Commentary

The way we are paid as doctors is changing. In some cases, the delivery of orthopedic care could change from healthcare institutions’ most significant financial asset to one of their most detrimental liabilities. These changes provide a chance to improve both the quality and efficiency of the care we deliver, but we are unlikely to capitalize on this opportunity unless we understand this shifting paradigm. This change requires us to first appreciate the recent history of our reimbursement environment.

Traditionally, healthcare has been a relatively lucrative field, especially for those providing surgical care: doctors are paid “physician fees” by insurance companies (including Medicare), and institutions where procedures are performed are paid “facility fees.” Profits are measured as revenue (ie, reimbursement) minus costs of providing care, and while there has always been the potential to make more money by lowering costs, providers have historically had much more to gain by increasing their revenue. This fact has been exacerbated by the “fee-for-service” (FFS) payment model, which unintentionally encourages physicians to provide high volumes of care by “paying more for doing more.” For example, rather than being paid a fixed sum to care for a patient’s knee arthritis, each provider involved in the patient’s care is paid for each intervention. Clearly, this system encourages providers to maximize their interventions (ie, earning revenue) rather than search for ways to cut costs.

The Centers for Medicare and Medicaid Services (CMS) partially addressed this issue during the 1980s by introducing the Diagnosis Related Group (DRG).^1,2 Under this classification scheme, hospitals would be paid a pre-specified amount for a particular type of admission, often based on a specific procedure. For example, there is a DRG with a set payment for total knee arthroplasty (TKA).³ When reimbursement for the condition is set at a fixed amount, facilities are motivated to decrease their expenses since this is the only way to maximize the financial return for a given patient. This change, theoretically, encourages providers to cut their costs for providing a TKA as much as possible, potentially even to the point of sacrificing quality of care. As usual, when CMS makes a sweeping change, private insurers followed suit, and as a result, both government and corporate insurance is now structured around DRGs.

However, this was not a complete departure from FFS payment. We were still not paid to manage a patient’s knee arthritis as cheaply as possible; we were paid for each steroid injection, preoperative clinic visit, TKA (with numerous coding modifiers for complexity or comorbidities) as well as post-discharge admissions to skilled nursing and acute rehabilitation facilities. However, it was a start: for example, hospitals were no longer incentivized to keep TKA patients in house with a growing bill for each administered drug or therapy session. Yet, it is noteworthy that hospitals and physicians were still paid separately. This is important because doctors have historically made almost all treatment decisions and thereby determined the cost of care, yet hospitals have borne most of those costs, such as expensive implants or unplanned admissions, without a commensurate increase in reimbursement. As long as physicians are guaranteed their “fee,” they have little motivation to reduce those costs. Unsurprisingly, and as we well know, the advent of DRGs did not successfully curb our growing healthcare budget.

Recently, TKA and total hip arthroplasty reimbursement changed more dramatically. After experimenting with several pilots, CMS rolled out the Comprehensive Care for Joint Replacement (CJR) bundled payment program in 2015.^1,4 Participation in CJR is mandatory for most arthroplasty providers in approximately half of all “metropolitan” areas. In this scheme, hospital and physician pay is intertwined. Specifically, hospitals are held accountable for costs, so if the total Medicare bill for a patient’s TKA exceeds the “target price,” the hospital faces a penalty. Conversely, a charge below the target can earn a bonus payment.⁴ The hospital and surgeons must decide how they will share the bonus (or penalty), which creates an incentive to work together to lower costs.

Continue to: While bundled payments like CJR shift some...

While bundled payments like CJR shift some of the risk for high costs to the hospital and surgeon, a much more extreme example of this type of shift is capitation (ie, paying a healthcare institution a set amount per patient to care for whatever maladies arise). Insurers have experimented with various forms of capitation in the past, which led to the expansion of health management organizations (HMOs) during the 1990s. In theory, capitation should encourage providers to invest in disease prevention to minimize the need for costly interventions. However, more nefarious incentives developed, resulting in “cherry picking” healthy patients, which restricts access to care for sicker patients, and even withholds care from patients in need. The most infamous example was arguably “drive-through deliveries,” where newborns and their mothers were prematurely discharged following birth.⁵ As a result, the “HMO backlash” occurred, and capitation temporarily fell out of favor. The heart of the problem was a strong incentive to reduce the cost of care without a counterbalancing incentive to maintain quality. CJR and other modern programs attempt to avoid similar adverse incentives by requiring participants to meet certain quality criteria.⁶

Since the passage of the Affordable Care Act in 2010, capitation has reemerged under a new name: Accountable Care Organizations (ACOs). Numerous forms of ACO’s exist with differing payment schemes⁷, but the most comprehensive version, named Next Generation (Next Gen), allows providers to choose full capitation.⁸ While early ACOs focused on individual patients, Next Gen ACOs are also focused on “population health.” That is, they must demonstrate outcomes for individuals and the patient population as a whole, while simultaneously assuming all financial risk via capitation. Specifically, these ACO’s are paid an “all-inclusive population-based payment” for each patient based on how much that type of patient’s care is expected to cost for the year.⁹ The ACO then provides all necessary treatment and, if the ACO cannot provide a necessary intervention, it is responsible for funding that care at another institution. Appropriately, there has been an increased focus on quality to avoid unintentional incentives to withhold care. Specifically, CMS has introduced mandatory quality metrics in the domains of patient experience, care coordination, preventive care, and management of at-risk populations.¹⁰ At present, unfortunately, these metrics are not nearly comprehensive enough nor adequately validated to assess the quality of care,¹¹ especially for subspecialized fields like orthopedics where functional outcome scores are needed.

To date, very limited attention in the media or academic literature has been dedicated to subspecialty surgical care in the setting of ACOs even though implications for specialized surgeons could be immense. While ACOs bring numerous reporting requirements, the most essential first step for orthopedists in transition to this new reimbursement scheme will be a change in mindset. As explained above, orthopedics and other forms of specialized surgical care have traditionally been extremely profitable for healthcare institutions through relatively high revenue. However, within a capitated ACO all revenue has been paid upfront for each patient, and every orthopedic surgery performed represents a substantial cost to the institution rather than a large profit. For example, it has been reported that the average contribution margin earned by a hospital for an episode of care to provide a TKA (which includes postoperative care such as clinic visits, unplanned readmissions, and reoperations for complications) based on Medicare reimbursement is $11,726.¹² This figure consists of reimbursement (median, $24,149) less variable costs (median, $10,190). Additionally, the surgeon currently receives $1400 in physician fees.¹³ These earnings represent a significant financial benefit for both the facility and doctor in the current FFS environment. However, a capitated ACO caring for a TKA patient would already have received full payment for his care for the year. As a result, providing a TKA would not afford any further financial benefit and would, instead, mean a loss of $10,190 (the aforementioned variable cost for the episode of care) directly from the bottom line. The orthopedic department within that ACO, along with other departments, can be expected to share that loss. This implies that upon becoming an ACO, an institution’s orthopedics department will change from a major profit-center to a major cost-center.

Continue to: CMS must establish adequate quality assurance...

CMS must establish adequate quality assurance measures to ensure that ACOs do not withhold cost-effective care, like TKAs,^14,15 from their patients. Hopefully, for both professional and ethical reasons, providers will be active partners in this process. Groups like the International Consortium for Health Outcome Measurement, which has convened international expert panels to agree on comprehensive outcome sets for total joint arthroplasty and the management of low back pain, among other non-orthopedic conditions, may be useful examples in this process.^16-18

At the provider level, surgeons will be more likely to be salaried employees, contracting directly with the ACO rather than primarily working to earn physician fees from insurance providers. Surgeons will likely be judged (and rewarded financially) on their ability to direct nonoperative care, to find non-surgical solutions to problems that may currently be treated operatively, and to reduce costs for patients that require surgery. Additionally, with an increased focus on quality assurance, there will likely be more pressure from ACOs and CMS to demonstrate results of both operative and nonoperative care, likely in the forms of patient-reported metrics and objective measures of physical function. Surgeons will have a strong incentive to be leaders in the process of collecting such data.

It is also worth considering the position of orthopedic practices that are not part of an ACO. Some ACOs will not have the capacity to provide all (or possibly any) of the orthopedic care their patients require. When necessary, they will contract with outside orthopedic practices. Compared with CMS, ACOs are much smaller purchasers and can be expected to be more sensitive to price, likely negotiating intensely between local orthopedic providers. As a result, even orthopedists outside of ACOs may feel the cost pressure created by this new reimbursement model and may be driven to implement cost-reduction measures such as standardized implant choices and discharge pathways.

ACOs are in an active growth phase,^19,20 and recent updates to ACO policies make it clear that CMS intends for this trend to continue.⁸ Since ACOs are still a nascent reimbursement model, orthopedists will still do better financially, in almost all markets, by continuing to expend their energy and resources pursuing revenue, rather than cutting costs or demonstrating outcomes. However, as ACOs and population health gain traction, those orthopedists who recognize this shift and plan accordingly will have a definite strategic advantage, whether their practice is within an ACO, interacting with external ACOs, or both.

The way we are paid as doctors is changing. In some cases, the delivery of orthopedic care could change from healthcare institutions’ most significant financial asset to one of their most detrimental liabilities. These changes provide a chance to improve both the quality and efficiency of the care we deliver, but we are unlikely to capitalize on this opportunity unless we understand this shifting paradigm. This change requires us to first appreciate the recent history of our reimbursement environment.

Traditionally, healthcare has been a relatively lucrative field, especially for those providing surgical care: doctors are paid “physician fees” by insurance companies (including Medicare), and institutions where procedures are performed are paid “facility fees.” Profits are measured as revenue (ie, reimbursement) minus costs of providing care, and while there has always been the potential to make more money by lowering costs, providers have historically had much more to gain by increasing their revenue. This fact has been exacerbated by the “fee-for-service” (FFS) payment model, which unintentionally encourages physicians to provide high volumes of care by “paying more for doing more.” For example, rather than being paid a fixed sum to care for a patient’s knee arthritis, each provider involved in the patient’s care is paid for each intervention. Clearly, this system encourages providers to maximize their interventions (ie, earning revenue) rather than search for ways to cut costs.

The Centers for Medicare and Medicaid Services (CMS) partially addressed this issue during the 1980s by introducing the Diagnosis Related Group (DRG).^1,2 Under this classification scheme, hospitals would be paid a pre-specified amount for a particular type of admission, often based on a specific procedure. For example, there is a DRG with a set payment for total knee arthroplasty (TKA).³ When reimbursement for the condition is set at a fixed amount, facilities are motivated to decrease their expenses since this is the only way to maximize the financial return for a given patient. This change, theoretically, encourages providers to cut their costs for providing a TKA as much as possible, potentially even to the point of sacrificing quality of care. As usual, when CMS makes a sweeping change, private insurers followed suit, and as a result, both government and corporate insurance is now structured around DRGs.

However, this was not a complete departure from FFS payment. We were still not paid to manage a patient’s knee arthritis as cheaply as possible; we were paid for each steroid injection, preoperative clinic visit, TKA (with numerous coding modifiers for complexity or comorbidities) as well as post-discharge admissions to skilled nursing and acute rehabilitation facilities. However, it was a start: for example, hospitals were no longer incentivized to keep TKA patients in house with a growing bill for each administered drug or therapy session. Yet, it is noteworthy that hospitals and physicians were still paid separately. This is important because doctors have historically made almost all treatment decisions and thereby determined the cost of care, yet hospitals have borne most of those costs, such as expensive implants or unplanned admissions, without a commensurate increase in reimbursement. As long as physicians are guaranteed their “fee,” they have little motivation to reduce those costs. Unsurprisingly, and as we well know, the advent of DRGs did not successfully curb our growing healthcare budget.

Recently, TKA and total hip arthroplasty reimbursement changed more dramatically. After experimenting with several pilots, CMS rolled out the Comprehensive Care for Joint Replacement (CJR) bundled payment program in 2015.^1,4 Participation in CJR is mandatory for most arthroplasty providers in approximately half of all “metropolitan” areas. In this scheme, hospital and physician pay is intertwined. Specifically, hospitals are held accountable for costs, so if the total Medicare bill for a patient’s TKA exceeds the “target price,” the hospital faces a penalty. Conversely, a charge below the target can earn a bonus payment.⁴ The hospital and surgeons must decide how they will share the bonus (or penalty), which creates an incentive to work together to lower costs.

Continue to: While bundled payments like CJR shift some...

While bundled payments like CJR shift some of the risk for high costs to the hospital and surgeon, a much more extreme example of this type of shift is capitation (ie, paying a healthcare institution a set amount per patient to care for whatever maladies arise). Insurers have experimented with various forms of capitation in the past, which led to the expansion of health management organizations (HMOs) during the 1990s. In theory, capitation should encourage providers to invest in disease prevention to minimize the need for costly interventions. However, more nefarious incentives developed, resulting in “cherry picking” healthy patients, which restricts access to care for sicker patients, and even withholds care from patients in need. The most infamous example was arguably “drive-through deliveries,” where newborns and their mothers were prematurely discharged following birth.⁵ As a result, the “HMO backlash” occurred, and capitation temporarily fell out of favor. The heart of the problem was a strong incentive to reduce the cost of care without a counterbalancing incentive to maintain quality. CJR and other modern programs attempt to avoid similar adverse incentives by requiring participants to meet certain quality criteria.⁶

Since the passage of the Affordable Care Act in 2010, capitation has reemerged under a new name: Accountable Care Organizations (ACOs). Numerous forms of ACO’s exist with differing payment schemes⁷, but the most comprehensive version, named Next Generation (Next Gen), allows providers to choose full capitation.⁸ While early ACOs focused on individual patients, Next Gen ACOs are also focused on “population health.” That is, they must demonstrate outcomes for individuals and the patient population as a whole, while simultaneously assuming all financial risk via capitation. Specifically, these ACO’s are paid an “all-inclusive population-based payment” for each patient based on how much that type of patient’s care is expected to cost for the year.⁹ The ACO then provides all necessary treatment and, if the ACO cannot provide a necessary intervention, it is responsible for funding that care at another institution. Appropriately, there has been an increased focus on quality to avoid unintentional incentives to withhold care. Specifically, CMS has introduced mandatory quality metrics in the domains of patient experience, care coordination, preventive care, and management of at-risk populations.¹⁰ At present, unfortunately, these metrics are not nearly comprehensive enough nor adequately validated to assess the quality of care,¹¹ especially for subspecialized fields like orthopedics where functional outcome scores are needed.

To date, very limited attention in the media or academic literature has been dedicated to subspecialty surgical care in the setting of ACOs even though implications for specialized surgeons could be immense. While ACOs bring numerous reporting requirements, the most essential first step for orthopedists in transition to this new reimbursement scheme will be a change in mindset. As explained above, orthopedics and other forms of specialized surgical care have traditionally been extremely profitable for healthcare institutions through relatively high revenue. However, within a capitated ACO all revenue has been paid upfront for each patient, and every orthopedic surgery performed represents a substantial cost to the institution rather than a large profit. For example, it has been reported that the average contribution margin earned by a hospital for an episode of care to provide a TKA (which includes postoperative care such as clinic visits, unplanned readmissions, and reoperations for complications) based on Medicare reimbursement is $11,726.¹² This figure consists of reimbursement (median, $24,149) less variable costs (median, $10,190). Additionally, the surgeon currently receives $1400 in physician fees.¹³ These earnings represent a significant financial benefit for both the facility and doctor in the current FFS environment. However, a capitated ACO caring for a TKA patient would already have received full payment for his care for the year. As a result, providing a TKA would not afford any further financial benefit and would, instead, mean a loss of $10,190 (the aforementioned variable cost for the episode of care) directly from the bottom line. The orthopedic department within that ACO, along with other departments, can be expected to share that loss. This implies that upon becoming an ACO, an institution’s orthopedics department will change from a major profit-center to a major cost-center.

Continue to: CMS must establish adequate quality assurance...

CMS must establish adequate quality assurance measures to ensure that ACOs do not withhold cost-effective care, like TKAs,^14,15 from their patients. Hopefully, for both professional and ethical reasons, providers will be active partners in this process. Groups like the International Consortium for Health Outcome Measurement, which has convened international expert panels to agree on comprehensive outcome sets for total joint arthroplasty and the management of low back pain, among other non-orthopedic conditions, may be useful examples in this process.^16-18

At the provider level, surgeons will be more likely to be salaried employees, contracting directly with the ACO rather than primarily working to earn physician fees from insurance providers. Surgeons will likely be judged (and rewarded financially) on their ability to direct nonoperative care, to find non-surgical solutions to problems that may currently be treated operatively, and to reduce costs for patients that require surgery. Additionally, with an increased focus on quality assurance, there will likely be more pressure from ACOs and CMS to demonstrate results of both operative and nonoperative care, likely in the forms of patient-reported metrics and objective measures of physical function. Surgeons will have a strong incentive to be leaders in the process of collecting such data.

It is also worth considering the position of orthopedic practices that are not part of an ACO. Some ACOs will not have the capacity to provide all (or possibly any) of the orthopedic care their patients require. When necessary, they will contract with outside orthopedic practices. Compared with CMS, ACOs are much smaller purchasers and can be expected to be more sensitive to price, likely negotiating intensely between local orthopedic providers. As a result, even orthopedists outside of ACOs may feel the cost pressure created by this new reimbursement model and may be driven to implement cost-reduction measures such as standardized implant choices and discharge pathways.

ACOs are in an active growth phase,^19,20 and recent updates to ACO policies make it clear that CMS intends for this trend to continue.⁸ Since ACOs are still a nascent reimbursement model, orthopedists will still do better financially, in almost all markets, by continuing to expend their energy and resources pursuing revenue, rather than cutting costs or demonstrating outcomes. However, as ACOs and population health gain traction, those orthopedists who recognize this shift and plan accordingly will have a definite strategic advantage, whether their practice is within an ACO, interacting with external ACOs, or both.

The way we are paid as doctors is changing. In some cases, the delivery of orthopedic care could change from healthcare institutions’ most significant financial asset to one of their most detrimental liabilities. These changes provide a chance to improve both the quality and efficiency of the care we deliver, but we are unlikely to capitalize on this opportunity unless we understand this shifting paradigm. This change requires us to first appreciate the recent history of our reimbursement environment.

Traditionally, healthcare has been a relatively lucrative field, especially for those providing surgical care: doctors are paid “physician fees” by insurance companies (including Medicare), and institutions where procedures are performed are paid “facility fees.” Profits are measured as revenue (ie, reimbursement) minus costs of providing care, and while there has always been the potential to make more money by lowering costs, providers have historically had much more to gain by increasing their revenue. This fact has been exacerbated by the “fee-for-service” (FFS) payment model, which unintentionally encourages physicians to provide high volumes of care by “paying more for doing more.” For example, rather than being paid a fixed sum to care for a patient’s knee arthritis, each provider involved in the patient’s care is paid for each intervention. Clearly, this system encourages providers to maximize their interventions (ie, earning revenue) rather than search for ways to cut costs.

The Centers for Medicare and Medicaid Services (CMS) partially addressed this issue during the 1980s by introducing the Diagnosis Related Group (DRG).^1,2 Under this classification scheme, hospitals would be paid a pre-specified amount for a particular type of admission, often based on a specific procedure. For example, there is a DRG with a set payment for total knee arthroplasty (TKA).³ When reimbursement for the condition is set at a fixed amount, facilities are motivated to decrease their expenses since this is the only way to maximize the financial return for a given patient. This change, theoretically, encourages providers to cut their costs for providing a TKA as much as possible, potentially even to the point of sacrificing quality of care. As usual, when CMS makes a sweeping change, private insurers followed suit, and as a result, both government and corporate insurance is now structured around DRGs.

However, this was not a complete departure from FFS payment. We were still not paid to manage a patient’s knee arthritis as cheaply as possible; we were paid for each steroid injection, preoperative clinic visit, TKA (with numerous coding modifiers for complexity or comorbidities) as well as post-discharge admissions to skilled nursing and acute rehabilitation facilities. However, it was a start: for example, hospitals were no longer incentivized to keep TKA patients in house with a growing bill for each administered drug or therapy session. Yet, it is noteworthy that hospitals and physicians were still paid separately. This is important because doctors have historically made almost all treatment decisions and thereby determined the cost of care, yet hospitals have borne most of those costs, such as expensive implants or unplanned admissions, without a commensurate increase in reimbursement. As long as physicians are guaranteed their “fee,” they have little motivation to reduce those costs. Unsurprisingly, and as we well know, the advent of DRGs did not successfully curb our growing healthcare budget.

Recently, TKA and total hip arthroplasty reimbursement changed more dramatically. After experimenting with several pilots, CMS rolled out the Comprehensive Care for Joint Replacement (CJR) bundled payment program in 2015.^1,4 Participation in CJR is mandatory for most arthroplasty providers in approximately half of all “metropolitan” areas. In this scheme, hospital and physician pay is intertwined. Specifically, hospitals are held accountable for costs, so if the total Medicare bill for a patient’s TKA exceeds the “target price,” the hospital faces a penalty. Conversely, a charge below the target can earn a bonus payment.⁴ The hospital and surgeons must decide how they will share the bonus (or penalty), which creates an incentive to work together to lower costs.

Continue to: While bundled payments like CJR shift some...

While bundled payments like CJR shift some of the risk for high costs to the hospital and surgeon, a much more extreme example of this type of shift is capitation (ie, paying a healthcare institution a set amount per patient to care for whatever maladies arise). Insurers have experimented with various forms of capitation in the past, which led to the expansion of health management organizations (HMOs) during the 1990s. In theory, capitation should encourage providers to invest in disease prevention to minimize the need for costly interventions. However, more nefarious incentives developed, resulting in “cherry picking” healthy patients, which restricts access to care for sicker patients, and even withholds care from patients in need. The most infamous example was arguably “drive-through deliveries,” where newborns and their mothers were prematurely discharged following birth.⁵ As a result, the “HMO backlash” occurred, and capitation temporarily fell out of favor. The heart of the problem was a strong incentive to reduce the cost of care without a counterbalancing incentive to maintain quality. CJR and other modern programs attempt to avoid similar adverse incentives by requiring participants to meet certain quality criteria.⁶

Since the passage of the Affordable Care Act in 2010, capitation has reemerged under a new name: Accountable Care Organizations (ACOs). Numerous forms of ACO’s exist with differing payment schemes⁷, but the most comprehensive version, named Next Generation (Next Gen), allows providers to choose full capitation.⁸ While early ACOs focused on individual patients, Next Gen ACOs are also focused on “population health.” That is, they must demonstrate outcomes for individuals and the patient population as a whole, while simultaneously assuming all financial risk via capitation. Specifically, these ACO’s are paid an “all-inclusive population-based payment” for each patient based on how much that type of patient’s care is expected to cost for the year.⁹ The ACO then provides all necessary treatment and, if the ACO cannot provide a necessary intervention, it is responsible for funding that care at another institution. Appropriately, there has been an increased focus on quality to avoid unintentional incentives to withhold care. Specifically, CMS has introduced mandatory quality metrics in the domains of patient experience, care coordination, preventive care, and management of at-risk populations.¹⁰ At present, unfortunately, these metrics are not nearly comprehensive enough nor adequately validated to assess the quality of care,¹¹ especially for subspecialized fields like orthopedics where functional outcome scores are needed.

To date, very limited attention in the media or academic literature has been dedicated to subspecialty surgical care in the setting of ACOs even though implications for specialized surgeons could be immense. While ACOs bring numerous reporting requirements, the most essential first step for orthopedists in transition to this new reimbursement scheme will be a change in mindset. As explained above, orthopedics and other forms of specialized surgical care have traditionally been extremely profitable for healthcare institutions through relatively high revenue. However, within a capitated ACO all revenue has been paid upfront for each patient, and every orthopedic surgery performed represents a substantial cost to the institution rather than a large profit. For example, it has been reported that the average contribution margin earned by a hospital for an episode of care to provide a TKA (which includes postoperative care such as clinic visits, unplanned readmissions, and reoperations for complications) based on Medicare reimbursement is $11,726.¹² This figure consists of reimbursement (median, $24,149) less variable costs (median, $10,190). Additionally, the surgeon currently receives $1400 in physician fees.¹³ These earnings represent a significant financial benefit for both the facility and doctor in the current FFS environment. However, a capitated ACO caring for a TKA patient would already have received full payment for his care for the year. As a result, providing a TKA would not afford any further financial benefit and would, instead, mean a loss of $10,190 (the aforementioned variable cost for the episode of care) directly from the bottom line. The orthopedic department within that ACO, along with other departments, can be expected to share that loss. This implies that upon becoming an ACO, an institution’s orthopedics department will change from a major profit-center to a major cost-center.

Continue to: CMS must establish adequate quality assurance...

CMS must establish adequate quality assurance measures to ensure that ACOs do not withhold cost-effective care, like TKAs,^14,15 from their patients. Hopefully, for both professional and ethical reasons, providers will be active partners in this process. Groups like the International Consortium for Health Outcome Measurement, which has convened international expert panels to agree on comprehensive outcome sets for total joint arthroplasty and the management of low back pain, among other non-orthopedic conditions, may be useful examples in this process.^16-18

At the provider level, surgeons will be more likely to be salaried employees, contracting directly with the ACO rather than primarily working to earn physician fees from insurance providers. Surgeons will likely be judged (and rewarded financially) on their ability to direct nonoperative care, to find non-surgical solutions to problems that may currently be treated operatively, and to reduce costs for patients that require surgery. Additionally, with an increased focus on quality assurance, there will likely be more pressure from ACOs and CMS to demonstrate results of both operative and nonoperative care, likely in the forms of patient-reported metrics and objective measures of physical function. Surgeons will have a strong incentive to be leaders in the process of collecting such data.

It is also worth considering the position of orthopedic practices that are not part of an ACO. Some ACOs will not have the capacity to provide all (or possibly any) of the orthopedic care their patients require. When necessary, they will contract with outside orthopedic practices. Compared with CMS, ACOs are much smaller purchasers and can be expected to be more sensitive to price, likely negotiating intensely between local orthopedic providers. As a result, even orthopedists outside of ACOs may feel the cost pressure created by this new reimbursement model and may be driven to implement cost-reduction measures such as standardized implant choices and discharge pathways.

ACOs are in an active growth phase,^19,20 and recent updates to ACO policies make it clear that CMS intends for this trend to continue.⁸ Since ACOs are still a nascent reimbursement model, orthopedists will still do better financially, in almost all markets, by continuing to expend their energy and resources pursuing revenue, rather than cutting costs or demonstrating outcomes. However, as ACOs and population health gain traction, those orthopedists who recognize this shift and plan accordingly will have a definite strategic advantage, whether their practice is within an ACO, interacting with external ACOs, or both.

With the bewildering array of new bureaucracies that private practices are now forced to contend with, it is easy to forget about the older ones – especially the Occupational Health and Safety Administration (OSHA).

Now might be a good time to get out your OSHA logs, walk through your office, and confirm that you remain in compliance with all the applicable regulations. Even if you hold regular safety meetings (which all too often is not the case), the occasional comprehensive review is always a good idea, and could save you a bundle in fines.

For starters, do you have an official OSHA poster, enumerating employee rights and explaining how to file complaints? Every office must have one posted in plain site, and it is the first thing an OSHA inspector will look for. You can download one from OSHA’s Web site or order it at no charge by calling 800-321-OSHA.

Next, how old is your written exposure control plan for blood-borne pathogens? It should document your use of such protective equipment as gloves, face and eye protection, needle guards, and gowns, and your implementation of universal precautions – and it is supposed to be updated annually, to reflect changes in technology.

You need not adopt every new safety device as it comes on the market, but you should document which ones you are using – and which you pass up – and why. For example, you and your employees may decide not to purchase a new safety needle because you don’t think it will improve safety, or that it will be more trouble than it’s worth; but you should document how you arrived at your decision and why you feel that your current protocol is as good or better.

Review your list of hazardous substances, which all employees have a right to know about. Keep in mind that OSHA’s list includes alcohol, hydrogen peroxide, acetone, and other substances that you might not consider particularly dangerous, but are nevertheless classified as “hazardous.” (My favorite in that category is liquid nitrogen; it’s hard to envision anything less hazardous, since it evaporates instantly if spilled, and cannot injure skin, or anything else, without purposeful, sustained exposure – and is great, incidentally, for extinguishing small fires.) For each substance, your employees must have access to the manufacturer-supplied Material Safety Data Sheet, which outlines the proper procedures for working with a specific material, and for handling and containing it in a spill or other emergency.

Check out your building’s exits. Everyone must be able to evacuate your office quickly in case of fire or other emergencies. At a minimum, you (or the owner of the building) are expected to establish exit routes to accommodate all employees and to post easily visible evacuation diagrams.

Examine all electrical devices and their power sources. All electrically powered equipment – medical, clerical, or anything else in the office – must operate safely. Pay particular attention to the way wall outlets are set up. Make sure each outlet has sufficient power to run the equipment plugged into it and that circuit breakers are present and functioning. And beware the common situation of too many gadgets running off a single circuit.

You must provide all at-risk employees with hepatitis B vaccine at no cost to them. You also must provide and pay for appropriate medical treatment and follow-up after any exposure to a dangerous pathogen.

Other components of the rule include proper containment of regulated medical waste, identification of regulated-waste containers, sharps disposal boxes, and periodic employee training regarding all of these things.

Federal OSHA regulations do not require medical and dental offices to keep an injury and illness log, as other businesses must; but your state may have a requirement that supersedes the federal law. Check with your state, or with your local OSHA office, regarding any such requirements.

It is a mistake to take OSHA regulations lightly; failure to comply with them can result in stiff penalties running into many thousands of dollars.

How can you be certain you are complying with all the rules? The easiest and cheapest way is to call your local OSHA office and request an inspection. Why would you do that? Because OSHA issues no citations during voluntary inspections, as long as you agree to remedy any violations they find.
 

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

With the bewildering array of new bureaucracies that private practices are now forced to contend with, it is easy to forget about the older ones – especially the Occupational Health and Safety Administration (OSHA).

Now might be a good time to get out your OSHA logs, walk through your office, and confirm that you remain in compliance with all the applicable regulations. Even if you hold regular safety meetings (which all too often is not the case), the occasional comprehensive review is always a good idea, and could save you a bundle in fines.

For starters, do you have an official OSHA poster, enumerating employee rights and explaining how to file complaints? Every office must have one posted in plain site, and it is the first thing an OSHA inspector will look for. You can download one from OSHA’s Web site or order it at no charge by calling 800-321-OSHA.

Next, how old is your written exposure control plan for blood-borne pathogens? It should document your use of such protective equipment as gloves, face and eye protection, needle guards, and gowns, and your implementation of universal precautions – and it is supposed to be updated annually, to reflect changes in technology.

You need not adopt every new safety device as it comes on the market, but you should document which ones you are using – and which you pass up – and why. For example, you and your employees may decide not to purchase a new safety needle because you don’t think it will improve safety, or that it will be more trouble than it’s worth; but you should document how you arrived at your decision and why you feel that your current protocol is as good or better.

Review your list of hazardous substances, which all employees have a right to know about. Keep in mind that OSHA’s list includes alcohol, hydrogen peroxide, acetone, and other substances that you might not consider particularly dangerous, but are nevertheless classified as “hazardous.” (My favorite in that category is liquid nitrogen; it’s hard to envision anything less hazardous, since it evaporates instantly if spilled, and cannot injure skin, or anything else, without purposeful, sustained exposure – and is great, incidentally, for extinguishing small fires.) For each substance, your employees must have access to the manufacturer-supplied Material Safety Data Sheet, which outlines the proper procedures for working with a specific material, and for handling and containing it in a spill or other emergency.

Check out your building’s exits. Everyone must be able to evacuate your office quickly in case of fire or other emergencies. At a minimum, you (or the owner of the building) are expected to establish exit routes to accommodate all employees and to post easily visible evacuation diagrams.

Examine all electrical devices and their power sources. All electrically powered equipment – medical, clerical, or anything else in the office – must operate safely. Pay particular attention to the way wall outlets are set up. Make sure each outlet has sufficient power to run the equipment plugged into it and that circuit breakers are present and functioning. And beware the common situation of too many gadgets running off a single circuit.

You must provide all at-risk employees with hepatitis B vaccine at no cost to them. You also must provide and pay for appropriate medical treatment and follow-up after any exposure to a dangerous pathogen.

Other components of the rule include proper containment of regulated medical waste, identification of regulated-waste containers, sharps disposal boxes, and periodic employee training regarding all of these things.

Federal OSHA regulations do not require medical and dental offices to keep an injury and illness log, as other businesses must; but your state may have a requirement that supersedes the federal law. Check with your state, or with your local OSHA office, regarding any such requirements.

It is a mistake to take OSHA regulations lightly; failure to comply with them can result in stiff penalties running into many thousands of dollars.

How can you be certain you are complying with all the rules? The easiest and cheapest way is to call your local OSHA office and request an inspection. Why would you do that? Because OSHA issues no citations during voluntary inspections, as long as you agree to remedy any violations they find.
 

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

With the bewildering array of new bureaucracies that private practices are now forced to contend with, it is easy to forget about the older ones – especially the Occupational Health and Safety Administration (OSHA).

Now might be a good time to get out your OSHA logs, walk through your office, and confirm that you remain in compliance with all the applicable regulations. Even if you hold regular safety meetings (which all too often is not the case), the occasional comprehensive review is always a good idea, and could save you a bundle in fines.

For starters, do you have an official OSHA poster, enumerating employee rights and explaining how to file complaints? Every office must have one posted in plain site, and it is the first thing an OSHA inspector will look for. You can download one from OSHA’s Web site or order it at no charge by calling 800-321-OSHA.

Next, how old is your written exposure control plan for blood-borne pathogens? It should document your use of such protective equipment as gloves, face and eye protection, needle guards, and gowns, and your implementation of universal precautions – and it is supposed to be updated annually, to reflect changes in technology.

You need not adopt every new safety device as it comes on the market, but you should document which ones you are using – and which you pass up – and why. For example, you and your employees may decide not to purchase a new safety needle because you don’t think it will improve safety, or that it will be more trouble than it’s worth; but you should document how you arrived at your decision and why you feel that your current protocol is as good or better.

Review your list of hazardous substances, which all employees have a right to know about. Keep in mind that OSHA’s list includes alcohol, hydrogen peroxide, acetone, and other substances that you might not consider particularly dangerous, but are nevertheless classified as “hazardous.” (My favorite in that category is liquid nitrogen; it’s hard to envision anything less hazardous, since it evaporates instantly if spilled, and cannot injure skin, or anything else, without purposeful, sustained exposure – and is great, incidentally, for extinguishing small fires.) For each substance, your employees must have access to the manufacturer-supplied Material Safety Data Sheet, which outlines the proper procedures for working with a specific material, and for handling and containing it in a spill or other emergency.

Check out your building’s exits. Everyone must be able to evacuate your office quickly in case of fire or other emergencies. At a minimum, you (or the owner of the building) are expected to establish exit routes to accommodate all employees and to post easily visible evacuation diagrams.

Examine all electrical devices and their power sources. All electrically powered equipment – medical, clerical, or anything else in the office – must operate safely. Pay particular attention to the way wall outlets are set up. Make sure each outlet has sufficient power to run the equipment plugged into it and that circuit breakers are present and functioning. And beware the common situation of too many gadgets running off a single circuit.

You must provide all at-risk employees with hepatitis B vaccine at no cost to them. You also must provide and pay for appropriate medical treatment and follow-up after any exposure to a dangerous pathogen.

Other components of the rule include proper containment of regulated medical waste, identification of regulated-waste containers, sharps disposal boxes, and periodic employee training regarding all of these things.

Federal OSHA regulations do not require medical and dental offices to keep an injury and illness log, as other businesses must; but your state may have a requirement that supersedes the federal law. Check with your state, or with your local OSHA office, regarding any such requirements.

It is a mistake to take OSHA regulations lightly; failure to comply with them can result in stiff penalties running into many thousands of dollars.

How can you be certain you are complying with all the rules? The easiest and cheapest way is to call your local OSHA office and request an inspection. Why would you do that? Because OSHA issues no citations during voluntary inspections, as long as you agree to remedy any violations they find.
 

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

Why do patients no-show?

The reasons are, obviously, widely variable among patients and circumstances. Some are more understandable than others, but all of them add up to an empty chair across the desk and loss of income for that time slot.

CherriesJD/Thinkstock

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Why do patients no-show?

The reasons are, obviously, widely variable among patients and circumstances. Some are more understandable than others, but all of them add up to an empty chair across the desk and loss of income for that time slot.

CherriesJD/Thinkstock

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Why do patients no-show?

The reasons are, obviously, widely variable among patients and circumstances. Some are more understandable than others, but all of them add up to an empty chair across the desk and loss of income for that time slot.

CherriesJD/Thinkstock

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

We live in the era of evidence-based medicine, so new interventions must meet criteria for both safety and efficacy before they are adopted. However, we have inherited many practices adopted before the current standards were in place, and we have not always been rigorous in reevaluating traditional remedies. A conservative belief in established practice or the influence of vested interests may account for this lack of rigor in reappraisal.¹ Calcium and vitamin D supplements are possible examples of this phenomenon.

BONE METABOLISM IS TIGHTLY REGULATED

Bone is a connective tissue, its matrix composed principally of type 1 collagen, which provides tensile strength. Hydroxyapatite crystals, composed predominantly of calcium and phosphate, lie between the collagen fibers and provide compressive strength. In a tightly regulated process, osteoblasts lay down the collagenous matrix, and osteoclasts remove it. Mineralization of newly formed bone proceeds if normal levels of extracellular calcium and phosphate are present, in the absence of inhibitors of mineralization.

High calcium intake does not drive bone formation

The endocrine system is critical in maintaining normocalcemia. A decrease in calcium intake results in increased parathyroid hormone secretion, resulting in increased renal tubular calcium reabsorption, increased bone turnover (both formation and resorption), and increased activation of vitamin D leading to increased intestinal absorption of calcium. High calcium intake reverses these changes.

Reid IR, Bristow SM, Bolland MJ. Calcium supplements: benefits and risks. J Intern Med 2015; 278(4):354–368. Copyright 2015, The Association for the Publication of the Journal of Internal Medicine.

If calcium intake is very low, hypocalcemia and secondary hyperparathyroidism develop,³ and bone mineralization may be impaired. However, levels of calcium intake in Africa and in East and Southeast Asia are typically less than 400 mg/day,⁴ yet there is no evidence that these levels adversely affect skeletal health. In fact, fracture risk is lower in these regions than in North America, where calcium intake is several times greater.

Thus, some calcium intake is required to maintain circulating concentrations, but there is no mechanism by which high calcium intake can drive bone formation. Quite the opposite, in fact.

Vitamin D deficiency has little relationship with diet

Vitamin D is a biologically inactive secosteroid activated by hydroxylation in the liver and kidney to function as the key regulator of intestinal calcium absorption. As with calcium, its deficiency results in hypocalcemia and impaired bone mineralization.

Paradoxically, high levels of vitamin D stimulate bone resorption and inhibit bone mineralization in mice,⁵ and large doses increase bone resorption markers acutely in clinical studies.⁶ Thus, it is important to ensure an adequate vitamin D supply, but not an oversupply.

In the absence of supplements, most vitamin D is produced in the skin as a result of the action of ultraviolet light (from sunlight) on 7-dehydrocholesterol. Thus, vitamin D deficiency occurs in those deprived of skin exposure to sunlight (eg, due to veiling, living at high latitude, staying permanently indoors), but it has little relationship with diet.

ARE CALCIUM SUPPLEMENTS EFFECTIVE?

Calcium supplements are certainly biologically active. They transiently increase serum calcium concentrations, suppress parathyroid hormone, and reduce bone resorption.² In the first year of use, they increase bone density by about 1% compared with placebo.⁷ However, longer use does not result in further bone density advantage over placebo,⁷ suggesting that the response simply reflects a decreased number of osteoclastic resorption sites and does not indicate a sustained change in bone balance.

A 1% difference in bone density would not be expected to reduce fracture risk, and a number of large, carefully conducted randomized controlled trials published over the last 15 years have failed to demonstrate anti­fracture efficacy for calcium.^8–12 As a result, the US Preventive Services Task Force recommends against the routine use of calcium supplements in community-dwelling adults.¹³

In contrast, in a placebo-controlled trial published in 1992, Chapuy et al¹⁴ found that elderly women residing in nursing homes who received calcium and vitamin D supplements had fewer fractures. At 18 months, by intention-to-treat analysis, nonvertebral fractures had occurred in 160 (12%) of 1,387 women in the supplement group compared with 215 (15%) of 1,403 women in the placebo group (P < .001). However, these women were severely vitamin D-deficient (the mean serum 25-hydroxyvitamin D level at baseline in the placebo group was 13 ng/mL, normal range 15–50), to the extent that many must have had osteomalacia.

Thus, this study shows that calcium and vitamin D are effective in managing osteomalacia, but the subsequent trials^8–12 did not observe any benefit in community-dwelling cohorts. Meta-analyses that pool the Chapuy study with community-based studies generally find that calcium with vitamin D is beneficial, but the heterogeneity of these populations means that such pooling is inappropriate.¹⁵

It is sometimes stated that calcium and vitamin D should always be given with osteoporosis medications because the efficacy of these drugs has only been demonstrated when coadministered with these supplements. This is incorrect. The addition of calcium to alendronate does not alter its effects on bone density,¹⁶ and the antifracture efficacy of both bisphosphonates¹⁷ and estrogen^18,19 has been demonstrated in the absence of supplementation with calcium or vitamin D. The evidence that bisphosphonates prevent fractures in the absence of calcium supplements has recently been strengthened by the results of a randomized controlled trial comparing zoledronate with placebo in women over age 65 with osteopenia.²⁰

Calcium supplements often cause gastrointestinal symptoms, particularly constipation. They have been shown to double the risk of hospital admission due to abdominal symptoms.²¹ In the absence of clear evidence of benefit, these facts alone should militate against their routine use. Calcium supplements also cause hypercalcemia and hypercalciuria²² and increase the risk of renal calculi (by 17% in the Women’s Health Initiative⁸).

Over the last decade, evidence has emerged that calcium supplements may also increase the risk of myocardial infarction, and possibly stroke. This finding was not statistically significant in any single study, but is consistently present in meta-analyses.²³

Evidence from the Women’s Health Initiative

When studies of calcium with vitamin D are added to these meta-analyses, the results are less consistent. This is because such meta-analyses are dominated by the Women's Health Initiative (because of its large size, with 36,282 participants). There have been 2 different analyses of this trial with respect to cardiovascular events.

When the Women’s Health Initiative as a whole was analyzed, there was no significant effect of calcium plus vitamin D on vascular end points. However, there is a significant interaction between body mass index and the effect of supplements, such that nonobese women demonstrated a 17% increase in myocardial infarction.²⁴ This study was unusual in that it included women already taking calcium and vitamin D supplements.

Bolland MJ, Grey A, Avenell A, Gamble GD, Reid IR. Calcium supplements with or without vitamin D and risk of cardiovascular events: reanalysis of the Women’s Health Initiative limited access dataset and meta-analysis. BMJ 2011; 342:d2040.

There was a significant interaction between baseline use of supplements and the effects of the trial intervention on vascular events, justifying analyzing the supplement-naive individuals separately. In this group of 16,000 women, an increase in clinical myocardial infarction of 22% was found, similar to the findings with calcium supplements alone.²⁵

Thus, there is consistent evidence that introducing a calcium supplement de novo increases the risk of myocardial infarction (Figure 2).^16,25–31 We calculate that treating 1,000 patients with calcium or calcium plus vitamin D for 5 years would cause an additional 6 myocardial infarctions or strokes (number needed to harm 178) and prevent only 3 fractures (number needed to treat 302).²⁵

ARE VITAMIN D SUPPLEMENTS EFFECTIVE?

Vitamin D is highly effective in treating osteomalacia, improving symptoms within days and increasing bone density by as much as 50% over 1 year.^32,33 In contrast, randomized controlled trials of vitamin D supplements alone in people without osteomalacia have not shown increases in bone density or changes in fracture risk.^34–37

Reid IR, Horne AM, Mihov B, et al. Effect of monthly high-dose vitamin D on bone density in community-dwelling older adults substudy of a randomized controlled trial. J Intern Med 2017; 282(5):452–460. Copyright 2017, Assoc for Publication of J Int Med

In 2017, my colleagues and I published a trial showing that vitamin D supplementation increases bone density by 2% to 3% in the spine and femoral neck in participants with baseline 25-hydroxyvitamin D levels below 30- nmol/L (12 ng/mL), but those starting above this level showed no effect (Figure 3).³⁸ And a reanalysis of an earlier study confirmed this 30 nmol/L threshold for an effect of vitamin D on bone density.³⁹ The finding of a clear-cut threshold for vitamin D effects is predicted by the physiologic considerations set out above.

Belief that higher levels of 25-hydroxyvitamin D are better is based on observational data. However, correlation does not prove causation, and it is likely that causation is reversed here. Those with better health are likely to spend more time exercising outdoors, are less likely to be obese, and are less likely to have inflammatory conditions; and as a result, they are more likely to have better vitamin D status. We should now be using trial-based definitions of vitamin D deficiency as opposed to thresholds derived from disease associations in observational studies.

Vitamin D supplements have also been suggested to benefit cardiovascular health and to reduce cancer risk, though current clinical trial data provide no support for these hypotheses.^36,40 Other trials addressing these questions are ongoing.

ARE VITAMIN D SUPPLEMENTS SAFE?

The safety of vitamin D supplements has generally been assessed with respect to the incidence of hypercalcemia. On this basis, very high doses have been promoted. However, there is now evidence that doses of 4,000 IU/day, 60,000 IU/month, and 500,000 IU/year increase the risk of falls and fractures.^41,42

The threshold for bone benefits discussed above (12 ng/mL) is easily exceeded with doses of vitamin D of 400 to 1,000 IU/day. At these levels, vitamin D supplements have no known adverse effects and can be widely endorsed for individuals at risk of deficiency. Supplement doses greater than 2,000 IU/day should be used only in exceptional circumstances, and with appropriate monitoring.

LITTLE USE FOR CALCIUM AND VITAMIN D SUPPLEMENTS

Extensive clinical trials have failed to demonstrate meaningful benefit from calcium supplements in the management of osteoporosis. Calcium supplements are often prescribed in patients who are receiving other treatments for osteoporosis, which may be justified with interventions that have the potential to cause hypocalcemia, but their coadministration with bisphosphonates has been shown to be unnecessary.

Calcium supplements commonly cause gastrointestinal symptoms that are sometimes severe and are likely to contribute to high levels of noncompliance with osteoporosis medications. They increase the risk of kidney stones,⁸ and there is reasonable evidence to suggest an adverse effect on vascular risk as well.²³

Vitamin D deficiency is common in frail elderly people, particularly those with dark skin or living at high latitudes. Low doses of vitamin D are safe and highly effective in preventing osteomalacia. But vitamin D supplements are unnecessary in those who regularly have sun exposure. And high doses of vitamin D have no demonstrated advantage and have been shown to increase the risk of falls and fractures.

Our decision to prescribe calcium and vitamin D supplements should be based on evidence that is of the same quality as for any other intervention we prescribe. Current evidence suggests that there is little reason to prescribe calcium, and that vitamin D should be targeted at those at risk of 25-hydroxyvitamin D levels less than 12 ng/mL.

We live in the era of evidence-based medicine, so new interventions must meet criteria for both safety and efficacy before they are adopted. However, we have inherited many practices adopted before the current standards were in place, and we have not always been rigorous in reevaluating traditional remedies. A conservative belief in established practice or the influence of vested interests may account for this lack of rigor in reappraisal.¹ Calcium and vitamin D supplements are possible examples of this phenomenon.

BONE METABOLISM IS TIGHTLY REGULATED

Bone is a connective tissue, its matrix composed principally of type 1 collagen, which provides tensile strength. Hydroxyapatite crystals, composed predominantly of calcium and phosphate, lie between the collagen fibers and provide compressive strength. In a tightly regulated process, osteoblasts lay down the collagenous matrix, and osteoclasts remove it. Mineralization of newly formed bone proceeds if normal levels of extracellular calcium and phosphate are present, in the absence of inhibitors of mineralization.

High calcium intake does not drive bone formation

The endocrine system is critical in maintaining normocalcemia. A decrease in calcium intake results in increased parathyroid hormone secretion, resulting in increased renal tubular calcium reabsorption, increased bone turnover (both formation and resorption), and increased activation of vitamin D leading to increased intestinal absorption of calcium. High calcium intake reverses these changes.

Reid IR, Bristow SM, Bolland MJ. Calcium supplements: benefits and risks. J Intern Med 2015; 278(4):354–368. Copyright 2015, The Association for the Publication of the Journal of Internal Medicine.

If calcium intake is very low, hypocalcemia and secondary hyperparathyroidism develop,³ and bone mineralization may be impaired. However, levels of calcium intake in Africa and in East and Southeast Asia are typically less than 400 mg/day,⁴ yet there is no evidence that these levels adversely affect skeletal health. In fact, fracture risk is lower in these regions than in North America, where calcium intake is several times greater.

Thus, some calcium intake is required to maintain circulating concentrations, but there is no mechanism by which high calcium intake can drive bone formation. Quite the opposite, in fact.

Vitamin D deficiency has little relationship with diet

Vitamin D is a biologically inactive secosteroid activated by hydroxylation in the liver and kidney to function as the key regulator of intestinal calcium absorption. As with calcium, its deficiency results in hypocalcemia and impaired bone mineralization.

Paradoxically, high levels of vitamin D stimulate bone resorption and inhibit bone mineralization in mice,⁵ and large doses increase bone resorption markers acutely in clinical studies.⁶ Thus, it is important to ensure an adequate vitamin D supply, but not an oversupply.

In the absence of supplements, most vitamin D is produced in the skin as a result of the action of ultraviolet light (from sunlight) on 7-dehydrocholesterol. Thus, vitamin D deficiency occurs in those deprived of skin exposure to sunlight (eg, due to veiling, living at high latitude, staying permanently indoors), but it has little relationship with diet.

ARE CALCIUM SUPPLEMENTS EFFECTIVE?

Calcium supplements are certainly biologically active. They transiently increase serum calcium concentrations, suppress parathyroid hormone, and reduce bone resorption.² In the first year of use, they increase bone density by about 1% compared with placebo.⁷ However, longer use does not result in further bone density advantage over placebo,⁷ suggesting that the response simply reflects a decreased number of osteoclastic resorption sites and does not indicate a sustained change in bone balance.

A 1% difference in bone density would not be expected to reduce fracture risk, and a number of large, carefully conducted randomized controlled trials published over the last 15 years have failed to demonstrate anti­fracture efficacy for calcium.^8–12 As a result, the US Preventive Services Task Force recommends against the routine use of calcium supplements in community-dwelling adults.¹³

In contrast, in a placebo-controlled trial published in 1992, Chapuy et al¹⁴ found that elderly women residing in nursing homes who received calcium and vitamin D supplements had fewer fractures. At 18 months, by intention-to-treat analysis, nonvertebral fractures had occurred in 160 (12%) of 1,387 women in the supplement group compared with 215 (15%) of 1,403 women in the placebo group (P < .001). However, these women were severely vitamin D-deficient (the mean serum 25-hydroxyvitamin D level at baseline in the placebo group was 13 ng/mL, normal range 15–50), to the extent that many must have had osteomalacia.

Thus, this study shows that calcium and vitamin D are effective in managing osteomalacia, but the subsequent trials^8–12 did not observe any benefit in community-dwelling cohorts. Meta-analyses that pool the Chapuy study with community-based studies generally find that calcium with vitamin D is beneficial, but the heterogeneity of these populations means that such pooling is inappropriate.¹⁵

It is sometimes stated that calcium and vitamin D should always be given with osteoporosis medications because the efficacy of these drugs has only been demonstrated when coadministered with these supplements. This is incorrect. The addition of calcium to alendronate does not alter its effects on bone density,¹⁶ and the antifracture efficacy of both bisphosphonates¹⁷ and estrogen^18,19 has been demonstrated in the absence of supplementation with calcium or vitamin D. The evidence that bisphosphonates prevent fractures in the absence of calcium supplements has recently been strengthened by the results of a randomized controlled trial comparing zoledronate with placebo in women over age 65 with osteopenia.²⁰

Calcium supplements often cause gastrointestinal symptoms, particularly constipation. They have been shown to double the risk of hospital admission due to abdominal symptoms.²¹ In the absence of clear evidence of benefit, these facts alone should militate against their routine use. Calcium supplements also cause hypercalcemia and hypercalciuria²² and increase the risk of renal calculi (by 17% in the Women’s Health Initiative⁸).

Over the last decade, evidence has emerged that calcium supplements may also increase the risk of myocardial infarction, and possibly stroke. This finding was not statistically significant in any single study, but is consistently present in meta-analyses.²³

Evidence from the Women’s Health Initiative

When studies of calcium with vitamin D are added to these meta-analyses, the results are less consistent. This is because such meta-analyses are dominated by the Women's Health Initiative (because of its large size, with 36,282 participants). There have been 2 different analyses of this trial with respect to cardiovascular events.

When the Women’s Health Initiative as a whole was analyzed, there was no significant effect of calcium plus vitamin D on vascular end points. However, there is a significant interaction between body mass index and the effect of supplements, such that nonobese women demonstrated a 17% increase in myocardial infarction.²⁴ This study was unusual in that it included women already taking calcium and vitamin D supplements.

Bolland MJ, Grey A, Avenell A, Gamble GD, Reid IR. Calcium supplements with or without vitamin D and risk of cardiovascular events: reanalysis of the Women’s Health Initiative limited access dataset and meta-analysis. BMJ 2011; 342:d2040.

There was a significant interaction between baseline use of supplements and the effects of the trial intervention on vascular events, justifying analyzing the supplement-naive individuals separately. In this group of 16,000 women, an increase in clinical myocardial infarction of 22% was found, similar to the findings with calcium supplements alone.²⁵

Thus, there is consistent evidence that introducing a calcium supplement de novo increases the risk of myocardial infarction (Figure 2).^16,25–31 We calculate that treating 1,000 patients with calcium or calcium plus vitamin D for 5 years would cause an additional 6 myocardial infarctions or strokes (number needed to harm 178) and prevent only 3 fractures (number needed to treat 302).²⁵

ARE VITAMIN D SUPPLEMENTS EFFECTIVE?

Vitamin D is highly effective in treating osteomalacia, improving symptoms within days and increasing bone density by as much as 50% over 1 year.^32,33 In contrast, randomized controlled trials of vitamin D supplements alone in people without osteomalacia have not shown increases in bone density or changes in fracture risk.^34–37

Reid IR, Horne AM, Mihov B, et al. Effect of monthly high-dose vitamin D on bone density in community-dwelling older adults substudy of a randomized controlled trial. J Intern Med 2017; 282(5):452–460. Copyright 2017, Assoc for Publication of J Int Med

In 2017, my colleagues and I published a trial showing that vitamin D supplementation increases bone density by 2% to 3% in the spine and femoral neck in participants with baseline 25-hydroxyvitamin D levels below 30- nmol/L (12 ng/mL), but those starting above this level showed no effect (Figure 3).³⁸ And a reanalysis of an earlier study confirmed this 30 nmol/L threshold for an effect of vitamin D on bone density.³⁹ The finding of a clear-cut threshold for vitamin D effects is predicted by the physiologic considerations set out above.

Belief that higher levels of 25-hydroxyvitamin D are better is based on observational data. However, correlation does not prove causation, and it is likely that causation is reversed here. Those with better health are likely to spend more time exercising outdoors, are less likely to be obese, and are less likely to have inflammatory conditions; and as a result, they are more likely to have better vitamin D status. We should now be using trial-based definitions of vitamin D deficiency as opposed to thresholds derived from disease associations in observational studies.

Vitamin D supplements have also been suggested to benefit cardiovascular health and to reduce cancer risk, though current clinical trial data provide no support for these hypotheses.^36,40 Other trials addressing these questions are ongoing.

ARE VITAMIN D SUPPLEMENTS SAFE?

The safety of vitamin D supplements has generally been assessed with respect to the incidence of hypercalcemia. On this basis, very high doses have been promoted. However, there is now evidence that doses of 4,000 IU/day, 60,000 IU/month, and 500,000 IU/year increase the risk of falls and fractures.^41,42

The threshold for bone benefits discussed above (12 ng/mL) is easily exceeded with doses of vitamin D of 400 to 1,000 IU/day. At these levels, vitamin D supplements have no known adverse effects and can be widely endorsed for individuals at risk of deficiency. Supplement doses greater than 2,000 IU/day should be used only in exceptional circumstances, and with appropriate monitoring.

LITTLE USE FOR CALCIUM AND VITAMIN D SUPPLEMENTS

Extensive clinical trials have failed to demonstrate meaningful benefit from calcium supplements in the management of osteoporosis. Calcium supplements are often prescribed in patients who are receiving other treatments for osteoporosis, which may be justified with interventions that have the potential to cause hypocalcemia, but their coadministration with bisphosphonates has been shown to be unnecessary.

Calcium supplements commonly cause gastrointestinal symptoms that are sometimes severe and are likely to contribute to high levels of noncompliance with osteoporosis medications. They increase the risk of kidney stones,⁸ and there is reasonable evidence to suggest an adverse effect on vascular risk as well.²³

Vitamin D deficiency is common in frail elderly people, particularly those with dark skin or living at high latitudes. Low doses of vitamin D are safe and highly effective in preventing osteomalacia. But vitamin D supplements are unnecessary in those who regularly have sun exposure. And high doses of vitamin D have no demonstrated advantage and have been shown to increase the risk of falls and fractures.

Our decision to prescribe calcium and vitamin D supplements should be based on evidence that is of the same quality as for any other intervention we prescribe. Current evidence suggests that there is little reason to prescribe calcium, and that vitamin D should be targeted at those at risk of 25-hydroxyvitamin D levels less than 12 ng/mL.

We live in the era of evidence-based medicine, so new interventions must meet criteria for both safety and efficacy before they are adopted. However, we have inherited many practices adopted before the current standards were in place, and we have not always been rigorous in reevaluating traditional remedies. A conservative belief in established practice or the influence of vested interests may account for this lack of rigor in reappraisal.¹ Calcium and vitamin D supplements are possible examples of this phenomenon.

BONE METABOLISM IS TIGHTLY REGULATED

Bone is a connective tissue, its matrix composed principally of type 1 collagen, which provides tensile strength. Hydroxyapatite crystals, composed predominantly of calcium and phosphate, lie between the collagen fibers and provide compressive strength. In a tightly regulated process, osteoblasts lay down the collagenous matrix, and osteoclasts remove it. Mineralization of newly formed bone proceeds if normal levels of extracellular calcium and phosphate are present, in the absence of inhibitors of mineralization.

High calcium intake does not drive bone formation

The endocrine system is critical in maintaining normocalcemia. A decrease in calcium intake results in increased parathyroid hormone secretion, resulting in increased renal tubular calcium reabsorption, increased bone turnover (both formation and resorption), and increased activation of vitamin D leading to increased intestinal absorption of calcium. High calcium intake reverses these changes.

Reid IR, Bristow SM, Bolland MJ. Calcium supplements: benefits and risks. J Intern Med 2015; 278(4):354–368. Copyright 2015, The Association for the Publication of the Journal of Internal Medicine.

If calcium intake is very low, hypocalcemia and secondary hyperparathyroidism develop,³ and bone mineralization may be impaired. However, levels of calcium intake in Africa and in East and Southeast Asia are typically less than 400 mg/day,⁴ yet there is no evidence that these levels adversely affect skeletal health. In fact, fracture risk is lower in these regions than in North America, where calcium intake is several times greater.

Thus, some calcium intake is required to maintain circulating concentrations, but there is no mechanism by which high calcium intake can drive bone formation. Quite the opposite, in fact.

Vitamin D deficiency has little relationship with diet

Vitamin D is a biologically inactive secosteroid activated by hydroxylation in the liver and kidney to function as the key regulator of intestinal calcium absorption. As with calcium, its deficiency results in hypocalcemia and impaired bone mineralization.

Paradoxically, high levels of vitamin D stimulate bone resorption and inhibit bone mineralization in mice,⁵ and large doses increase bone resorption markers acutely in clinical studies.⁶ Thus, it is important to ensure an adequate vitamin D supply, but not an oversupply.

In the absence of supplements, most vitamin D is produced in the skin as a result of the action of ultraviolet light (from sunlight) on 7-dehydrocholesterol. Thus, vitamin D deficiency occurs in those deprived of skin exposure to sunlight (eg, due to veiling, living at high latitude, staying permanently indoors), but it has little relationship with diet.

ARE CALCIUM SUPPLEMENTS EFFECTIVE?

Calcium supplements are certainly biologically active. They transiently increase serum calcium concentrations, suppress parathyroid hormone, and reduce bone resorption.² In the first year of use, they increase bone density by about 1% compared with placebo.⁷ However, longer use does not result in further bone density advantage over placebo,⁷ suggesting that the response simply reflects a decreased number of osteoclastic resorption sites and does not indicate a sustained change in bone balance.

A 1% difference in bone density would not be expected to reduce fracture risk, and a number of large, carefully conducted randomized controlled trials published over the last 15 years have failed to demonstrate anti­fracture efficacy for calcium.^8–12 As a result, the US Preventive Services Task Force recommends against the routine use of calcium supplements in community-dwelling adults.¹³

In contrast, in a placebo-controlled trial published in 1992, Chapuy et al¹⁴ found that elderly women residing in nursing homes who received calcium and vitamin D supplements had fewer fractures. At 18 months, by intention-to-treat analysis, nonvertebral fractures had occurred in 160 (12%) of 1,387 women in the supplement group compared with 215 (15%) of 1,403 women in the placebo group (P < .001). However, these women were severely vitamin D-deficient (the mean serum 25-hydroxyvitamin D level at baseline in the placebo group was 13 ng/mL, normal range 15–50), to the extent that many must have had osteomalacia.

Thus, this study shows that calcium and vitamin D are effective in managing osteomalacia, but the subsequent trials^8–12 did not observe any benefit in community-dwelling cohorts. Meta-analyses that pool the Chapuy study with community-based studies generally find that calcium with vitamin D is beneficial, but the heterogeneity of these populations means that such pooling is inappropriate.¹⁵

It is sometimes stated that calcium and vitamin D should always be given with osteoporosis medications because the efficacy of these drugs has only been demonstrated when coadministered with these supplements. This is incorrect. The addition of calcium to alendronate does not alter its effects on bone density,¹⁶ and the antifracture efficacy of both bisphosphonates¹⁷ and estrogen^18,19 has been demonstrated in the absence of supplementation with calcium or vitamin D. The evidence that bisphosphonates prevent fractures in the absence of calcium supplements has recently been strengthened by the results of a randomized controlled trial comparing zoledronate with placebo in women over age 65 with osteopenia.²⁰

Calcium supplements often cause gastrointestinal symptoms, particularly constipation. They have been shown to double the risk of hospital admission due to abdominal symptoms.²¹ In the absence of clear evidence of benefit, these facts alone should militate against their routine use. Calcium supplements also cause hypercalcemia and hypercalciuria²² and increase the risk of renal calculi (by 17% in the Women’s Health Initiative⁸).

Over the last decade, evidence has emerged that calcium supplements may also increase the risk of myocardial infarction, and possibly stroke. This finding was not statistically significant in any single study, but is consistently present in meta-analyses.²³

Evidence from the Women’s Health Initiative

When studies of calcium with vitamin D are added to these meta-analyses, the results are less consistent. This is because such meta-analyses are dominated by the Women's Health Initiative (because of its large size, with 36,282 participants). There have been 2 different analyses of this trial with respect to cardiovascular events.

When the Women’s Health Initiative as a whole was analyzed, there was no significant effect of calcium plus vitamin D on vascular end points. However, there is a significant interaction between body mass index and the effect of supplements, such that nonobese women demonstrated a 17% increase in myocardial infarction.²⁴ This study was unusual in that it included women already taking calcium and vitamin D supplements.

Bolland MJ, Grey A, Avenell A, Gamble GD, Reid IR. Calcium supplements with or without vitamin D and risk of cardiovascular events: reanalysis of the Women’s Health Initiative limited access dataset and meta-analysis. BMJ 2011; 342:d2040.

There was a significant interaction between baseline use of supplements and the effects of the trial intervention on vascular events, justifying analyzing the supplement-naive individuals separately. In this group of 16,000 women, an increase in clinical myocardial infarction of 22% was found, similar to the findings with calcium supplements alone.²⁵

Thus, there is consistent evidence that introducing a calcium supplement de novo increases the risk of myocardial infarction (Figure 2).^16,25–31 We calculate that treating 1,000 patients with calcium or calcium plus vitamin D for 5 years would cause an additional 6 myocardial infarctions or strokes (number needed to harm 178) and prevent only 3 fractures (number needed to treat 302).²⁵

ARE VITAMIN D SUPPLEMENTS EFFECTIVE?

Vitamin D is highly effective in treating osteomalacia, improving symptoms within days and increasing bone density by as much as 50% over 1 year.^32,33 In contrast, randomized controlled trials of vitamin D supplements alone in people without osteomalacia have not shown increases in bone density or changes in fracture risk.^34–37

Reid IR, Horne AM, Mihov B, et al. Effect of monthly high-dose vitamin D on bone density in community-dwelling older adults substudy of a randomized controlled trial. J Intern Med 2017; 282(5):452–460. Copyright 2017, Assoc for Publication of J Int Med

In 2017, my colleagues and I published a trial showing that vitamin D supplementation increases bone density by 2% to 3% in the spine and femoral neck in participants with baseline 25-hydroxyvitamin D levels below 30- nmol/L (12 ng/mL), but those starting above this level showed no effect (Figure 3).³⁸ And a reanalysis of an earlier study confirmed this 30 nmol/L threshold for an effect of vitamin D on bone density.³⁹ The finding of a clear-cut threshold for vitamin D effects is predicted by the physiologic considerations set out above.

Belief that higher levels of 25-hydroxyvitamin D are better is based on observational data. However, correlation does not prove causation, and it is likely that causation is reversed here. Those with better health are likely to spend more time exercising outdoors, are less likely to be obese, and are less likely to have inflammatory conditions; and as a result, they are more likely to have better vitamin D status. We should now be using trial-based definitions of vitamin D deficiency as opposed to thresholds derived from disease associations in observational studies.

Vitamin D supplements have also been suggested to benefit cardiovascular health and to reduce cancer risk, though current clinical trial data provide no support for these hypotheses.^36,40 Other trials addressing these questions are ongoing.

ARE VITAMIN D SUPPLEMENTS SAFE?

The safety of vitamin D supplements has generally been assessed with respect to the incidence of hypercalcemia. On this basis, very high doses have been promoted. However, there is now evidence that doses of 4,000 IU/day, 60,000 IU/month, and 500,000 IU/year increase the risk of falls and fractures.^41,42

The threshold for bone benefits discussed above (12 ng/mL) is easily exceeded with doses of vitamin D of 400 to 1,000 IU/day. At these levels, vitamin D supplements have no known adverse effects and can be widely endorsed for individuals at risk of deficiency. Supplement doses greater than 2,000 IU/day should be used only in exceptional circumstances, and with appropriate monitoring.

LITTLE USE FOR CALCIUM AND VITAMIN D SUPPLEMENTS

Extensive clinical trials have failed to demonstrate meaningful benefit from calcium supplements in the management of osteoporosis. Calcium supplements are often prescribed in patients who are receiving other treatments for osteoporosis, which may be justified with interventions that have the potential to cause hypocalcemia, but their coadministration with bisphosphonates has been shown to be unnecessary.

Calcium supplements commonly cause gastrointestinal symptoms that are sometimes severe and are likely to contribute to high levels of noncompliance with osteoporosis medications. They increase the risk of kidney stones,⁸ and there is reasonable evidence to suggest an adverse effect on vascular risk as well.²³

Vitamin D deficiency is common in frail elderly people, particularly those with dark skin or living at high latitudes. Low doses of vitamin D are safe and highly effective in preventing osteomalacia. But vitamin D supplements are unnecessary in those who regularly have sun exposure. And high doses of vitamin D have no demonstrated advantage and have been shown to increase the risk of falls and fractures.

Our decision to prescribe calcium and vitamin D supplements should be based on evidence that is of the same quality as for any other intervention we prescribe. Current evidence suggests that there is little reason to prescribe calcium, and that vitamin D should be targeted at those at risk of 25-hydroxyvitamin D levels less than 12 ng/mL.

Musculoskeletal complaints are one of the top reasons patients visit family physicians, with more than 24 million encounters per year.¹ Two articles in this month’s issue of JFP discuss treatments for musculoskeletal pain.

The article by Drs. Stephen and Peter Carek summarizes the value of specific exercises for hip and knee osteoarthritis (OA), chronic back pain, chronic shoulder pain, Achilles tendinitis, and lateral epicondylitis. This month’s PURL summarizes a negative randomized trial of treatment of knee OA with the popular over-the-counter combination of glucosamine and chondroitin. The findings? The group taking placebo actually had superior pain relief at 6 months!

What else works … and doesn’t? You may find that the following 4 “pearls,” taken from the literature, are also useful to know as you seek to manage patients’ musculoskeletal pain.

Studies remind us to harness the placebo effect, rather than dismiss it.

Pearl #1. Don’t use diazepam (valium) for acute low back pain. It doesn’t improve pain or function for this back pain. One hundred fourteen patients with acute low back pain were randomized to naproxen 500 mg bid as needed plus either placebo or diazepam 5 mg, 1 or 2 tablets, every 12 hours prn. At 7 days, 32% of the diazepam group reported moderate to severe pain and 22% of the placebo group did.²

Pearl #2. Use naproxen alone when treating acute low back pain. Three hundred twenty-three patients with acute low back pain were randomized to receive naproxen 500 mg bid plus placebo; naproxen plus oxycodone/acetaminophen; or naproxen plus cyclobenzaprine.³ At 7 days and 3 months, pain and function scores did not differ between groups.

Pearl #3. Don’t inject knees with corticosteroids. Enroll these patients in exercise and walking programs, which do provide benefit. One hundred forty patients with moderately severe knee OA were randomized to saline or triamcinolone 40 mg intra-articular injections every 3 months for 2 years.⁴ There was no difference in pain or function scores measured every 3 months and there was more cartilage degeneration in the triamcinolone group.

Continue to: Pearl #4

Pearl #4. Don’t dismiss the placebo effect. Eighty-three patients with chronic low back pain were randomized to either continue their current pain medications or to continue their current pain medication plus a placebo tablet twice daily for 3 weeks.⁵ They were told that placebos can have significant pain-relieving qualities. At 3 weeks, the patients taking placebo had less pain than those not taking placebo.

I’m not sure if we should start prescribing placebos, but this study is a strong reminder that we should harness the placebo effect, rather than dismiss it.

Musculoskeletal complaints are one of the top reasons patients visit family physicians, with more than 24 million encounters per year.¹ Two articles in this month’s issue of JFP discuss treatments for musculoskeletal pain.

The article by Drs. Stephen and Peter Carek summarizes the value of specific exercises for hip and knee osteoarthritis (OA), chronic back pain, chronic shoulder pain, Achilles tendinitis, and lateral epicondylitis. This month’s PURL summarizes a negative randomized trial of treatment of knee OA with the popular over-the-counter combination of glucosamine and chondroitin. The findings? The group taking placebo actually had superior pain relief at 6 months!

What else works … and doesn’t? You may find that the following 4 “pearls,” taken from the literature, are also useful to know as you seek to manage patients’ musculoskeletal pain.

Studies remind us to harness the placebo effect, rather than dismiss it.

Pearl #1. Don’t use diazepam (valium) for acute low back pain. It doesn’t improve pain or function for this back pain. One hundred fourteen patients with acute low back pain were randomized to naproxen 500 mg bid as needed plus either placebo or diazepam 5 mg, 1 or 2 tablets, every 12 hours prn. At 7 days, 32% of the diazepam group reported moderate to severe pain and 22% of the placebo group did.²

Pearl #2. Use naproxen alone when treating acute low back pain. Three hundred twenty-three patients with acute low back pain were randomized to receive naproxen 500 mg bid plus placebo; naproxen plus oxycodone/acetaminophen; or naproxen plus cyclobenzaprine.³ At 7 days and 3 months, pain and function scores did not differ between groups.

Pearl #3. Don’t inject knees with corticosteroids. Enroll these patients in exercise and walking programs, which do provide benefit. One hundred forty patients with moderately severe knee OA were randomized to saline or triamcinolone 40 mg intra-articular injections every 3 months for 2 years.⁴ There was no difference in pain or function scores measured every 3 months and there was more cartilage degeneration in the triamcinolone group.

Continue to: Pearl #4

Pearl #4. Don’t dismiss the placebo effect. Eighty-three patients with chronic low back pain were randomized to either continue their current pain medications or to continue their current pain medication plus a placebo tablet twice daily for 3 weeks.⁵ They were told that placebos can have significant pain-relieving qualities. At 3 weeks, the patients taking placebo had less pain than those not taking placebo.

I’m not sure if we should start prescribing placebos, but this study is a strong reminder that we should harness the placebo effect, rather than dismiss it.

Musculoskeletal complaints are one of the top reasons patients visit family physicians, with more than 24 million encounters per year.¹ Two articles in this month’s issue of JFP discuss treatments for musculoskeletal pain.

The article by Drs. Stephen and Peter Carek summarizes the value of specific exercises for hip and knee osteoarthritis (OA), chronic back pain, chronic shoulder pain, Achilles tendinitis, and lateral epicondylitis. This month’s PURL summarizes a negative randomized trial of treatment of knee OA with the popular over-the-counter combination of glucosamine and chondroitin. The findings? The group taking placebo actually had superior pain relief at 6 months!

What else works … and doesn’t? You may find that the following 4 “pearls,” taken from the literature, are also useful to know as you seek to manage patients’ musculoskeletal pain.

Studies remind us to harness the placebo effect, rather than dismiss it.

Pearl #1. Don’t use diazepam (valium) for acute low back pain. It doesn’t improve pain or function for this back pain. One hundred fourteen patients with acute low back pain were randomized to naproxen 500 mg bid as needed plus either placebo or diazepam 5 mg, 1 or 2 tablets, every 12 hours prn. At 7 days, 32% of the diazepam group reported moderate to severe pain and 22% of the placebo group did.²

Pearl #2. Use naproxen alone when treating acute low back pain. Three hundred twenty-three patients with acute low back pain were randomized to receive naproxen 500 mg bid plus placebo; naproxen plus oxycodone/acetaminophen; or naproxen plus cyclobenzaprine.³ At 7 days and 3 months, pain and function scores did not differ between groups.

Pearl #3. Don’t inject knees with corticosteroids. Enroll these patients in exercise and walking programs, which do provide benefit. One hundred forty patients with moderately severe knee OA were randomized to saline or triamcinolone 40 mg intra-articular injections every 3 months for 2 years.⁴ There was no difference in pain or function scores measured every 3 months and there was more cartilage degeneration in the triamcinolone group.

Continue to: Pearl #4

Pearl #4. Don’t dismiss the placebo effect. Eighty-three patients with chronic low back pain were randomized to either continue their current pain medications or to continue their current pain medication plus a placebo tablet twice daily for 3 weeks.⁵ They were told that placebos can have significant pain-relieving qualities. At 3 weeks, the patients taking placebo had less pain than those not taking placebo.

I’m not sure if we should start prescribing placebos, but this study is a strong reminder that we should harness the placebo effect, rather than dismiss it.

Martha Boxer (not her real name) had mentally prepared herself that this could happen, but the news still hit hard. Her doctors on the leukemia service broke the facts as gently as we could: The chemotherapy she had been suffering through for the last 2 weeks hadn’t worked. The results of her latest bone marrow biopsy showed it remained packed with cancer cells.

As Martha absorbed the news quietly, her son, sitting next to her bedside with his hand on hers, spoke first. “What now?”

I looked at my attending and nodded, as we were fully ready to answer this question. From the outset, we knew that Martha’s leukemia carried a genetic mutation that unfortunately put her in a high-risk category. The chances of her cancer responding to the first round of chemotherapy were low. When this happens, what we typically do next is reinduction, we explained. It’s a different combination of chemotherapy drugs, with a somewhat different side effect profile. But it would give her the best chance of response, we believed. We could start the new chemotherapy as early as today, we said.

Martha took this in. “Okay,” she said pensively. “I’ve been thinking. And I think maybe … I won’t do chemotherapy anymore.”

Her words caught me off guard because, frankly, they seemed premature. Her leukemia had not budged with the first round of treatment. But we still had an option B, and then an option C. It was usually at a later, more dire stage – when multiple lines of treatment had not worked, and instead had only caused harm – or, when the decision was forced by the medical system’s admission that we had nothing left to offer – that I’d heard patients express similar preferences. It was then that I’d seen patients and their loved ones flip a mental switch and choose to focus the time they had left on what really mattered to them.

It didn’t feel like we were at that point.

And so, as we debriefed outside her room, my first instinct was to convince her otherwise.

However, Martha had other priorities, as I would come to learn. Above all else, she hated the hospital. She hated feeling trapped in a strange room that wasn’t hers; she hated how the chemotherapy stole her energy and made her feel too weak to even shower. She wanted to be in her own home. She wanted to eat her own food, sleep in her own bed, and be surrounded by what she recognized.

But, she also wanted to live. Two paths lay ahead of her. It was a trade-off of more suffering with a small chance at remission, versus accepting no chance of cure but feeling well for as long as she could. She soon clarified that she wasn’t definitely against chemotherapy. She couldn’t decide. She needed more information from us to make this decision, the hardest of her life.

Over the next few days, I watched as our attending physician expertly provided just that. There were actually three options, she laid out. There was aggressive chemotherapy, entailing at least 3 more weeks in the hospital and coming with significant risk of infection, nausea, vomiting, and fatigue. The chances of inducing a remission were about one in three to one in two, and that remission would likely last between several months and 2 years before the leukemia would relapse. The second option was a chemotherapy pill she could take at home, an option with fewer side effects but no longer aimed at cure. The third option was home hospice support, focused on symptoms, without any anticancer medication.

I noticed a few things during those conversations. I noticed how my attending took a navigator role, not pushing Martha in one direction or another, but rather imparting all the relevant information to empower Martha to decide for herself. I noticed how she provided realistic estimates, not hedging away from numbers, but giving the honest, nitty-gritty facts, as best as she could predict. I noticed how she took the time and never rushed, even in spite of external pressures to discharge the patient from the hospital.

There was no right or wrong answer. I no longer felt that we had something in our grasp – a clear-cut, best decision – to persuade Martha toward. Is one in three good odds, or bad odds? Is 2 years a long period of time, or a short one? Of course, there is no actual answer to these questions; the answer is as elusive and personal as if we had asked Martha: What do you think?

What I learned from Martha is that, with a devastating diagnosis, there isn’t a right time to make this decision. There isn’t one defining moment where we flip a switch and change course. It isn’t only when we run out of treatment options that the choice to forgo it makes sense. That option is on a flexible line, different for every person and priority. As my attending later said, with Martha’s diagnosis and her values, it wouldn’t have been unreasonable to decide against chemotherapy from the start.

The language we use can sometimes mask that reality. As doctors, we may casually slip in words like “need” and “have to” in response to patients’ questions about what to do next. “You need more chemotherapy,” we might say. “We’d have to treat it.” We have “treatment,” after all, and so we go down the line of offering what’s next in the medical algorithm. That word, too, can be deceivingly tempting, enticing down a road that makes it seem like the obvious answer – or the only one. If the choices are treatment versus not, who wouldn’t want the treatment? But the details are where things get murky. What does that treatment involve? What are the chances it will work, and for how long?

Surreptitiously missing from this language is the fact that there’s a choice. There’s always a choice, and it’s on the table at any point. You can start chemotherapy without committing to stick it out until the end. You can go home, if that is what’s important to you. The best treatment option is the one the patient wants.

After 4 days, Martha decided to go home with palliative chemotherapy and a bridge to hospice. Each member of our team hugged her goodbye and wished her luck. She was nervous. But she packed her hospital room, and she left.

I recently pulled up her medical chart, bracing myself for bad news. But the interesting thing about hospice is that even though the focus is no longer on prolonging life, people sometimes live longer.

She felt well, the most recent palliative note said. She was spending her time writing, getting her finances in order, and finishing a legacy project for her grandchildren.

For Martha, it seemed to be the right choice.

Dr. Yurkiewicz is a fellow in hematology and oncology at Stanford (Calif.) University. Follow her on Twitter @ilanayurkiewicz.

Martha Boxer (not her real name) had mentally prepared herself that this could happen, but the news still hit hard. Her doctors on the leukemia service broke the facts as gently as we could: The chemotherapy she had been suffering through for the last 2 weeks hadn’t worked. The results of her latest bone marrow biopsy showed it remained packed with cancer cells.

As Martha absorbed the news quietly, her son, sitting next to her bedside with his hand on hers, spoke first. “What now?”

I looked at my attending and nodded, as we were fully ready to answer this question. From the outset, we knew that Martha’s leukemia carried a genetic mutation that unfortunately put her in a high-risk category. The chances of her cancer responding to the first round of chemotherapy were low. When this happens, what we typically do next is reinduction, we explained. It’s a different combination of chemotherapy drugs, with a somewhat different side effect profile. But it would give her the best chance of response, we believed. We could start the new chemotherapy as early as today, we said.

Martha took this in. “Okay,” she said pensively. “I’ve been thinking. And I think maybe … I won’t do chemotherapy anymore.”

Her words caught me off guard because, frankly, they seemed premature. Her leukemia had not budged with the first round of treatment. But we still had an option B, and then an option C. It was usually at a later, more dire stage – when multiple lines of treatment had not worked, and instead had only caused harm – or, when the decision was forced by the medical system’s admission that we had nothing left to offer – that I’d heard patients express similar preferences. It was then that I’d seen patients and their loved ones flip a mental switch and choose to focus the time they had left on what really mattered to them.

It didn’t feel like we were at that point.

And so, as we debriefed outside her room, my first instinct was to convince her otherwise.

However, Martha had other priorities, as I would come to learn. Above all else, she hated the hospital. She hated feeling trapped in a strange room that wasn’t hers; she hated how the chemotherapy stole her energy and made her feel too weak to even shower. She wanted to be in her own home. She wanted to eat her own food, sleep in her own bed, and be surrounded by what she recognized.

But, she also wanted to live. Two paths lay ahead of her. It was a trade-off of more suffering with a small chance at remission, versus accepting no chance of cure but feeling well for as long as she could. She soon clarified that she wasn’t definitely against chemotherapy. She couldn’t decide. She needed more information from us to make this decision, the hardest of her life.

Over the next few days, I watched as our attending physician expertly provided just that. There were actually three options, she laid out. There was aggressive chemotherapy, entailing at least 3 more weeks in the hospital and coming with significant risk of infection, nausea, vomiting, and fatigue. The chances of inducing a remission were about one in three to one in two, and that remission would likely last between several months and 2 years before the leukemia would relapse. The second option was a chemotherapy pill she could take at home, an option with fewer side effects but no longer aimed at cure. The third option was home hospice support, focused on symptoms, without any anticancer medication.

I noticed a few things during those conversations. I noticed how my attending took a navigator role, not pushing Martha in one direction or another, but rather imparting all the relevant information to empower Martha to decide for herself. I noticed how she provided realistic estimates, not hedging away from numbers, but giving the honest, nitty-gritty facts, as best as she could predict. I noticed how she took the time and never rushed, even in spite of external pressures to discharge the patient from the hospital.

There was no right or wrong answer. I no longer felt that we had something in our grasp – a clear-cut, best decision – to persuade Martha toward. Is one in three good odds, or bad odds? Is 2 years a long period of time, or a short one? Of course, there is no actual answer to these questions; the answer is as elusive and personal as if we had asked Martha: What do you think?

What I learned from Martha is that, with a devastating diagnosis, there isn’t a right time to make this decision. There isn’t one defining moment where we flip a switch and change course. It isn’t only when we run out of treatment options that the choice to forgo it makes sense. That option is on a flexible line, different for every person and priority. As my attending later said, with Martha’s diagnosis and her values, it wouldn’t have been unreasonable to decide against chemotherapy from the start.

The language we use can sometimes mask that reality. As doctors, we may casually slip in words like “need” and “have to” in response to patients’ questions about what to do next. “You need more chemotherapy,” we might say. “We’d have to treat it.” We have “treatment,” after all, and so we go down the line of offering what’s next in the medical algorithm. That word, too, can be deceivingly tempting, enticing down a road that makes it seem like the obvious answer – or the only one. If the choices are treatment versus not, who wouldn’t want the treatment? But the details are where things get murky. What does that treatment involve? What are the chances it will work, and for how long?

Surreptitiously missing from this language is the fact that there’s a choice. There’s always a choice, and it’s on the table at any point. You can start chemotherapy without committing to stick it out until the end. You can go home, if that is what’s important to you. The best treatment option is the one the patient wants.

After 4 days, Martha decided to go home with palliative chemotherapy and a bridge to hospice. Each member of our team hugged her goodbye and wished her luck. She was nervous. But she packed her hospital room, and she left.

I recently pulled up her medical chart, bracing myself for bad news. But the interesting thing about hospice is that even though the focus is no longer on prolonging life, people sometimes live longer.

She felt well, the most recent palliative note said. She was spending her time writing, getting her finances in order, and finishing a legacy project for her grandchildren.

For Martha, it seemed to be the right choice.

Dr. Yurkiewicz is a fellow in hematology and oncology at Stanford (Calif.) University. Follow her on Twitter @ilanayurkiewicz.

Martha Boxer (not her real name) had mentally prepared herself that this could happen, but the news still hit hard. Her doctors on the leukemia service broke the facts as gently as we could: The chemotherapy she had been suffering through for the last 2 weeks hadn’t worked. The results of her latest bone marrow biopsy showed it remained packed with cancer cells.

As Martha absorbed the news quietly, her son, sitting next to her bedside with his hand on hers, spoke first. “What now?”

I looked at my attending and nodded, as we were fully ready to answer this question. From the outset, we knew that Martha’s leukemia carried a genetic mutation that unfortunately put her in a high-risk category. The chances of her cancer responding to the first round of chemotherapy were low. When this happens, what we typically do next is reinduction, we explained. It’s a different combination of chemotherapy drugs, with a somewhat different side effect profile. But it would give her the best chance of response, we believed. We could start the new chemotherapy as early as today, we said.

Martha took this in. “Okay,” she said pensively. “I’ve been thinking. And I think maybe … I won’t do chemotherapy anymore.”

Her words caught me off guard because, frankly, they seemed premature. Her leukemia had not budged with the first round of treatment. But we still had an option B, and then an option C. It was usually at a later, more dire stage – when multiple lines of treatment had not worked, and instead had only caused harm – or, when the decision was forced by the medical system’s admission that we had nothing left to offer – that I’d heard patients express similar preferences. It was then that I’d seen patients and their loved ones flip a mental switch and choose to focus the time they had left on what really mattered to them.

It didn’t feel like we were at that point.

And so, as we debriefed outside her room, my first instinct was to convince her otherwise.

However, Martha had other priorities, as I would come to learn. Above all else, she hated the hospital. She hated feeling trapped in a strange room that wasn’t hers; she hated how the chemotherapy stole her energy and made her feel too weak to even shower. She wanted to be in her own home. She wanted to eat her own food, sleep in her own bed, and be surrounded by what she recognized.

But, she also wanted to live. Two paths lay ahead of her. It was a trade-off of more suffering with a small chance at remission, versus accepting no chance of cure but feeling well for as long as she could. She soon clarified that she wasn’t definitely against chemotherapy. She couldn’t decide. She needed more information from us to make this decision, the hardest of her life.

Over the next few days, I watched as our attending physician expertly provided just that. There were actually three options, she laid out. There was aggressive chemotherapy, entailing at least 3 more weeks in the hospital and coming with significant risk of infection, nausea, vomiting, and fatigue. The chances of inducing a remission were about one in three to one in two, and that remission would likely last between several months and 2 years before the leukemia would relapse. The second option was a chemotherapy pill she could take at home, an option with fewer side effects but no longer aimed at cure. The third option was home hospice support, focused on symptoms, without any anticancer medication.

I noticed a few things during those conversations. I noticed how my attending took a navigator role, not pushing Martha in one direction or another, but rather imparting all the relevant information to empower Martha to decide for herself. I noticed how she provided realistic estimates, not hedging away from numbers, but giving the honest, nitty-gritty facts, as best as she could predict. I noticed how she took the time and never rushed, even in spite of external pressures to discharge the patient from the hospital.

There was no right or wrong answer. I no longer felt that we had something in our grasp – a clear-cut, best decision – to persuade Martha toward. Is one in three good odds, or bad odds? Is 2 years a long period of time, or a short one? Of course, there is no actual answer to these questions; the answer is as elusive and personal as if we had asked Martha: What do you think?

What I learned from Martha is that, with a devastating diagnosis, there isn’t a right time to make this decision. There isn’t one defining moment where we flip a switch and change course. It isn’t only when we run out of treatment options that the choice to forgo it makes sense. That option is on a flexible line, different for every person and priority. As my attending later said, with Martha’s diagnosis and her values, it wouldn’t have been unreasonable to decide against chemotherapy from the start.

The language we use can sometimes mask that reality. As doctors, we may casually slip in words like “need” and “have to” in response to patients’ questions about what to do next. “You need more chemotherapy,” we might say. “We’d have to treat it.” We have “treatment,” after all, and so we go down the line of offering what’s next in the medical algorithm. That word, too, can be deceivingly tempting, enticing down a road that makes it seem like the obvious answer – or the only one. If the choices are treatment versus not, who wouldn’t want the treatment? But the details are where things get murky. What does that treatment involve? What are the chances it will work, and for how long?

Surreptitiously missing from this language is the fact that there’s a choice. There’s always a choice, and it’s on the table at any point. You can start chemotherapy without committing to stick it out until the end. You can go home, if that is what’s important to you. The best treatment option is the one the patient wants.

After 4 days, Martha decided to go home with palliative chemotherapy and a bridge to hospice. Each member of our team hugged her goodbye and wished her luck. She was nervous. But she packed her hospital room, and she left.

I recently pulled up her medical chart, bracing myself for bad news. But the interesting thing about hospice is that even though the focus is no longer on prolonging life, people sometimes live longer.

She felt well, the most recent palliative note said. She was spending her time writing, getting her finances in order, and finishing a legacy project for her grandchildren.

For Martha, it seemed to be the right choice.

Dr. Yurkiewicz is a fellow in hematology and oncology at Stanford (Calif.) University. Follow her on Twitter @ilanayurkiewicz.

In the world of research, an “n of 1” is considered an insufficient sample size to make an inference about a population. While distinguishing significance in research is vital in the scientific world, this statistical view often feels invalid when the “n of 1” is you or someone you know. And when the statistic is a diagnosis of cancer, that “1” feels even more noteworthy.

We know that cancer is a devastating disease that results in an increasing number of diagnoses each day. Case in point, the American Cancer Society estimates that more than 4,700 new cancers will be diagnosed each day in 2018.¹ Most of us know that breast, colon, lung, and prostate cancer are the main contributors to those staggering numbers. But did you know that the incidence of oropharyngeal cancers (OPCs) is increasing? I didn’t.

It is estimated that 51,540 new cancer cases in 2018 will be of the oral cavity and pharynx and will cause approximately 10,000 deaths in the United States (US).¹ Included in this estimate is the increasing incidence of human papillomavirus–associated oropharyngeal cancers (HPV-OPCs). The “n of 1” that started this discussion? That was a colleague of mine, who received just such a diagnosis. And the causative factor was surprising to me.

Now, please don’t misunderstand me—I know that HPV, a group of more than 150 related viruses, is the most common sexually transmitted infection (STI) in the US.² I also know that HPV is implicated in genital warts and in cervical and anal cancers. The virus, which is transmitted through intimate skin-to-skin contact, is acquired by many during their adolescent and young adult years.² Currently, 84 million Americans have HPV, and 14 million new cases are diagnosed each year.³ And while many of these infections resolve on their own, others can cause serious health problems.

The most serious of those health problems, HPV-related cancers (which include cervical, vulvovaginal, anal, and oropharyngeal), are on the rise in the US.⁴ The prevalence of HPV in oropharyngeal tumors increased from 16.3% during the 1980s to 72.7% during the 2000s.⁵ Moreover, HPV has been implicated in 12% to 63% of all oropharyngeal cancers.⁶ Fifteen years ago, researchers concluded that HPV type 16 was the cause of 90% of cases of HPV-positive squamous cell carcinomas of the head and neck.^7,8 At any given time, 7% of the population between ages 14 and 69 are infected by the virus within the oral mucosa.⁹

For my colleague—and many of us—the ship of prevention has sailed. But what disconcerts me most about this rise in HPV-related cancers is that, as of 2006, we have a vaccine that protects against infection with the two most prevalent cancer-causing HPV types. And yet, our vaccination rates continue to fall short of the Office of Disease Prevention and Health Promotion’s goal of having 80% of females ages 13 to 15 fully vaccinated against HPV.¹⁰

Continue to: Research has shown that parents of young adolescents...

Research has shown that parents of young adolescents are often upset by the recommendation that their children receive the HPV vaccine.¹¹ Common beliefs are that the vaccine will give adolescents permission to become sexually active—or, conversely, that the adolescent isn’t sexually active, so the vaccine isn’t necessary. The reality of the situation: Adolescents don’t consider oral sex as having sexual relations, and oral sex is often the first sexual encounter for young people. Adolescents also regard oral sex as less risky than vaginal sex.¹² So, many have unknowingly put themselves at risk while thinking they are actually being “safe.”

There are ways to reduce cancer risk, but few interventions are more effective than HPV vaccination.¹³ Given the incidence of HPV-OPC, it’s time to debunk the misbeliefs about sexual activity and move on to a concerted effort to promote HPV vaccination. Recent advertising about the HPV vaccine has emphasized the consequence of cancer in its messages. I applaud this new direction—it could be key to reversing the persistently low rate of HPV vaccination and changing that “n of 1” to zero. Share your trials and triumphs in promoting HPV vaccination with me at [email protected].

In the world of research, an “n of 1” is considered an insufficient sample size to make an inference about a population. While distinguishing significance in research is vital in the scientific world, this statistical view often feels invalid when the “n of 1” is you or someone you know. And when the statistic is a diagnosis of cancer, that “1” feels even more noteworthy.

We know that cancer is a devastating disease that results in an increasing number of diagnoses each day. Case in point, the American Cancer Society estimates that more than 4,700 new cancers will be diagnosed each day in 2018.¹ Most of us know that breast, colon, lung, and prostate cancer are the main contributors to those staggering numbers. But did you know that the incidence of oropharyngeal cancers (OPCs) is increasing? I didn’t.

It is estimated that 51,540 new cancer cases in 2018 will be of the oral cavity and pharynx and will cause approximately 10,000 deaths in the United States (US).¹ Included in this estimate is the increasing incidence of human papillomavirus–associated oropharyngeal cancers (HPV-OPCs). The “n of 1” that started this discussion? That was a colleague of mine, who received just such a diagnosis. And the causative factor was surprising to me.

Now, please don’t misunderstand me—I know that HPV, a group of more than 150 related viruses, is the most common sexually transmitted infection (STI) in the US.² I also know that HPV is implicated in genital warts and in cervical and anal cancers. The virus, which is transmitted through intimate skin-to-skin contact, is acquired by many during their adolescent and young adult years.² Currently, 84 million Americans have HPV, and 14 million new cases are diagnosed each year.³ And while many of these infections resolve on their own, others can cause serious health problems.

The most serious of those health problems, HPV-related cancers (which include cervical, vulvovaginal, anal, and oropharyngeal), are on the rise in the US.⁴ The prevalence of HPV in oropharyngeal tumors increased from 16.3% during the 1980s to 72.7% during the 2000s.⁵ Moreover, HPV has been implicated in 12% to 63% of all oropharyngeal cancers.⁶ Fifteen years ago, researchers concluded that HPV type 16 was the cause of 90% of cases of HPV-positive squamous cell carcinomas of the head and neck.^7,8 At any given time, 7% of the population between ages 14 and 69 are infected by the virus within the oral mucosa.⁹

For my colleague—and many of us—the ship of prevention has sailed. But what disconcerts me most about this rise in HPV-related cancers is that, as of 2006, we have a vaccine that protects against infection with the two most prevalent cancer-causing HPV types. And yet, our vaccination rates continue to fall short of the Office of Disease Prevention and Health Promotion’s goal of having 80% of females ages 13 to 15 fully vaccinated against HPV.¹⁰

Continue to: Research has shown that parents of young adolescents...

Research has shown that parents of young adolescents are often upset by the recommendation that their children receive the HPV vaccine.¹¹ Common beliefs are that the vaccine will give adolescents permission to become sexually active—or, conversely, that the adolescent isn’t sexually active, so the vaccine isn’t necessary. The reality of the situation: Adolescents don’t consider oral sex as having sexual relations, and oral sex is often the first sexual encounter for young people. Adolescents also regard oral sex as less risky than vaginal sex.¹² So, many have unknowingly put themselves at risk while thinking they are actually being “safe.”

There are ways to reduce cancer risk, but few interventions are more effective than HPV vaccination.¹³ Given the incidence of HPV-OPC, it’s time to debunk the misbeliefs about sexual activity and move on to a concerted effort to promote HPV vaccination. Recent advertising about the HPV vaccine has emphasized the consequence of cancer in its messages. I applaud this new direction—it could be key to reversing the persistently low rate of HPV vaccination and changing that “n of 1” to zero. Share your trials and triumphs in promoting HPV vaccination with me at [email protected].

In the world of research, an “n of 1” is considered an insufficient sample size to make an inference about a population. While distinguishing significance in research is vital in the scientific world, this statistical view often feels invalid when the “n of 1” is you or someone you know. And when the statistic is a diagnosis of cancer, that “1” feels even more noteworthy.

We know that cancer is a devastating disease that results in an increasing number of diagnoses each day. Case in point, the American Cancer Society estimates that more than 4,700 new cancers will be diagnosed each day in 2018.¹ Most of us know that breast, colon, lung, and prostate cancer are the main contributors to those staggering numbers. But did you know that the incidence of oropharyngeal cancers (OPCs) is increasing? I didn’t.

It is estimated that 51,540 new cancer cases in 2018 will be of the oral cavity and pharynx and will cause approximately 10,000 deaths in the United States (US).¹ Included in this estimate is the increasing incidence of human papillomavirus–associated oropharyngeal cancers (HPV-OPCs). The “n of 1” that started this discussion? That was a colleague of mine, who received just such a diagnosis. And the causative factor was surprising to me.

Now, please don’t misunderstand me—I know that HPV, a group of more than 150 related viruses, is the most common sexually transmitted infection (STI) in the US.² I also know that HPV is implicated in genital warts and in cervical and anal cancers. The virus, which is transmitted through intimate skin-to-skin contact, is acquired by many during their adolescent and young adult years.² Currently, 84 million Americans have HPV, and 14 million new cases are diagnosed each year.³ And while many of these infections resolve on their own, others can cause serious health problems.

The most serious of those health problems, HPV-related cancers (which include cervical, vulvovaginal, anal, and oropharyngeal), are on the rise in the US.⁴ The prevalence of HPV in oropharyngeal tumors increased from 16.3% during the 1980s to 72.7% during the 2000s.⁵ Moreover, HPV has been implicated in 12% to 63% of all oropharyngeal cancers.⁶ Fifteen years ago, researchers concluded that HPV type 16 was the cause of 90% of cases of HPV-positive squamous cell carcinomas of the head and neck.^7,8 At any given time, 7% of the population between ages 14 and 69 are infected by the virus within the oral mucosa.⁹

For my colleague—and many of us—the ship of prevention has sailed. But what disconcerts me most about this rise in HPV-related cancers is that, as of 2006, we have a vaccine that protects against infection with the two most prevalent cancer-causing HPV types. And yet, our vaccination rates continue to fall short of the Office of Disease Prevention and Health Promotion’s goal of having 80% of females ages 13 to 15 fully vaccinated against HPV.¹⁰

Continue to: Research has shown that parents of young adolescents...

Research has shown that parents of young adolescents are often upset by the recommendation that their children receive the HPV vaccine.¹¹ Common beliefs are that the vaccine will give adolescents permission to become sexually active—or, conversely, that the adolescent isn’t sexually active, so the vaccine isn’t necessary. The reality of the situation: Adolescents don’t consider oral sex as having sexual relations, and oral sex is often the first sexual encounter for young people. Adolescents also regard oral sex as less risky than vaginal sex.¹² So, many have unknowingly put themselves at risk while thinking they are actually being “safe.”

There are ways to reduce cancer risk, but few interventions are more effective than HPV vaccination.¹³ Given the incidence of HPV-OPC, it’s time to debunk the misbeliefs about sexual activity and move on to a concerted effort to promote HPV vaccination. Recent advertising about the HPV vaccine has emphasized the consequence of cancer in its messages. I applaud this new direction—it could be key to reversing the persistently low rate of HPV vaccination and changing that “n of 1” to zero. Share your trials and triumphs in promoting HPV vaccination with me at [email protected].

CMS has released its proposed rule (see related articles and a commentary) and included changes as substantial as I have seen in the last two decades. Additionally, the Affordable Care Act has been under continued attack despite its majority support from our citizenry. Loss of the individual mandate, allowance of “skinny” health plans, a rewrite of association plan rules, elimination of cost-sharing reductions and premium support – all have contributed to a shifting away from socialized medical costs and toward a system of individual responsibility for health. Depending on one’s political philosophy (and income), that may be bad or good.

Our article list this month will be interesting to many. The AGA produced a Clinical Practice Update about tumor seeding with endoscopic procedures. This should give us pause and make us reconsider our endoscopic practices. My wife (an endoscopy nurse in Minneapolis) has been asking for years whether pulling a PEG tube past an esophageal cancer might cause tumor seeding, and physicians have reassured her that there is no cause for worry. Turns out she was right (as usual). Deaths from liver disease in the U.S. have seen a dramatic increase since 1999, driven substantially by increasing alcohol use. Fecal transplants in irritable bowel syndrome? Possibly helpful, as reported in an article from Digestive Disease Week.^®

As summer comes to an end, we head into a tumultuous fall that will be dominated by November elections.

John I. Allen, MD, MBA, AGAF
Editor in Chief

CMS has released its proposed rule (see related articles and a commentary) and included changes as substantial as I have seen in the last two decades. Additionally, the Affordable Care Act has been under continued attack despite its majority support from our citizenry. Loss of the individual mandate, allowance of “skinny” health plans, a rewrite of association plan rules, elimination of cost-sharing reductions and premium support – all have contributed to a shifting away from socialized medical costs and toward a system of individual responsibility for health. Depending on one’s political philosophy (and income), that may be bad or good.

Our article list this month will be interesting to many. The AGA produced a Clinical Practice Update about tumor seeding with endoscopic procedures. This should give us pause and make us reconsider our endoscopic practices. My wife (an endoscopy nurse in Minneapolis) has been asking for years whether pulling a PEG tube past an esophageal cancer might cause tumor seeding, and physicians have reassured her that there is no cause for worry. Turns out she was right (as usual). Deaths from liver disease in the U.S. have seen a dramatic increase since 1999, driven substantially by increasing alcohol use. Fecal transplants in irritable bowel syndrome? Possibly helpful, as reported in an article from Digestive Disease Week.^®

As summer comes to an end, we head into a tumultuous fall that will be dominated by November elections.

John I. Allen, MD, MBA, AGAF
Editor in Chief

CMS has released its proposed rule (see related articles and a commentary) and included changes as substantial as I have seen in the last two decades. Additionally, the Affordable Care Act has been under continued attack despite its majority support from our citizenry. Loss of the individual mandate, allowance of “skinny” health plans, a rewrite of association plan rules, elimination of cost-sharing reductions and premium support – all have contributed to a shifting away from socialized medical costs and toward a system of individual responsibility for health. Depending on one’s political philosophy (and income), that may be bad or good.

Our article list this month will be interesting to many. The AGA produced a Clinical Practice Update about tumor seeding with endoscopic procedures. This should give us pause and make us reconsider our endoscopic practices. My wife (an endoscopy nurse in Minneapolis) has been asking for years whether pulling a PEG tube past an esophageal cancer might cause tumor seeding, and physicians have reassured her that there is no cause for worry. Turns out she was right (as usual). Deaths from liver disease in the U.S. have seen a dramatic increase since 1999, driven substantially by increasing alcohol use. Fecal transplants in irritable bowel syndrome? Possibly helpful, as reported in an article from Digestive Disease Week.^®

As summer comes to an end, we head into a tumultuous fall that will be dominated by November elections.

John I. Allen, MD, MBA, AGAF
Editor in Chief

“Alex, I understand that you are upset that you left your little bulldozer at home. Let’s try to think of something else you can play with here at the restaurant that is kind of like a bulldozer.”

Ambernectar 13/CC BY-ND 2.0

Sounds like a reasonable strategy to calm an unruly preschooler, and it might have been had it not been the fifth attempt in a 45-minute dialogue between a mother and her overtired, misbehaving 3-year-old. There had been a lot of “I understand how you feel” and “use your words” woven into a gag-worthy and futile effort to forge a collaborative parent-child solution to the problem of an exhausted preschooler who is up past his bedtime in a public place.

My wife and I enjoy a night out with friends and prefer a quiet dining atmosphere. However, some evenings we eat earlier and choose a restaurant we know appeals to families with young children. At those meals, we anticipate being serenaded by a loud background buzz punctuated by the occasional shriek or short bout of crying. We expect a degree of childish behavior to come with the territory, and watching the dramas unfold brings back fond “been there, done that” memories. But, listening to those behaviors being horribly mismanaged can ruin even the most tolerant adult’s appetite in less time than it takes a parent to say, “I can see you’re unhappy, and we need to talk about why.”

In an op-ed piece, a psychotherapist asks the legitimate question, and provides the correct quick answer (“Which Is Better, Rewards or Punishments? Neither,” New York Times, Aug. 21, 2018). I couldn’t agree more. In my experience, rewards have a very short half-life and can become disastrously inflationary in the blink of an eye. On the other hand, punishments can be either too heavy-handed or so irrational that the child fails to make a logical connection between his misbehavior and his sentence.

Unfortunately, many child behavior advisers, including the op-ed author, offer alternatives to rewards and punishment that are unworkable in real-world circumstances, such as the restaurant scenario my wife and I endured.

While it sounds very democratic to ask a 3-year-old why he is misbehaving, more often than not it should be the parent who is asking what he or she could have done differently to avoid the situation. It is likely the child has been allowed to become overtired and/or the parent may be in denial about his/her child’s intolerance for stimulating environments.

Too often the parent takes too long to realize that the water is spilling over the dam and it is time to head for shore. Children who are overtired and having a tantrum can’t participate in a rational discussion about their feelings. If that dialogue needs to happen, and that is seldom, it should be the next day after the parent has time to consider his or her own mistakes.

When it comes to managing misbehaving children, I prefer well-tailored consequences and my favorite is a humanely crafted time-out. When presented and executed properly, a time-out can break the cycle of misbehavior and give both parent and child a chance to reconsider their positions.

But at 7 p.m. on a Friday evening in a busy restaurant, neither a time-out nor philosophizing with a 3-year-old is going to work. It’s time to ask for the check and head home to bed.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

“Alex, I understand that you are upset that you left your little bulldozer at home. Let’s try to think of something else you can play with here at the restaurant that is kind of like a bulldozer.”

Ambernectar 13/CC BY-ND 2.0

Sounds like a reasonable strategy to calm an unruly preschooler, and it might have been had it not been the fifth attempt in a 45-minute dialogue between a mother and her overtired, misbehaving 3-year-old. There had been a lot of “I understand how you feel” and “use your words” woven into a gag-worthy and futile effort to forge a collaborative parent-child solution to the problem of an exhausted preschooler who is up past his bedtime in a public place.

My wife and I enjoy a night out with friends and prefer a quiet dining atmosphere. However, some evenings we eat earlier and choose a restaurant we know appeals to families with young children. At those meals, we anticipate being serenaded by a loud background buzz punctuated by the occasional shriek or short bout of crying. We expect a degree of childish behavior to come with the territory, and watching the dramas unfold brings back fond “been there, done that” memories. But, listening to those behaviors being horribly mismanaged can ruin even the most tolerant adult’s appetite in less time than it takes a parent to say, “I can see you’re unhappy, and we need to talk about why.”

In an op-ed piece, a psychotherapist asks the legitimate question, and provides the correct quick answer (“Which Is Better, Rewards or Punishments? Neither,” New York Times, Aug. 21, 2018). I couldn’t agree more. In my experience, rewards have a very short half-life and can become disastrously inflationary in the blink of an eye. On the other hand, punishments can be either too heavy-handed or so irrational that the child fails to make a logical connection between his misbehavior and his sentence.

Unfortunately, many child behavior advisers, including the op-ed author, offer alternatives to rewards and punishment that are unworkable in real-world circumstances, such as the restaurant scenario my wife and I endured.

While it sounds very democratic to ask a 3-year-old why he is misbehaving, more often than not it should be the parent who is asking what he or she could have done differently to avoid the situation. It is likely the child has been allowed to become overtired and/or the parent may be in denial about his/her child’s intolerance for stimulating environments.

Too often the parent takes too long to realize that the water is spilling over the dam and it is time to head for shore. Children who are overtired and having a tantrum can’t participate in a rational discussion about their feelings. If that dialogue needs to happen, and that is seldom, it should be the next day after the parent has time to consider his or her own mistakes.

When it comes to managing misbehaving children, I prefer well-tailored consequences and my favorite is a humanely crafted time-out. When presented and executed properly, a time-out can break the cycle of misbehavior and give both parent and child a chance to reconsider their positions.

But at 7 p.m. on a Friday evening in a busy restaurant, neither a time-out nor philosophizing with a 3-year-old is going to work. It’s time to ask for the check and head home to bed.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

“Alex, I understand that you are upset that you left your little bulldozer at home. Let’s try to think of something else you can play with here at the restaurant that is kind of like a bulldozer.”

Ambernectar 13/CC BY-ND 2.0

Sounds like a reasonable strategy to calm an unruly preschooler, and it might have been had it not been the fifth attempt in a 45-minute dialogue between a mother and her overtired, misbehaving 3-year-old. There had been a lot of “I understand how you feel” and “use your words” woven into a gag-worthy and futile effort to forge a collaborative parent-child solution to the problem of an exhausted preschooler who is up past his bedtime in a public place.

My wife and I enjoy a night out with friends and prefer a quiet dining atmosphere. However, some evenings we eat earlier and choose a restaurant we know appeals to families with young children. At those meals, we anticipate being serenaded by a loud background buzz punctuated by the occasional shriek or short bout of crying. We expect a degree of childish behavior to come with the territory, and watching the dramas unfold brings back fond “been there, done that” memories. But, listening to those behaviors being horribly mismanaged can ruin even the most tolerant adult’s appetite in less time than it takes a parent to say, “I can see you’re unhappy, and we need to talk about why.”

In an op-ed piece, a psychotherapist asks the legitimate question, and provides the correct quick answer (“Which Is Better, Rewards or Punishments? Neither,” New York Times, Aug. 21, 2018). I couldn’t agree more. In my experience, rewards have a very short half-life and can become disastrously inflationary in the blink of an eye. On the other hand, punishments can be either too heavy-handed or so irrational that the child fails to make a logical connection between his misbehavior and his sentence.

Unfortunately, many child behavior advisers, including the op-ed author, offer alternatives to rewards and punishment that are unworkable in real-world circumstances, such as the restaurant scenario my wife and I endured.

While it sounds very democratic to ask a 3-year-old why he is misbehaving, more often than not it should be the parent who is asking what he or she could have done differently to avoid the situation. It is likely the child has been allowed to become overtired and/or the parent may be in denial about his/her child’s intolerance for stimulating environments.

Too often the parent takes too long to realize that the water is spilling over the dam and it is time to head for shore. Children who are overtired and having a tantrum can’t participate in a rational discussion about their feelings. If that dialogue needs to happen, and that is seldom, it should be the next day after the parent has time to consider his or her own mistakes.

When it comes to managing misbehaving children, I prefer well-tailored consequences and my favorite is a humanely crafted time-out. When presented and executed properly, a time-out can break the cycle of misbehavior and give both parent and child a chance to reconsider their positions.

But at 7 p.m. on a Friday evening in a busy restaurant, neither a time-out nor philosophizing with a 3-year-old is going to work. It’s time to ask for the check and head home to bed.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].