapies.”¹⁸ 

In conclusion, there is an opportunity in the current climate of health care reform ushered in by the Affordable Care Act to address many of the discussed elements leading to the persistent racial mortality gap in breast cancer. We have argued that two substantial factors lead to this eroding gap. One is differences in tumor biology and genomics, and the second is a quality difference in patterns of care. In describing the perfect storm, Sebastian Junger¹⁹ wrote of the collision of two forces – a hurricane’s warm-air, low-pressure system and an anticyclone’s cool-air, high-pressure system – that combined to create a more powerful and devastating meteorological force. Similarly, we argue that it is the collision of these two factors – tumor biology and genomics with patterns of care – that leads to the breast cancer mortality gap. The delays, misuse, and underuse of treatment that we have underscored are of increased significance when patients present with more aggressive forms of breast cancer. Interventions to close this gap will take leaders at the patient, provider, payer, and community levels to drive system change.

1. Daly B, Olopade OI: A perfect storm: How tumor biology, genomics, and health care delivery patterns collide to create a racial survival disparity in breast cancer and proposed interventions for change. CA Cancer J Clin. 2015 Apr;65:221-38.

2. Fox J: Lessons from an oncology medical home collaborative. Am J Manag Care. 2013; 19:SP5-9.

3. Mehta AJ, Macklis RM: Overview of accountable care organizations for oncology specialists. J Oncol Pract. 2013 Jul; 9(4):216-21.

4. Daly B, Mort EA: A decade after to Err is Human: what should health care leaders be doing? Physician Exec. 2014 May-Jun; 40(3):50-2, 54.

5. Dangi-Garimella S: Oncology medical home: improved quality and cost of care. Am J Manag Care. 2014 Sep.

6. McAneny BL: The future of oncology? COME HOME, the oncology medical home. Am J Manag Care. 2013 Feb.

7. Goyal RK, Wheeler SB, Kohler RE, et al: Health care utilization from chemotherapy-related adverse events among low-income breast cancer patients: effect of enrollment in a medical home program. N C Med J. 2014 Jul-Aug;75(4):231-8.

8. Kuntz G, Tozer JM, Snegosky J, et al: Michigan Oncology Medical Home Demonstration Project: first-year results. J Oncol Pract. 2014 Sep. 10:294-7.

9. Moy B, Polite BN, Halpern MT, et al: American Society of Clinical Oncology policy statement: opportunities in the patient protection and affordable care act to reduce cancer care disparities. J Clin Oncol. 2011 Oct;29(28):3816-24.

10. Chin MH, Clarke AR, Nocon RS, et al: A roadmap and best practices for organizations to reduce racial and ethnic disparities in health care. J Gen Intern Med. 2012 Aug; 27(8):992-1000.

11. Emanuel EJ: How Well Is the Affordable Care Act Doing?: Reasons for Optimism. JAMA 315:1331-2, 2016.

12. Zhang SQ, Polite BN: Achieving a deeper understanding of the implemented provisions of the Affordable Care Act. Am Soc Clin Oncol Educ Book. 2014:e472-7.

13. Polite BN, Sylvester BE, Olopade OI: Race and subset analyses in clinical trials: time to get serious about data integration. J Natl Cancer Inst. 2011 Oct. 103(20):1486-8.

14. Hall MJ, Olopade OI: Disparities in genetic testing: thinking outside the BRCA box. J Clin Oncol. 2006 May; 24(14):2197-203.

15. Churpek JE, Walsh T, Zheng Y, et al: Inherited predisposition to breast cancer among African American women. Breast Cancer Res Treat. 2015 Jan;149(1):31-9.

16. Easton J: Genetic mutations more common among African American women with breast cancer: early testing could protect patients and their relatives. news.uchicago.edu/article/2013/06/03/genetic-mutations-more-common-among-african-american-women-breast-cancer. Published June 3, 2013. Accessed April 20, 2016.

17. Pear R: U.S. to collect genetic data to hone care. New York Times. January 30, 2015.

18. Subbiah V, Kurzrock R: Universal Genomic Testing Needed to Win the War Against Cancer: Genomics IS the Diagnosis. JAMA Oncol, 2016.

19. Junger S: The Perfect Storm. New York, NY: WW Norton and Co; 2009.

Bobby Daly, MD, MBA, is the chief fellow in the section of hematology/oncology at the University of Chicago Medicine. His clinical focus is breast and thoracic oncology, and his research focus is health services. Specifically, Dr. Daly researches disparities in oncology care delivery, oncology health care utilization, aggressive end-of-life oncology care, and oncology payment models. He received his MD and MBA from Harvard Medical School and Harvard Business School, both in Boston, and a BA in Economics and History from Stanford (Calif.) University. He was the recipient of the Dean’s Award at Harvard Medical and Business Schools.

Olufunmilayo Olopade, MD, FACP, OON, is the Walter L. Palmer Distinguished Service Professor of Medicine and Human Genetics, and director, Center for Global Health at the University of Chicago. She is adopting emerging high throughput genomic and informatics strategies to identify genetic and nongenetic risk factors for breast cancer in order to implement precision health care in diverse populations. This innovative approach has the potential to improve the quality of care and reduce costs while saving more lives.

Disclosures: Dr. Olopade serves on the Medical Advisory Board for CancerIQ. Dr. Daly serves as a director of Quadrant Holdings Corporation and receives compensation from this entity. Frontline Medical Communications is a subsidiary of Quadrant Holdings Corporation.

Published in conjunction with Susan G. Komen®.

A tic is described by the DSM-5 as a sudden, rapid, recurrent, nonrhythmic movement or vocalization. Tics are a common occurrence in childhood and can range from mild to severe, transient to chronic, simple to complex. It is not uncommon for parents to ask pediatric care providers when and how to manage tics in children. Here, we present a case to illustrate just such an issue.

Case summary

Adam is an 8-year-old with a previous diagnosis of attention-deficit/hyperactivity disorder (ADHD) who is being seen for follow-up after being started on a stimulant 3 months ago because of declining performance in school and at home, despite adequate accommodations, parent education, and nonpharmacologic treatments. He has done well on a small dose of methylphenidate (0.5 mg/kg per day), but in the context of being asked about other symptoms, his mother, Mary, mentions that she has noticed that Adam is frequently clearing his throat. This began about 6 weeks ago after experiencing allergic rhinitis for almost a week. Since that time, Mary has noticed that he clears his throat as frequently as once every 5 minutes.

The behavior was reported to occur in the classroom, but not nearly with the frequency experienced at home. If asked to not clear his throat, Adam can suppress it. None of his classmates have said anything or appear to have noticed. His parents have never noticed any tics previously. There is a family history of ADHD in his father. There is no other family history of neurodevelopmental disorders, including no obsessive compulsive disorder (OCD), Tourette’s disorder, or other chronic tic disorders. There is nothing else of concern on physical or mental status examination. His mother has concerns that the stimulant medication may be inducing a tic and wonders about stopping it.

Case discussion

Adam has a mild simple vocal tic. The vast majority of tics that develop in childhood will not last the requisite 1 year required to make the diagnosis of a persistent (chronic) motor or vocal tic, nor will they occur with both vocal and motor tics over 1 year required to make the diagnosis of Tourette’s disorder. In the DSM-IV, tics lasting less than 1 year would have been given the diagnosis of transient tic disorder.

In the DSM-5, the diagnosis is now provisional tic disorder because there is no way to tell which tics will be transient and which will be persistent or chronic. Chronic tics occur with a prevalence of between 0.5% and 3%¹, with a male predominance, and are more common in children with ADHD and OCD. In addition, children with chronic tic disorders often have higher incidence of learning problems and, perhaps, autism spectrum disorders. Simple motor and vocal tics (those involving a single muscle group) are more common than complex tics, in which coordinated movements are made. Despite the portrayal in the popular media, it is particularly rare to have complex tics that include copropraxia (an obscene gesture), coprolalia (an obscene movement), echolalia (repeating another’s words), or echopraxia (repeating another’s actions).

Tics tend to have their onset in early school age, with the highest prevalence and severity between the ages of 9 and 12 years.² When present, tics tend to be somewhat suppressed when the child is in school or when the child is engaged in a task. Furthermore, most tics, even when chronic, do not lead to impairment. When impairment does occur, it is often the result of social problems from teasing by peers. Most tics wax and wane over time, but eventually resolve without intervention.

In the case of Adam, there is no clear reason to begin to treat immediately. If one wanted to follow his tics, there are several parent and clinic measures that are available. Taking a history of his case would include ensuring that there are no other predisposing causes and no other psychiatric comorbidities. Induction of tics by the initiation of a stimulant might be considered, although recent data suggest that stimulants are less likely to induce or worsen tics in the course of treatment for ADHD than previously thought.^3,4 If concerned, however, alternative ADHD treatment such as alpha-2 agonist treatment could be considered. Education could be provided to the parents regarding the likelihood of resolution. Should the tics worsen in severity and/or become chronic, there are several behavioral interventions, including habit reversal training and the Comprehensive Behavioral Intervention for Tics, which could be considered as first line.

Medications could be considered if the tics are moderate to severe and behavioral interventions are not sufficient to reduce impairment. The only Food and Drug Administration–approved agents are haloperidol and pimozide, although there is ample support for other agents, and practitioners are most likely to use alternatives, given the side-effect profiles of these typical antipsychotics. Co-occurring symptoms should be considered when thinking about medication. Alpha-2 agonists appear to be most effective in the context of ADHD, while second-generation antipsychotics appear to be more useful if OCD is comorbid. In general, though, in cases like Adam’s, taking a watchful-waiting approach will most often lead to symptom resolution.

References

1. Eur Child Adolesc Psychiatry. 2012 Jan;21(1):5-13.

2. J Am Acad Child Adolesc Psychiatry. 2013 Dec;52(12):1341-59.

3. J Am Acad Child Adolesc Psychiatry. 2015 Sep;54(9):728-36.

4. Cochrane Database Syst Rev. 2011 Apr 13;(4):CD007990.

Dr. Althoff is associate professor of psychiatry, psychology, and pediatrics at the University of Vermont, Burlington. He is director of the division of behavioral genetics and conducts research on the development of self-regulation in children. Email him at [email protected].

A tic is described by the DSM-5 as a sudden, rapid, recurrent, nonrhythmic movement or vocalization. Tics are a common occurrence in childhood and can range from mild to severe, transient to chronic, simple to complex. It is not uncommon for parents to ask pediatric care providers when and how to manage tics in children. Here, we present a case to illustrate just such an issue.

Case summary

Adam is an 8-year-old with a previous diagnosis of attention-deficit/hyperactivity disorder (ADHD) who is being seen for follow-up after being started on a stimulant 3 months ago because of declining performance in school and at home, despite adequate accommodations, parent education, and nonpharmacologic treatments. He has done well on a small dose of methylphenidate (0.5 mg/kg per day), but in the context of being asked about other symptoms, his mother, Mary, mentions that she has noticed that Adam is frequently clearing his throat. This began about 6 weeks ago after experiencing allergic rhinitis for almost a week. Since that time, Mary has noticed that he clears his throat as frequently as once every 5 minutes.

The behavior was reported to occur in the classroom, but not nearly with the frequency experienced at home. If asked to not clear his throat, Adam can suppress it. None of his classmates have said anything or appear to have noticed. His parents have never noticed any tics previously. There is a family history of ADHD in his father. There is no other family history of neurodevelopmental disorders, including no obsessive compulsive disorder (OCD), Tourette’s disorder, or other chronic tic disorders. There is nothing else of concern on physical or mental status examination. His mother has concerns that the stimulant medication may be inducing a tic and wonders about stopping it.

Case discussion

Adam has a mild simple vocal tic. The vast majority of tics that develop in childhood will not last the requisite 1 year required to make the diagnosis of a persistent (chronic) motor or vocal tic, nor will they occur with both vocal and motor tics over 1 year required to make the diagnosis of Tourette’s disorder. In the DSM-IV, tics lasting less than 1 year would have been given the diagnosis of transient tic disorder.

In the DSM-5, the diagnosis is now provisional tic disorder because there is no way to tell which tics will be transient and which will be persistent or chronic. Chronic tics occur with a prevalence of between 0.5% and 3%¹, with a male predominance, and are more common in children with ADHD and OCD. In addition, children with chronic tic disorders often have higher incidence of learning problems and, perhaps, autism spectrum disorders. Simple motor and vocal tics (those involving a single muscle group) are more common than complex tics, in which coordinated movements are made. Despite the portrayal in the popular media, it is particularly rare to have complex tics that include copropraxia (an obscene gesture), coprolalia (an obscene movement), echolalia (repeating another’s words), or echopraxia (repeating another’s actions).

Tics tend to have their onset in early school age, with the highest prevalence and severity between the ages of 9 and 12 years.² When present, tics tend to be somewhat suppressed when the child is in school or when the child is engaged in a task. Furthermore, most tics, even when chronic, do not lead to impairment. When impairment does occur, it is often the result of social problems from teasing by peers. Most tics wax and wane over time, but eventually resolve without intervention.

In the case of Adam, there is no clear reason to begin to treat immediately. If one wanted to follow his tics, there are several parent and clinic measures that are available. Taking a history of his case would include ensuring that there are no other predisposing causes and no other psychiatric comorbidities. Induction of tics by the initiation of a stimulant might be considered, although recent data suggest that stimulants are less likely to induce or worsen tics in the course of treatment for ADHD than previously thought.^3,4 If concerned, however, alternative ADHD treatment such as alpha-2 agonist treatment could be considered. Education could be provided to the parents regarding the likelihood of resolution. Should the tics worsen in severity and/or become chronic, there are several behavioral interventions, including habit reversal training and the Comprehensive Behavioral Intervention for Tics, which could be considered as first line.

Medications could be considered if the tics are moderate to severe and behavioral interventions are not sufficient to reduce impairment. The only Food and Drug Administration–approved agents are haloperidol and pimozide, although there is ample support for other agents, and practitioners are most likely to use alternatives, given the side-effect profiles of these typical antipsychotics. Co-occurring symptoms should be considered when thinking about medication. Alpha-2 agonists appear to be most effective in the context of ADHD, while second-generation antipsychotics appear to be more useful if OCD is comorbid. In general, though, in cases like Adam’s, taking a watchful-waiting approach will most often lead to symptom resolution.

References

1. Eur Child Adolesc Psychiatry. 2012 Jan;21(1):5-13.

2. J Am Acad Child Adolesc Psychiatry. 2013 Dec;52(12):1341-59.

3. J Am Acad Child Adolesc Psychiatry. 2015 Sep;54(9):728-36.

4. Cochrane Database Syst Rev. 2011 Apr 13;(4):CD007990.

Dr. Althoff is associate professor of psychiatry, psychology, and pediatrics at the University of Vermont, Burlington. He is director of the division of behavioral genetics and conducts research on the development of self-regulation in children. Email him at [email protected].

A tic is described by the DSM-5 as a sudden, rapid, recurrent, nonrhythmic movement or vocalization. Tics are a common occurrence in childhood and can range from mild to severe, transient to chronic, simple to complex. It is not uncommon for parents to ask pediatric care providers when and how to manage tics in children. Here, we present a case to illustrate just such an issue.

Case summary

Adam is an 8-year-old with a previous diagnosis of attention-deficit/hyperactivity disorder (ADHD) who is being seen for follow-up after being started on a stimulant 3 months ago because of declining performance in school and at home, despite adequate accommodations, parent education, and nonpharmacologic treatments. He has done well on a small dose of methylphenidate (0.5 mg/kg per day), but in the context of being asked about other symptoms, his mother, Mary, mentions that she has noticed that Adam is frequently clearing his throat. This began about 6 weeks ago after experiencing allergic rhinitis for almost a week. Since that time, Mary has noticed that he clears his throat as frequently as once every 5 minutes.

The behavior was reported to occur in the classroom, but not nearly with the frequency experienced at home. If asked to not clear his throat, Adam can suppress it. None of his classmates have said anything or appear to have noticed. His parents have never noticed any tics previously. There is a family history of ADHD in his father. There is no other family history of neurodevelopmental disorders, including no obsessive compulsive disorder (OCD), Tourette’s disorder, or other chronic tic disorders. There is nothing else of concern on physical or mental status examination. His mother has concerns that the stimulant medication may be inducing a tic and wonders about stopping it.

Case discussion

Adam has a mild simple vocal tic. The vast majority of tics that develop in childhood will not last the requisite 1 year required to make the diagnosis of a persistent (chronic) motor or vocal tic, nor will they occur with both vocal and motor tics over 1 year required to make the diagnosis of Tourette’s disorder. In the DSM-IV, tics lasting less than 1 year would have been given the diagnosis of transient tic disorder.

In the DSM-5, the diagnosis is now provisional tic disorder because there is no way to tell which tics will be transient and which will be persistent or chronic. Chronic tics occur with a prevalence of between 0.5% and 3%¹, with a male predominance, and are more common in children with ADHD and OCD. In addition, children with chronic tic disorders often have higher incidence of learning problems and, perhaps, autism spectrum disorders. Simple motor and vocal tics (those involving a single muscle group) are more common than complex tics, in which coordinated movements are made. Despite the portrayal in the popular media, it is particularly rare to have complex tics that include copropraxia (an obscene gesture), coprolalia (an obscene movement), echolalia (repeating another’s words), or echopraxia (repeating another’s actions).

Tics tend to have their onset in early school age, with the highest prevalence and severity between the ages of 9 and 12 years.² When present, tics tend to be somewhat suppressed when the child is in school or when the child is engaged in a task. Furthermore, most tics, even when chronic, do not lead to impairment. When impairment does occur, it is often the result of social problems from teasing by peers. Most tics wax and wane over time, but eventually resolve without intervention.

In the case of Adam, there is no clear reason to begin to treat immediately. If one wanted to follow his tics, there are several parent and clinic measures that are available. Taking a history of his case would include ensuring that there are no other predisposing causes and no other psychiatric comorbidities. Induction of tics by the initiation of a stimulant might be considered, although recent data suggest that stimulants are less likely to induce or worsen tics in the course of treatment for ADHD than previously thought.^3,4 If concerned, however, alternative ADHD treatment such as alpha-2 agonist treatment could be considered. Education could be provided to the parents regarding the likelihood of resolution. Should the tics worsen in severity and/or become chronic, there are several behavioral interventions, including habit reversal training and the Comprehensive Behavioral Intervention for Tics, which could be considered as first line.

Medications could be considered if the tics are moderate to severe and behavioral interventions are not sufficient to reduce impairment. The only Food and Drug Administration–approved agents are haloperidol and pimozide, although there is ample support for other agents, and practitioners are most likely to use alternatives, given the side-effect profiles of these typical antipsychotics. Co-occurring symptoms should be considered when thinking about medication. Alpha-2 agonists appear to be most effective in the context of ADHD, while second-generation antipsychotics appear to be more useful if OCD is comorbid. In general, though, in cases like Adam’s, taking a watchful-waiting approach will most often lead to symptom resolution.

References

1. Eur Child Adolesc Psychiatry. 2012 Jan;21(1):5-13.

2. J Am Acad Child Adolesc Psychiatry. 2013 Dec;52(12):1341-59.

3. J Am Acad Child Adolesc Psychiatry. 2015 Sep;54(9):728-36.

4. Cochrane Database Syst Rev. 2011 Apr 13;(4):CD007990.

Dr. Althoff is associate professor of psychiatry, psychology, and pediatrics at the University of Vermont, Burlington. He is director of the division of behavioral genetics and conducts research on the development of self-regulation in children. Email him at [email protected].

“READER REACTIONS TO THE PROBLEM OF INADEQUATE CONTRACEPTION FOR HIGH-RISK WOMEN”(COMMENT & CONTROVERSY; APRIL 2016)

Focus on decreasing unintended pregnanciesI found the letters in response to Dr. Barbieri’s Editorial on inadequate contraception to be much overwrought. Dr. Will’s suggestion to have “automatic contraception … for all reproductive-age women including ‘children’ who are … menstruating” is excessive. Shouldn’t parents have the final decision making in their minor children’s health care?

An anonymous clinician ex-presses frustration with a Catholichealth care system for not allowing prescription of contraceptives, which does actually stay true to the religious beliefs of the institution, and proposes decreased reimbursements to these facilities across the board as a form of financial punishment for these practices. Not only would that be illegal and unconstitutional but it also demonstrates a lack of understanding of our First Amendment protections.

Overall, these letters and Dr. Barbieri’s response show a very narrow understanding of the issues involved. I think we can and should be focused on decreasing unintended pregnancies while also respecting the rights of all without resorting to Draconian and totalitarian solutions.

Myles Dotto, MD
Oradell, New Jersey

Dr. Barbieri respondsI share Dr. Dotto’s concern that government mandates regarding health care are potentially very dangerous. It is better for communities of clinicians and patients to develop optimal approaches to health care, without government interference.

“THE CRUSHING OF INNOVATION FOR TREATING FEMALE PELVIC FLOOR DISORDERS: A STORY OF ‘LEAD OR BE LED’”ANDREW CASSIDENTI, MD (GUEST EDITORIAL; APRIL 2016)Stand up for research benefiting our patientsI salute Dr. Cassidenti’s courage to call surgeons and the respective professional organizations to step up to defend the research and expose inappropriate expert testimony. We should be ashamed to be scattered like dogs because of fear and lack of courage to be advocates for what is in the best interest of our patients. Please continue the campaign to encourage physicians and surgeons to stand up.

Cleve Waters, MD
Chattanooga, Tennessee

Caving to class action litigation is a mistakeIn his Guest Editorial Dr. Cassidenti clarifies the importance of looking forward regarding mesh devices for pelvic organ prolapse (POP) treatment. As an advocate for women with POP and Founder/Executive Director of the Association for Pelvic Organ Prolapse Support—a US-based 501(c)(3)advocacy agency with global arms focused on generating awareness of POP and providing guidance and support to women navigating POP treatment—I found Endo International’s decision to close its Astora Women’s Health division extremely unsettling.

The nature of medicine is to continually advance, and that includes learning from experience and recognizing paths to evolution. Caving to class action litigation is a mistake. Research findings frequently indicate that up to half of the female population will experience POP and/or comorbid conditions.¹ It is imperative that health care, industry, research, academia, policy, and advocacy agencies continue to shine a light on this much needed field in women’s health.

Sherrie Palm
Milwaukee, Wisconsin

Reference

“INTRACTABLE SHOULDER DYSTOCIA: A POSTERIOR AXILLA MANEUVER MAY SAVE THE DAY”ROBERT L. BARBIERI, MD (APRIL 2016)

Avoidance: the greatest tool to address shoulder dystociaAlthough avoiding endometrial injury at cesarean delivery, including the possibility of later pathologic implantation, can be attained with vaginal delivery, vaginal birth at all cost leads to a dangerous situation. The emergency environment of shoulder dystocia is not a preferable or safer stratagem.

It is granted that shoulder dystocia will happen at some point but avoidance, by employing cesarean delivery when it is indicated, is the greatest tool for addressing this very dangerous problem.

J. Michael Arnold, MD
Oconto Falls, Wisconsin

Another suggestion for shoulder dystociaMy senior partner taught me a technique that works well, although I do not know its name. After suprapubic and McRoberts maneuvers fail and the shoulders do not deliver with gentle downward guidance in one direction, I rotate the head 180° and try again. Usually this works. I have taught this technique to several midwives, and they swear by it.

Annette Fineberg, MD
Davis, California

Dr. Barbieri respondsI thank Drs. Arnold and Fineberg for sharing their perspective and experience with our readers. Dr. Arnold notes that recommending cesarean delivery in high-risk situations such as cases in which the mother has diabetes and the fetus is macrosomic would surely reduce the frequency of shoulder dystocia. I respect Dr. Fineberg’s recommendation, based on extensive clinical experience, that by rotating the fetal head the shoulder dystocia may be resolved. My concern with this technique is that the torque transmitted to the neck might cause fetal damage. I think that rotating the shoulders (Rubin or Wood maneuver) would be less likely to result in fetal injury.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

“READER REACTIONS TO THE PROBLEM OF INADEQUATE CONTRACEPTION FOR HIGH-RISK WOMEN”(COMMENT & CONTROVERSY; APRIL 2016)

Focus on decreasing unintended pregnanciesI found the letters in response to Dr. Barbieri’s Editorial on inadequate contraception to be much overwrought. Dr. Will’s suggestion to have “automatic contraception … for all reproductive-age women including ‘children’ who are … menstruating” is excessive. Shouldn’t parents have the final decision making in their minor children’s health care?

An anonymous clinician ex-presses frustration with a Catholichealth care system for not allowing prescription of contraceptives, which does actually stay true to the religious beliefs of the institution, and proposes decreased reimbursements to these facilities across the board as a form of financial punishment for these practices. Not only would that be illegal and unconstitutional but it also demonstrates a lack of understanding of our First Amendment protections.

Overall, these letters and Dr. Barbieri’s response show a very narrow understanding of the issues involved. I think we can and should be focused on decreasing unintended pregnancies while also respecting the rights of all without resorting to Draconian and totalitarian solutions.

Myles Dotto, MD
Oradell, New Jersey

Dr. Barbieri respondsI share Dr. Dotto’s concern that government mandates regarding health care are potentially very dangerous. It is better for communities of clinicians and patients to develop optimal approaches to health care, without government interference.

“THE CRUSHING OF INNOVATION FOR TREATING FEMALE PELVIC FLOOR DISORDERS: A STORY OF ‘LEAD OR BE LED’”ANDREW CASSIDENTI, MD (GUEST EDITORIAL; APRIL 2016)Stand up for research benefiting our patientsI salute Dr. Cassidenti’s courage to call surgeons and the respective professional organizations to step up to defend the research and expose inappropriate expert testimony. We should be ashamed to be scattered like dogs because of fear and lack of courage to be advocates for what is in the best interest of our patients. Please continue the campaign to encourage physicians and surgeons to stand up.

Cleve Waters, MD
Chattanooga, Tennessee

Caving to class action litigation is a mistakeIn his Guest Editorial Dr. Cassidenti clarifies the importance of looking forward regarding mesh devices for pelvic organ prolapse (POP) treatment. As an advocate for women with POP and Founder/Executive Director of the Association for Pelvic Organ Prolapse Support—a US-based 501(c)(3)advocacy agency with global arms focused on generating awareness of POP and providing guidance and support to women navigating POP treatment—I found Endo International’s decision to close its Astora Women’s Health division extremely unsettling.

The nature of medicine is to continually advance, and that includes learning from experience and recognizing paths to evolution. Caving to class action litigation is a mistake. Research findings frequently indicate that up to half of the female population will experience POP and/or comorbid conditions.¹ It is imperative that health care, industry, research, academia, policy, and advocacy agencies continue to shine a light on this much needed field in women’s health.

Sherrie Palm
Milwaukee, Wisconsin

Reference

“INTRACTABLE SHOULDER DYSTOCIA: A POSTERIOR AXILLA MANEUVER MAY SAVE THE DAY”ROBERT L. BARBIERI, MD (APRIL 2016)

Avoidance: the greatest tool to address shoulder dystociaAlthough avoiding endometrial injury at cesarean delivery, including the possibility of later pathologic implantation, can be attained with vaginal delivery, vaginal birth at all cost leads to a dangerous situation. The emergency environment of shoulder dystocia is not a preferable or safer stratagem.

It is granted that shoulder dystocia will happen at some point but avoidance, by employing cesarean delivery when it is indicated, is the greatest tool for addressing this very dangerous problem.

J. Michael Arnold, MD
Oconto Falls, Wisconsin

Another suggestion for shoulder dystociaMy senior partner taught me a technique that works well, although I do not know its name. After suprapubic and McRoberts maneuvers fail and the shoulders do not deliver with gentle downward guidance in one direction, I rotate the head 180° and try again. Usually this works. I have taught this technique to several midwives, and they swear by it.

Annette Fineberg, MD
Davis, California

Dr. Barbieri respondsI thank Drs. Arnold and Fineberg for sharing their perspective and experience with our readers. Dr. Arnold notes that recommending cesarean delivery in high-risk situations such as cases in which the mother has diabetes and the fetus is macrosomic would surely reduce the frequency of shoulder dystocia. I respect Dr. Fineberg’s recommendation, based on extensive clinical experience, that by rotating the fetal head the shoulder dystocia may be resolved. My concern with this technique is that the torque transmitted to the neck might cause fetal damage. I think that rotating the shoulders (Rubin or Wood maneuver) would be less likely to result in fetal injury.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

“READER REACTIONS TO THE PROBLEM OF INADEQUATE CONTRACEPTION FOR HIGH-RISK WOMEN”(COMMENT & CONTROVERSY; APRIL 2016)

Focus on decreasing unintended pregnanciesI found the letters in response to Dr. Barbieri’s Editorial on inadequate contraception to be much overwrought. Dr. Will’s suggestion to have “automatic contraception … for all reproductive-age women including ‘children’ who are … menstruating” is excessive. Shouldn’t parents have the final decision making in their minor children’s health care?

An anonymous clinician ex-presses frustration with a Catholichealth care system for not allowing prescription of contraceptives, which does actually stay true to the religious beliefs of the institution, and proposes decreased reimbursements to these facilities across the board as a form of financial punishment for these practices. Not only would that be illegal and unconstitutional but it also demonstrates a lack of understanding of our First Amendment protections.

Overall, these letters and Dr. Barbieri’s response show a very narrow understanding of the issues involved. I think we can and should be focused on decreasing unintended pregnancies while also respecting the rights of all without resorting to Draconian and totalitarian solutions.

Myles Dotto, MD
Oradell, New Jersey

Dr. Barbieri respondsI share Dr. Dotto’s concern that government mandates regarding health care are potentially very dangerous. It is better for communities of clinicians and patients to develop optimal approaches to health care, without government interference.

“THE CRUSHING OF INNOVATION FOR TREATING FEMALE PELVIC FLOOR DISORDERS: A STORY OF ‘LEAD OR BE LED’”ANDREW CASSIDENTI, MD (GUEST EDITORIAL; APRIL 2016)Stand up for research benefiting our patientsI salute Dr. Cassidenti’s courage to call surgeons and the respective professional organizations to step up to defend the research and expose inappropriate expert testimony. We should be ashamed to be scattered like dogs because of fear and lack of courage to be advocates for what is in the best interest of our patients. Please continue the campaign to encourage physicians and surgeons to stand up.

Cleve Waters, MD
Chattanooga, Tennessee

Caving to class action litigation is a mistakeIn his Guest Editorial Dr. Cassidenti clarifies the importance of looking forward regarding mesh devices for pelvic organ prolapse (POP) treatment. As an advocate for women with POP and Founder/Executive Director of the Association for Pelvic Organ Prolapse Support—a US-based 501(c)(3)advocacy agency with global arms focused on generating awareness of POP and providing guidance and support to women navigating POP treatment—I found Endo International’s decision to close its Astora Women’s Health division extremely unsettling.

The nature of medicine is to continually advance, and that includes learning from experience and recognizing paths to evolution. Caving to class action litigation is a mistake. Research findings frequently indicate that up to half of the female population will experience POP and/or comorbid conditions.¹ It is imperative that health care, industry, research, academia, policy, and advocacy agencies continue to shine a light on this much needed field in women’s health.

Sherrie Palm
Milwaukee, Wisconsin

Reference

“INTRACTABLE SHOULDER DYSTOCIA: A POSTERIOR AXILLA MANEUVER MAY SAVE THE DAY”ROBERT L. BARBIERI, MD (APRIL 2016)

Avoidance: the greatest tool to address shoulder dystociaAlthough avoiding endometrial injury at cesarean delivery, including the possibility of later pathologic implantation, can be attained with vaginal delivery, vaginal birth at all cost leads to a dangerous situation. The emergency environment of shoulder dystocia is not a preferable or safer stratagem.

It is granted that shoulder dystocia will happen at some point but avoidance, by employing cesarean delivery when it is indicated, is the greatest tool for addressing this very dangerous problem.

J. Michael Arnold, MD
Oconto Falls, Wisconsin

Another suggestion for shoulder dystociaMy senior partner taught me a technique that works well, although I do not know its name. After suprapubic and McRoberts maneuvers fail and the shoulders do not deliver with gentle downward guidance in one direction, I rotate the head 180° and try again. Usually this works. I have taught this technique to several midwives, and they swear by it.

Annette Fineberg, MD
Davis, California

Dr. Barbieri respondsI thank Drs. Arnold and Fineberg for sharing their perspective and experience with our readers. Dr. Arnold notes that recommending cesarean delivery in high-risk situations such as cases in which the mother has diabetes and the fetus is macrosomic would surely reduce the frequency of shoulder dystocia. I respect Dr. Fineberg’s recommendation, based on extensive clinical experience, that by rotating the fetal head the shoulder dystocia may be resolved. My concern with this technique is that the torque transmitted to the neck might cause fetal damage. I think that rotating the shoulders (Rubin or Wood maneuver) would be less likely to result in fetal injury.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

The figures and trends behind the obesity epidemic are alarming: More than one-third of all adults in the United States are obese, as are 34% of women aged 20-39, and 17% of youth aged 2-19, according to data for 2011-2014 from the National Health and Nutrition Examination Survey.

In our ob.gyn. practices, many of us have witnessed the significant climb in national obesity rates over the past several decades. We’ve seen a continued increase in the prevalence of obesity among childbearing women, and a steady increase in the incidence of high-birth-weight babies. The percentage of women weighing 200 pounds has more than doubled since 1980, and up to 3-4 times as many children and teens in various age subsets are obese today as in the 1970s.

The obesity epidemic is often attributed to a high-fat and/or calorie-dense diet and decreased activity levels. However, this is only part of the picture. There has been growing recognition in recent years that obesity may be programmed by the in utero and newborn environment, particularly as it relates to nutritional permutations. We now have evidence, in fact, that developmental programming is likely a primary cause of the obesity epidemic.

Exposure to maternal obesity and being born with a low birth weight – especially a low birth weight paired with rapid catch-up growth – are both associated with a significantly increased risk of childhood and adult obesity.

Research has demonstrated that newborns may be programmed, in both of these scenarios, with an increased appetite and a predisposition to storing calories as fat. In addition, data are accumulating that exposure to bisphenol A and other endocrine-disruptive chemicals, other environmental toxins, and corticosteroids may exert similar programming effects.

This window into the origins of obesity has significant implications for the practice of ob.gyn., where we have the opportunity to address the programming effects of the in utero and early life environment. Most importantly, we must counsel women before pregnancy about the importance of losing weight, guide them during pregnancy to achieve optimal pregnancy nutrition and weight gain, and prepare them to adopt optimal newborn feeding strategies that will guard against overconsumption.

Programming of obesity

The current obesity epidemic is only minimally due to genetics. Although select genetic mutations may be associated with obesity, these mutations account for an exceedingly small proportion of the obese population. Instead, much of the obesity epidemic involves epigenetic change – in this case, largely epigenetic deregulation of gene expression – and more broadly what we call gestational, or developmental, programming.

Developmental programming is a process by which a stress or stimulus at a critical or sensitive period of development has long-term effects. The major part of the developmental process pertaining to cell division occurs during intrauterine life; more than 90% of the cell divisions necessary to make an adult human occur before birth. Although there are important effects of the early newborn period, developmental programming is therefore largely gestational programming. Depending on when an in utero stress or perturbation occurs, it may permanently change cell number and/or cell differentiation, organ structure, metabolic set points, and gene expression.

The late physician Dr. David Barker got us thinking about in utero programming when he demonstrated an association between low birth weight, rapid weight gain in early life, and adult cardiovascular mortality. His theory about how nutrition and growth before birth may affect cardiovascular health later on, as well as other adult chronic diseases and conditions, became known as the Barker Hypothesis.

Many studies, both animal research and human epidemiological studies, have since confirmed and expanded our understanding of this phenomena. Research has demonstrated associations, for instance, between low birth weight and later risks of insulin resistance, diabetes, fatty liver, and the often-underlying metabolic syndrome.

Obesity is also central to the development of the metabolic syndrome, and we now have irrefutable evidence to show that low birth weight infants have a higher risk of obesity than do normal weight infants. We also know, as Dr. Barker and his colleagues had surmised, that the greatest risks occur when there is rapid catch-up growth of low-birth-weight infants in the early years of life.

Moreover, we now understand that maternal obesity has programming effects that are similar to those of an in utero environment of undernutrition and growth restriction. In the past several decades, the marked increase in maternal obesity has resulted in this programming process having an ever-increasing impact.

Both animal and human studies have shown that infants born to obese mothers have the same increased risks for adult chronic disease – including the risk of becoming obese – as those of low birth weight infants. This increased risk is often, but not always, associated with high birth weight, and it is independent of whether the mother has gestational diabetes mellitus (GDM). Having a high birth weight is more likely in the setting of maternal obesity and itself raises the risk of eventual obesity (as does GDM), but an infant’s exposure to maternal obesity in and of itself is a risk factor.

The mechanisms

The programming mechanisms that predispose offspring to obesity are similar in infants of obese mothers and intrauterine growth restricted newborns, though they involve different epigenetic signals. Both involve dysregulation of appetite/satiety and of adipogenesis.

Appetite is primarily controlled by a complex circuit of neurons in the hypothalamus of the brain called the hypothalamic arcuate nucleus. Some neurons are orexigenic and stimulate or increase appetite, while others are anorexigenic and suppress appetite by promoting satiety.

During fetal development, hypothalamic neural stem cells proliferate and differentiate into various cell types. Neurons destined for the arcuate nucleus then differentiate into these so-called appetite neurons and satiety neurons. Though there is continued neural development and maturation during newborn life, hypothalamic control of appetite and satiety is largely set during this period.

Differentiation to appetite or satiety neurons is regulated by a complex interplay of pathways that may be significantly altered by the nutrient environment. Research in our laboratory and others has shown that both limited and excess nutrition can program the structure and function of the arcuate nucleus – changing its wiring, in essence – such that there is an increased ratio of appetite to satiety neurons (Clin Obstet Gynecol. 2013 Sep;56[3]:529-36).

There also appears to be a programmed down-regulation in the reward pathway of the brain, and some studies have shown that children of obese mothers and children who were born with low birth weights have a higher preference for sweet and high-calorie foods. This all begins at the neural stem cell level.

©moodboard/thinkstockphotos.com

With more appetite neurons and fewer satiety neurons, as well as a down-regulation of reward – and an abundance of available food – a newborn is at high risk of becoming obese. Eating for this child will not only be pleasurable; it will be driven by an enhanced appetite, an inability to feel full after reasonable amounts of food, and a down-regulation of reward (potentially requiring greater amounts of food or a shift in preference for high fat/sweet food to achieve the pleasure from eating).

In addition to alterations in appetite/satiety, the nutrition environment in utero can alter adipose tissue development and function.

Like neural development, adipogenesis – the process by which preadipocytes proliferate and differentiate into mature adipocytes – is tightly regulated by a cascade of transcription factors that are expressed in response to stimuli, including nutrients. In animal studies we have found an up-regulation of adipogenic and lipogenic transcription factors in intrauterine growth restricted offspring as well as in offspring of obese mothers (Reprod Sci. 2008 Oct;15[8]:785-96 and Curr Diab Rep. 2013 Feb;13[1]:27-33).

This up-regulation leads to greater proliferation of preadipocytes and greater lipid synthesis and storage in mature adipocytes. Not only will the newborn have an increased number of adipocytes, but he or she will have an increased number of hypertrophic lipid-filled fat cells. The enhanced adipogenesis will contribute to the newborn’s programmed propensity for obesity, and the directive to “just eat less” will likely be ineffective throughout childhood and beyond.

Programmed offspring are resistant to both central and peripheral effects of leptin and insulin, resulting in impaired satiety (i.e., overeating) and manifestations of GDM. Responses to an array of additional energy regulatory factors (e.g., ghrelin) demonstrate a similar programmed dysfunction.

In practice

There are several approaches that ob.gyns. can take to prevent childhood and lifelong obesity. Most importantly, we must counsel our obese patients to lose weight before pregnancy. In doing so, it may be meaningful and effective to ask the patient to think about her baby’s future as an obese adult.

Patients who have experienced the challenges of trying to lose weight, and who are told about the developmental origins of obesity and how obesity can be programmed, may be more motivated to lose weight to avoid passing on to their children the burden and challenges that they’ve experienced. We can tell obese patients that their children may well be predisposed through the current in utero environment to have an increased appetite and a propensity to store body fat, and that they subsequently will face higher risks of diabetes and other serious chronic conditions.

We should also appropriately counsel women on healthy weight gain during pregnancy, and urge them not to gain excessive weight.

Newborn feeding strategies are also important for babies exposed to gestational programming of obesity, but especially small babies given the high risk of obesity when there is rapid catch-up growth. We must encourage good growth of both the low-birth-weight and macrosomic infant during the newborn period, but not overgrowth.

The importance of breastfeeding cannot be overestimated, as it has been demonstrated to reduce the occurrence of excessive newborn weight gain and improve long term infant health. We should encourage breastfeeding for the natural opportunity it provides to avoid excessive feeding, in addition to its other benefits. And for newborns who are bottle fed, we should counsel the new mother on optimal feeding and strategies for comforting a crying baby, which will protect against overfeeding.

Regarding environmental exposures, this area of developmental programming is continuing to evolve at a rapid rate. Both animal research and epidemiological studies support the association of developmental exposure to BPA and other chemicals with obesity.

For the present, we should educate our patients regarding optimal nutrition prior to and during pregnancy, and the avoidance of potentially toxic or metabolically-active chemicals or drugs. We look forward to continued research into the mechanisms and preventive/therapeutic strategies for optimization of childhood and adult health.

Dr. Ross is professor of obstetrics and gynecology at the University of California, Los Angeles. Dr. Desai is assistant professor of ob.gyn. at the university. They reported having no relevant financial disclosures.

The figures and trends behind the obesity epidemic are alarming: More than one-third of all adults in the United States are obese, as are 34% of women aged 20-39, and 17% of youth aged 2-19, according to data for 2011-2014 from the National Health and Nutrition Examination Survey.

In our ob.gyn. practices, many of us have witnessed the significant climb in national obesity rates over the past several decades. We’ve seen a continued increase in the prevalence of obesity among childbearing women, and a steady increase in the incidence of high-birth-weight babies. The percentage of women weighing 200 pounds has more than doubled since 1980, and up to 3-4 times as many children and teens in various age subsets are obese today as in the 1970s.

The obesity epidemic is often attributed to a high-fat and/or calorie-dense diet and decreased activity levels. However, this is only part of the picture. There has been growing recognition in recent years that obesity may be programmed by the in utero and newborn environment, particularly as it relates to nutritional permutations. We now have evidence, in fact, that developmental programming is likely a primary cause of the obesity epidemic.

Exposure to maternal obesity and being born with a low birth weight – especially a low birth weight paired with rapid catch-up growth – are both associated with a significantly increased risk of childhood and adult obesity.

Research has demonstrated that newborns may be programmed, in both of these scenarios, with an increased appetite and a predisposition to storing calories as fat. In addition, data are accumulating that exposure to bisphenol A and other endocrine-disruptive chemicals, other environmental toxins, and corticosteroids may exert similar programming effects.

This window into the origins of obesity has significant implications for the practice of ob.gyn., where we have the opportunity to address the programming effects of the in utero and early life environment. Most importantly, we must counsel women before pregnancy about the importance of losing weight, guide them during pregnancy to achieve optimal pregnancy nutrition and weight gain, and prepare them to adopt optimal newborn feeding strategies that will guard against overconsumption.

Programming of obesity

The current obesity epidemic is only minimally due to genetics. Although select genetic mutations may be associated with obesity, these mutations account for an exceedingly small proportion of the obese population. Instead, much of the obesity epidemic involves epigenetic change – in this case, largely epigenetic deregulation of gene expression – and more broadly what we call gestational, or developmental, programming.

Developmental programming is a process by which a stress or stimulus at a critical or sensitive period of development has long-term effects. The major part of the developmental process pertaining to cell division occurs during intrauterine life; more than 90% of the cell divisions necessary to make an adult human occur before birth. Although there are important effects of the early newborn period, developmental programming is therefore largely gestational programming. Depending on when an in utero stress or perturbation occurs, it may permanently change cell number and/or cell differentiation, organ structure, metabolic set points, and gene expression.

The late physician Dr. David Barker got us thinking about in utero programming when he demonstrated an association between low birth weight, rapid weight gain in early life, and adult cardiovascular mortality. His theory about how nutrition and growth before birth may affect cardiovascular health later on, as well as other adult chronic diseases and conditions, became known as the Barker Hypothesis.

Many studies, both animal research and human epidemiological studies, have since confirmed and expanded our understanding of this phenomena. Research has demonstrated associations, for instance, between low birth weight and later risks of insulin resistance, diabetes, fatty liver, and the often-underlying metabolic syndrome.

Obesity is also central to the development of the metabolic syndrome, and we now have irrefutable evidence to show that low birth weight infants have a higher risk of obesity than do normal weight infants. We also know, as Dr. Barker and his colleagues had surmised, that the greatest risks occur when there is rapid catch-up growth of low-birth-weight infants in the early years of life.

Moreover, we now understand that maternal obesity has programming effects that are similar to those of an in utero environment of undernutrition and growth restriction. In the past several decades, the marked increase in maternal obesity has resulted in this programming process having an ever-increasing impact.

Both animal and human studies have shown that infants born to obese mothers have the same increased risks for adult chronic disease – including the risk of becoming obese – as those of low birth weight infants. This increased risk is often, but not always, associated with high birth weight, and it is independent of whether the mother has gestational diabetes mellitus (GDM). Having a high birth weight is more likely in the setting of maternal obesity and itself raises the risk of eventual obesity (as does GDM), but an infant’s exposure to maternal obesity in and of itself is a risk factor.

The mechanisms

The programming mechanisms that predispose offspring to obesity are similar in infants of obese mothers and intrauterine growth restricted newborns, though they involve different epigenetic signals. Both involve dysregulation of appetite/satiety and of adipogenesis.

Appetite is primarily controlled by a complex circuit of neurons in the hypothalamus of the brain called the hypothalamic arcuate nucleus. Some neurons are orexigenic and stimulate or increase appetite, while others are anorexigenic and suppress appetite by promoting satiety.

During fetal development, hypothalamic neural stem cells proliferate and differentiate into various cell types. Neurons destined for the arcuate nucleus then differentiate into these so-called appetite neurons and satiety neurons. Though there is continued neural development and maturation during newborn life, hypothalamic control of appetite and satiety is largely set during this period.

Differentiation to appetite or satiety neurons is regulated by a complex interplay of pathways that may be significantly altered by the nutrient environment. Research in our laboratory and others has shown that both limited and excess nutrition can program the structure and function of the arcuate nucleus – changing its wiring, in essence – such that there is an increased ratio of appetite to satiety neurons (Clin Obstet Gynecol. 2013 Sep;56[3]:529-36).

There also appears to be a programmed down-regulation in the reward pathway of the brain, and some studies have shown that children of obese mothers and children who were born with low birth weights have a higher preference for sweet and high-calorie foods. This all begins at the neural stem cell level.

©moodboard/thinkstockphotos.com

With more appetite neurons and fewer satiety neurons, as well as a down-regulation of reward – and an abundance of available food – a newborn is at high risk of becoming obese. Eating for this child will not only be pleasurable; it will be driven by an enhanced appetite, an inability to feel full after reasonable amounts of food, and a down-regulation of reward (potentially requiring greater amounts of food or a shift in preference for high fat/sweet food to achieve the pleasure from eating).

In addition to alterations in appetite/satiety, the nutrition environment in utero can alter adipose tissue development and function.

Like neural development, adipogenesis – the process by which preadipocytes proliferate and differentiate into mature adipocytes – is tightly regulated by a cascade of transcription factors that are expressed in response to stimuli, including nutrients. In animal studies we have found an up-regulation of adipogenic and lipogenic transcription factors in intrauterine growth restricted offspring as well as in offspring of obese mothers (Reprod Sci. 2008 Oct;15[8]:785-96 and Curr Diab Rep. 2013 Feb;13[1]:27-33).

This up-regulation leads to greater proliferation of preadipocytes and greater lipid synthesis and storage in mature adipocytes. Not only will the newborn have an increased number of adipocytes, but he or she will have an increased number of hypertrophic lipid-filled fat cells. The enhanced adipogenesis will contribute to the newborn’s programmed propensity for obesity, and the directive to “just eat less” will likely be ineffective throughout childhood and beyond.

Programmed offspring are resistant to both central and peripheral effects of leptin and insulin, resulting in impaired satiety (i.e., overeating) and manifestations of GDM. Responses to an array of additional energy regulatory factors (e.g., ghrelin) demonstrate a similar programmed dysfunction.

In practice

There are several approaches that ob.gyns. can take to prevent childhood and lifelong obesity. Most importantly, we must counsel our obese patients to lose weight before pregnancy. In doing so, it may be meaningful and effective to ask the patient to think about her baby’s future as an obese adult.

Patients who have experienced the challenges of trying to lose weight, and who are told about the developmental origins of obesity and how obesity can be programmed, may be more motivated to lose weight to avoid passing on to their children the burden and challenges that they’ve experienced. We can tell obese patients that their children may well be predisposed through the current in utero environment to have an increased appetite and a propensity to store body fat, and that they subsequently will face higher risks of diabetes and other serious chronic conditions.

We should also appropriately counsel women on healthy weight gain during pregnancy, and urge them not to gain excessive weight.

Newborn feeding strategies are also important for babies exposed to gestational programming of obesity, but especially small babies given the high risk of obesity when there is rapid catch-up growth. We must encourage good growth of both the low-birth-weight and macrosomic infant during the newborn period, but not overgrowth.

The importance of breastfeeding cannot be overestimated, as it has been demonstrated to reduce the occurrence of excessive newborn weight gain and improve long term infant health. We should encourage breastfeeding for the natural opportunity it provides to avoid excessive feeding, in addition to its other benefits. And for newborns who are bottle fed, we should counsel the new mother on optimal feeding and strategies for comforting a crying baby, which will protect against overfeeding.

Regarding environmental exposures, this area of developmental programming is continuing to evolve at a rapid rate. Both animal research and epidemiological studies support the association of developmental exposure to BPA and other chemicals with obesity.

For the present, we should educate our patients regarding optimal nutrition prior to and during pregnancy, and the avoidance of potentially toxic or metabolically-active chemicals or drugs. We look forward to continued research into the mechanisms and preventive/therapeutic strategies for optimization of childhood and adult health.

Dr. Ross is professor of obstetrics and gynecology at the University of California, Los Angeles. Dr. Desai is assistant professor of ob.gyn. at the university. They reported having no relevant financial disclosures.

The figures and trends behind the obesity epidemic are alarming: More than one-third of all adults in the United States are obese, as are 34% of women aged 20-39, and 17% of youth aged 2-19, according to data for 2011-2014 from the National Health and Nutrition Examination Survey.

In our ob.gyn. practices, many of us have witnessed the significant climb in national obesity rates over the past several decades. We’ve seen a continued increase in the prevalence of obesity among childbearing women, and a steady increase in the incidence of high-birth-weight babies. The percentage of women weighing 200 pounds has more than doubled since 1980, and up to 3-4 times as many children and teens in various age subsets are obese today as in the 1970s.

The obesity epidemic is often attributed to a high-fat and/or calorie-dense diet and decreased activity levels. However, this is only part of the picture. There has been growing recognition in recent years that obesity may be programmed by the in utero and newborn environment, particularly as it relates to nutritional permutations. We now have evidence, in fact, that developmental programming is likely a primary cause of the obesity epidemic.

Exposure to maternal obesity and being born with a low birth weight – especially a low birth weight paired with rapid catch-up growth – are both associated with a significantly increased risk of childhood and adult obesity.

Research has demonstrated that newborns may be programmed, in both of these scenarios, with an increased appetite and a predisposition to storing calories as fat. In addition, data are accumulating that exposure to bisphenol A and other endocrine-disruptive chemicals, other environmental toxins, and corticosteroids may exert similar programming effects.

This window into the origins of obesity has significant implications for the practice of ob.gyn., where we have the opportunity to address the programming effects of the in utero and early life environment. Most importantly, we must counsel women before pregnancy about the importance of losing weight, guide them during pregnancy to achieve optimal pregnancy nutrition and weight gain, and prepare them to adopt optimal newborn feeding strategies that will guard against overconsumption.

Programming of obesity

The current obesity epidemic is only minimally due to genetics. Although select genetic mutations may be associated with obesity, these mutations account for an exceedingly small proportion of the obese population. Instead, much of the obesity epidemic involves epigenetic change – in this case, largely epigenetic deregulation of gene expression – and more broadly what we call gestational, or developmental, programming.

Developmental programming is a process by which a stress or stimulus at a critical or sensitive period of development has long-term effects. The major part of the developmental process pertaining to cell division occurs during intrauterine life; more than 90% of the cell divisions necessary to make an adult human occur before birth. Although there are important effects of the early newborn period, developmental programming is therefore largely gestational programming. Depending on when an in utero stress or perturbation occurs, it may permanently change cell number and/or cell differentiation, organ structure, metabolic set points, and gene expression.

The late physician Dr. David Barker got us thinking about in utero programming when he demonstrated an association between low birth weight, rapid weight gain in early life, and adult cardiovascular mortality. His theory about how nutrition and growth before birth may affect cardiovascular health later on, as well as other adult chronic diseases and conditions, became known as the Barker Hypothesis.

Many studies, both animal research and human epidemiological studies, have since confirmed and expanded our understanding of this phenomena. Research has demonstrated associations, for instance, between low birth weight and later risks of insulin resistance, diabetes, fatty liver, and the often-underlying metabolic syndrome.

Obesity is also central to the development of the metabolic syndrome, and we now have irrefutable evidence to show that low birth weight infants have a higher risk of obesity than do normal weight infants. We also know, as Dr. Barker and his colleagues had surmised, that the greatest risks occur when there is rapid catch-up growth of low-birth-weight infants in the early years of life.

Moreover, we now understand that maternal obesity has programming effects that are similar to those of an in utero environment of undernutrition and growth restriction. In the past several decades, the marked increase in maternal obesity has resulted in this programming process having an ever-increasing impact.

Both animal and human studies have shown that infants born to obese mothers have the same increased risks for adult chronic disease – including the risk of becoming obese – as those of low birth weight infants. This increased risk is often, but not always, associated with high birth weight, and it is independent of whether the mother has gestational diabetes mellitus (GDM). Having a high birth weight is more likely in the setting of maternal obesity and itself raises the risk of eventual obesity (as does GDM), but an infant’s exposure to maternal obesity in and of itself is a risk factor.

The mechanisms

The programming mechanisms that predispose offspring to obesity are similar in infants of obese mothers and intrauterine growth restricted newborns, though they involve different epigenetic signals. Both involve dysregulation of appetite/satiety and of adipogenesis.

Appetite is primarily controlled by a complex circuit of neurons in the hypothalamus of the brain called the hypothalamic arcuate nucleus. Some neurons are orexigenic and stimulate or increase appetite, while others are anorexigenic and suppress appetite by promoting satiety.

During fetal development, hypothalamic neural stem cells proliferate and differentiate into various cell types. Neurons destined for the arcuate nucleus then differentiate into these so-called appetite neurons and satiety neurons. Though there is continued neural development and maturation during newborn life, hypothalamic control of appetite and satiety is largely set during this period.

Differentiation to appetite or satiety neurons is regulated by a complex interplay of pathways that may be significantly altered by the nutrient environment. Research in our laboratory and others has shown that both limited and excess nutrition can program the structure and function of the arcuate nucleus – changing its wiring, in essence – such that there is an increased ratio of appetite to satiety neurons (Clin Obstet Gynecol. 2013 Sep;56[3]:529-36).

There also appears to be a programmed down-regulation in the reward pathway of the brain, and some studies have shown that children of obese mothers and children who were born with low birth weights have a higher preference for sweet and high-calorie foods. This all begins at the neural stem cell level.

©moodboard/thinkstockphotos.com

With more appetite neurons and fewer satiety neurons, as well as a down-regulation of reward – and an abundance of available food – a newborn is at high risk of becoming obese. Eating for this child will not only be pleasurable; it will be driven by an enhanced appetite, an inability to feel full after reasonable amounts of food, and a down-regulation of reward (potentially requiring greater amounts of food or a shift in preference for high fat/sweet food to achieve the pleasure from eating).

In addition to alterations in appetite/satiety, the nutrition environment in utero can alter adipose tissue development and function.

Like neural development, adipogenesis – the process by which preadipocytes proliferate and differentiate into mature adipocytes – is tightly regulated by a cascade of transcription factors that are expressed in response to stimuli, including nutrients. In animal studies we have found an up-regulation of adipogenic and lipogenic transcription factors in intrauterine growth restricted offspring as well as in offspring of obese mothers (Reprod Sci. 2008 Oct;15[8]:785-96 and Curr Diab Rep. 2013 Feb;13[1]:27-33).

This up-regulation leads to greater proliferation of preadipocytes and greater lipid synthesis and storage in mature adipocytes. Not only will the newborn have an increased number of adipocytes, but he or she will have an increased number of hypertrophic lipid-filled fat cells. The enhanced adipogenesis will contribute to the newborn’s programmed propensity for obesity, and the directive to “just eat less” will likely be ineffective throughout childhood and beyond.

Programmed offspring are resistant to both central and peripheral effects of leptin and insulin, resulting in impaired satiety (i.e., overeating) and manifestations of GDM. Responses to an array of additional energy regulatory factors (e.g., ghrelin) demonstrate a similar programmed dysfunction.

In practice

There are several approaches that ob.gyns. can take to prevent childhood and lifelong obesity. Most importantly, we must counsel our obese patients to lose weight before pregnancy. In doing so, it may be meaningful and effective to ask the patient to think about her baby’s future as an obese adult.

Patients who have experienced the challenges of trying to lose weight, and who are told about the developmental origins of obesity and how obesity can be programmed, may be more motivated to lose weight to avoid passing on to their children the burden and challenges that they’ve experienced. We can tell obese patients that their children may well be predisposed through the current in utero environment to have an increased appetite and a propensity to store body fat, and that they subsequently will face higher risks of diabetes and other serious chronic conditions.

We should also appropriately counsel women on healthy weight gain during pregnancy, and urge them not to gain excessive weight.

Newborn feeding strategies are also important for babies exposed to gestational programming of obesity, but especially small babies given the high risk of obesity when there is rapid catch-up growth. We must encourage good growth of both the low-birth-weight and macrosomic infant during the newborn period, but not overgrowth.

The importance of breastfeeding cannot be overestimated, as it has been demonstrated to reduce the occurrence of excessive newborn weight gain and improve long term infant health. We should encourage breastfeeding for the natural opportunity it provides to avoid excessive feeding, in addition to its other benefits. And for newborns who are bottle fed, we should counsel the new mother on optimal feeding and strategies for comforting a crying baby, which will protect against overfeeding.

Regarding environmental exposures, this area of developmental programming is continuing to evolve at a rapid rate. Both animal research and epidemiological studies support the association of developmental exposure to BPA and other chemicals with obesity.

For the present, we should educate our patients regarding optimal nutrition prior to and during pregnancy, and the avoidance of potentially toxic or metabolically-active chemicals or drugs. We look forward to continued research into the mechanisms and preventive/therapeutic strategies for optimization of childhood and adult health.

Dr. Ross is professor of obstetrics and gynecology at the University of California, Los Angeles. Dr. Desai is assistant professor of ob.gyn. at the university. They reported having no relevant financial disclosures.