Photo from Novartis

The US Food and Drug Administration (FDA) has approved tisagenlecleucel (Kymriah®) for its second indication.

The chimeric antigen receptor (CAR) T-cell therapy is now approved to treat adults with relapsed or refractory large B-cell lymphoma after 2 or more lines of systemic therapy.

This includes patients with diffuse large B-cell lymphoma (DLBCL) not otherwise specified, high grade B-cell lymphoma, and DLBCL arising from follicular lymphoma.

The application for tisagenlecleucel in B-cell lymphoma was granted priority review. The FDA aims to take action on a priority review application within 6 months of receiving it, rather than the standard 10 months.

Tisagenlecleucel is also FDA-approved to treat patients age 25 and younger who have B-cell precursor acute lymphoblastic leukemia that is refractory or in second or later relapse.

Access to tisagenlecleucel

The prescribing information for tisagenlecleucel includes a boxed warning detailing the risk of cytokine release syndrome (CRS) and neurological toxicities for patients receiving tisagenlecleucel.

Because of these risks, tisagenlecleucel is only available through a Risk Evaluation and Mitigation Strategy (REMS) program. The REMS program serves to inform and educate healthcare professionals about the risks associated with tisagenlecleucel treatment.

Novartis, the company marketing tisagenlecleucel, has established a network of certified treatment centers throughout the US. Staff at these centers are trained on the use of tisagenlecleucel and appropriate patient care.

Tisagenlecleucel is manufactured at a Novartis facility in Morris Plains, New Jersey. In the US, the target turnaround time for manufacturing tisagenlecleucel is 22 days.

Tisagenlecleucel costs $475,000 for a single course of treatment. However, Novartis said it is collaborating with the US Centers for Medicare and Medicaid Services on the creation of an appropriate value-based pricing approach.

The company also has a program called KYMRIAH CARES™, which offers financial assistance to eligible patients to help them gain access to tisagenlecleucel.

Phase 2 trial

The FDA approval of tisagenlecleucel for adults with relapsed/refractory B-cell lymphoma is based on results of the phase 2 JULIET trial.

The prescribing information for tisagenlecleucel includes data on 106 patients treated on this trial.

Only 68 of these patients were evaluable for efficacy. They had a median age of 56 (range, 22 to 74), and 71% were male.

Seventy-eight percent of patients had primary DLBCL not otherwise specified, and 22% had DLBCL following transformation from follicular lymphoma. Seventeen percent had high grade DLBCL.

Fifty-six percent of patients had refractory disease, and 44% had relapsed after their last therapy. The median number of prior therapies was 3 (range, 1 to 6), and 44% of patients had undergone autologous transplant.

Ninety percent of patients received lymphodepleting chemotherapy (66% fludarabine and 24% bendamustine) prior to tisagenlecleucel, and 10% did not. The median dose of tisagenlecleucel was 3.5 × 10⁸ CAR+ T cells (range, 1.0 to 5.2 × 10⁸).

The overall response rate was 50%, with 32% of patients achieving a complete response and 18% achieving a partial response. The median duration of response was not reached with a median follow-up of 9.4 months.

In all 106 patients infused with tisagenlecleucel, the most common grade 3/4 adverse events were infections (25%), CRS (23%), neurologic events (18%), febrile neutropenia (17%), encephalopathy (11%), lymphopenia (94%), neutropenia (81%), leukopenia (77%), anemia (58%), thrombocytopenia (54%), hypophosphatemia (24%), hypokalemia (12%), and hyponatremia (11%).

Three patients died within 30 days of tisagenlecleucel infusion. All of them had CRS and either stable or progressive disease. One of these patients developed bowel necrosis.

One patient died of infection. There were no deaths attributed to neurological events, and no fatal cases of cerebral edema.

Photo from Novartis

The US Food and Drug Administration (FDA) has approved tisagenlecleucel (Kymriah®) for its second indication.

The chimeric antigen receptor (CAR) T-cell therapy is now approved to treat adults with relapsed or refractory large B-cell lymphoma after 2 or more lines of systemic therapy.

This includes patients with diffuse large B-cell lymphoma (DLBCL) not otherwise specified, high grade B-cell lymphoma, and DLBCL arising from follicular lymphoma.

The application for tisagenlecleucel in B-cell lymphoma was granted priority review. The FDA aims to take action on a priority review application within 6 months of receiving it, rather than the standard 10 months.

Tisagenlecleucel is also FDA-approved to treat patients age 25 and younger who have B-cell precursor acute lymphoblastic leukemia that is refractory or in second or later relapse.

Access to tisagenlecleucel

The prescribing information for tisagenlecleucel includes a boxed warning detailing the risk of cytokine release syndrome (CRS) and neurological toxicities for patients receiving tisagenlecleucel.

Because of these risks, tisagenlecleucel is only available through a Risk Evaluation and Mitigation Strategy (REMS) program. The REMS program serves to inform and educate healthcare professionals about the risks associated with tisagenlecleucel treatment.

Novartis, the company marketing tisagenlecleucel, has established a network of certified treatment centers throughout the US. Staff at these centers are trained on the use of tisagenlecleucel and appropriate patient care.

Tisagenlecleucel is manufactured at a Novartis facility in Morris Plains, New Jersey. In the US, the target turnaround time for manufacturing tisagenlecleucel is 22 days.

Tisagenlecleucel costs $475,000 for a single course of treatment. However, Novartis said it is collaborating with the US Centers for Medicare and Medicaid Services on the creation of an appropriate value-based pricing approach.

The company also has a program called KYMRIAH CARES™, which offers financial assistance to eligible patients to help them gain access to tisagenlecleucel.

Phase 2 trial

The FDA approval of tisagenlecleucel for adults with relapsed/refractory B-cell lymphoma is based on results of the phase 2 JULIET trial.

The prescribing information for tisagenlecleucel includes data on 106 patients treated on this trial.

Only 68 of these patients were evaluable for efficacy. They had a median age of 56 (range, 22 to 74), and 71% were male.

Seventy-eight percent of patients had primary DLBCL not otherwise specified, and 22% had DLBCL following transformation from follicular lymphoma. Seventeen percent had high grade DLBCL.

Fifty-six percent of patients had refractory disease, and 44% had relapsed after their last therapy. The median number of prior therapies was 3 (range, 1 to 6), and 44% of patients had undergone autologous transplant.

Ninety percent of patients received lymphodepleting chemotherapy (66% fludarabine and 24% bendamustine) prior to tisagenlecleucel, and 10% did not. The median dose of tisagenlecleucel was 3.5 × 10⁸ CAR+ T cells (range, 1.0 to 5.2 × 10⁸).

The overall response rate was 50%, with 32% of patients achieving a complete response and 18% achieving a partial response. The median duration of response was not reached with a median follow-up of 9.4 months.

In all 106 patients infused with tisagenlecleucel, the most common grade 3/4 adverse events were infections (25%), CRS (23%), neurologic events (18%), febrile neutropenia (17%), encephalopathy (11%), lymphopenia (94%), neutropenia (81%), leukopenia (77%), anemia (58%), thrombocytopenia (54%), hypophosphatemia (24%), hypokalemia (12%), and hyponatremia (11%).

Three patients died within 30 days of tisagenlecleucel infusion. All of them had CRS and either stable or progressive disease. One of these patients developed bowel necrosis.

One patient died of infection. There were no deaths attributed to neurological events, and no fatal cases of cerebral edema.

Photo from Novartis

The US Food and Drug Administration (FDA) has approved tisagenlecleucel (Kymriah®) for its second indication.

The chimeric antigen receptor (CAR) T-cell therapy is now approved to treat adults with relapsed or refractory large B-cell lymphoma after 2 or more lines of systemic therapy.

This includes patients with diffuse large B-cell lymphoma (DLBCL) not otherwise specified, high grade B-cell lymphoma, and DLBCL arising from follicular lymphoma.

The application for tisagenlecleucel in B-cell lymphoma was granted priority review. The FDA aims to take action on a priority review application within 6 months of receiving it, rather than the standard 10 months.

Tisagenlecleucel is also FDA-approved to treat patients age 25 and younger who have B-cell precursor acute lymphoblastic leukemia that is refractory or in second or later relapse.

Access to tisagenlecleucel

The prescribing information for tisagenlecleucel includes a boxed warning detailing the risk of cytokine release syndrome (CRS) and neurological toxicities for patients receiving tisagenlecleucel.

Because of these risks, tisagenlecleucel is only available through a Risk Evaluation and Mitigation Strategy (REMS) program. The REMS program serves to inform and educate healthcare professionals about the risks associated with tisagenlecleucel treatment.

Novartis, the company marketing tisagenlecleucel, has established a network of certified treatment centers throughout the US. Staff at these centers are trained on the use of tisagenlecleucel and appropriate patient care.

Tisagenlecleucel is manufactured at a Novartis facility in Morris Plains, New Jersey. In the US, the target turnaround time for manufacturing tisagenlecleucel is 22 days.

Tisagenlecleucel costs $475,000 for a single course of treatment. However, Novartis said it is collaborating with the US Centers for Medicare and Medicaid Services on the creation of an appropriate value-based pricing approach.

The company also has a program called KYMRIAH CARES™, which offers financial assistance to eligible patients to help them gain access to tisagenlecleucel.

Phase 2 trial

The FDA approval of tisagenlecleucel for adults with relapsed/refractory B-cell lymphoma is based on results of the phase 2 JULIET trial.

The prescribing information for tisagenlecleucel includes data on 106 patients treated on this trial.

Only 68 of these patients were evaluable for efficacy. They had a median age of 56 (range, 22 to 74), and 71% were male.

Seventy-eight percent of patients had primary DLBCL not otherwise specified, and 22% had DLBCL following transformation from follicular lymphoma. Seventeen percent had high grade DLBCL.

Fifty-six percent of patients had refractory disease, and 44% had relapsed after their last therapy. The median number of prior therapies was 3 (range, 1 to 6), and 44% of patients had undergone autologous transplant.

Ninety percent of patients received lymphodepleting chemotherapy (66% fludarabine and 24% bendamustine) prior to tisagenlecleucel, and 10% did not. The median dose of tisagenlecleucel was 3.5 × 10⁸ CAR+ T cells (range, 1.0 to 5.2 × 10⁸).

The overall response rate was 50%, with 32% of patients achieving a complete response and 18% achieving a partial response. The median duration of response was not reached with a median follow-up of 9.4 months.

In all 106 patients infused with tisagenlecleucel, the most common grade 3/4 adverse events were infections (25%), CRS (23%), neurologic events (18%), febrile neutropenia (17%), encephalopathy (11%), lymphopenia (94%), neutropenia (81%), leukopenia (77%), anemia (58%), thrombocytopenia (54%), hypophosphatemia (24%), hypokalemia (12%), and hyponatremia (11%).

Three patients died within 30 days of tisagenlecleucel infusion. All of them had CRS and either stable or progressive disease. One of these patients developed bowel necrosis.

One patient died of infection. There were no deaths attributed to neurological events, and no fatal cases of cerebral edema.

Photo from Business Wire

Researchers say they’ve discovered why multiple myeloma (MM) patients may experience chemotherapy-induced peripheral neuropathy (CIPN) when treated with bortezomib.

The group’s study also suggests fingolimod—a drug approved to treat multiple sclerosis—could mitigate CIPN without compromising the efficacy of bortezomib.

Daniela Salvemini, PhD, of the Saint Louis University School of Medicine in St. Louis, Missouri, and her colleagues reported these findings in the Journal of Experimental Medicine.

The researchers said bortezomib causes CIPN in more than 40% of patients, but the reasons for this are unclear.

With their study, Dr Salvemini and her colleagues found that bortezomib accelerates the production of sphingolipids, which have been linked to neuropathic pain.

Rats treated with bortezomib began to accumulate 2 sphingolipid metabolites—sphingosine 1-phosphate and dihydrosphingosine 1-phosphate—in their spinal cords at the time they began to show signs of neuropathic pain.

Blocking the production of these molecules prevented the animals from developing CIPN in response to bortezomib.

Sphingosine 1-phosphate and dihydrosphingosine 1-phosphate can activate a cell surface receptor protein called S1PR1. Dr Salvemini and her colleagues determined that the 2 metabolites cause CIPN by activating S1PR1 on the surface of astrocytes, resulting in neuroinflammation and enhanced release of the excitatory neurotransmitter glutamate.

Drugs that inhibit S1PR1 prevented rats from developing CIPN in response to bortezomib. One such inhibitor was fingolimod, a drug approved by the US Food and Drug Administration (FDA) to treat multiple sclerosis.

In addition to preventing CIPN, fingolimod did not inhibit bortezomib’s ability to kill MM cells. In fact, fingolimod has demonstrated anticancer activity in past studies.

“Because fingolimod shows promising anticancer potential and is already FDA-approved, we think that our findings in rats can be rapidly translated to the clinic to prevent and treat bortezomib-induced neuropathic pain,” Dr Salvemini said.

Photo from Business Wire

Researchers say they’ve discovered why multiple myeloma (MM) patients may experience chemotherapy-induced peripheral neuropathy (CIPN) when treated with bortezomib.

The group’s study also suggests fingolimod—a drug approved to treat multiple sclerosis—could mitigate CIPN without compromising the efficacy of bortezomib.

Daniela Salvemini, PhD, of the Saint Louis University School of Medicine in St. Louis, Missouri, and her colleagues reported these findings in the Journal of Experimental Medicine.

The researchers said bortezomib causes CIPN in more than 40% of patients, but the reasons for this are unclear.

With their study, Dr Salvemini and her colleagues found that bortezomib accelerates the production of sphingolipids, which have been linked to neuropathic pain.

Rats treated with bortezomib began to accumulate 2 sphingolipid metabolites—sphingosine 1-phosphate and dihydrosphingosine 1-phosphate—in their spinal cords at the time they began to show signs of neuropathic pain.

Blocking the production of these molecules prevented the animals from developing CIPN in response to bortezomib.

Sphingosine 1-phosphate and dihydrosphingosine 1-phosphate can activate a cell surface receptor protein called S1PR1. Dr Salvemini and her colleagues determined that the 2 metabolites cause CIPN by activating S1PR1 on the surface of astrocytes, resulting in neuroinflammation and enhanced release of the excitatory neurotransmitter glutamate.

Drugs that inhibit S1PR1 prevented rats from developing CIPN in response to bortezomib. One such inhibitor was fingolimod, a drug approved by the US Food and Drug Administration (FDA) to treat multiple sclerosis.

In addition to preventing CIPN, fingolimod did not inhibit bortezomib’s ability to kill MM cells. In fact, fingolimod has demonstrated anticancer activity in past studies.

“Because fingolimod shows promising anticancer potential and is already FDA-approved, we think that our findings in rats can be rapidly translated to the clinic to prevent and treat bortezomib-induced neuropathic pain,” Dr Salvemini said.

Photo from Business Wire

Researchers say they’ve discovered why multiple myeloma (MM) patients may experience chemotherapy-induced peripheral neuropathy (CIPN) when treated with bortezomib.

The group’s study also suggests fingolimod—a drug approved to treat multiple sclerosis—could mitigate CIPN without compromising the efficacy of bortezomib.

Daniela Salvemini, PhD, of the Saint Louis University School of Medicine in St. Louis, Missouri, and her colleagues reported these findings in the Journal of Experimental Medicine.

The researchers said bortezomib causes CIPN in more than 40% of patients, but the reasons for this are unclear.

With their study, Dr Salvemini and her colleagues found that bortezomib accelerates the production of sphingolipids, which have been linked to neuropathic pain.

Rats treated with bortezomib began to accumulate 2 sphingolipid metabolites—sphingosine 1-phosphate and dihydrosphingosine 1-phosphate—in their spinal cords at the time they began to show signs of neuropathic pain.

Blocking the production of these molecules prevented the animals from developing CIPN in response to bortezomib.

Sphingosine 1-phosphate and dihydrosphingosine 1-phosphate can activate a cell surface receptor protein called S1PR1. Dr Salvemini and her colleagues determined that the 2 metabolites cause CIPN by activating S1PR1 on the surface of astrocytes, resulting in neuroinflammation and enhanced release of the excitatory neurotransmitter glutamate.

Drugs that inhibit S1PR1 prevented rats from developing CIPN in response to bortezomib. One such inhibitor was fingolimod, a drug approved by the US Food and Drug Administration (FDA) to treat multiple sclerosis.

In addition to preventing CIPN, fingolimod did not inhibit bortezomib’s ability to kill MM cells. In fact, fingolimod has demonstrated anticancer activity in past studies.

“Because fingolimod shows promising anticancer potential and is already FDA-approved, we think that our findings in rats can be rapidly translated to the clinic to prevent and treat bortezomib-induced neuropathic pain,” Dr Salvemini said.

Lab mouse

Preclinical research suggests PI3K inhibitors could treat hereditary hemorrhagic telangiectasia (HHT).

Experiments in mice and patient samples revealed that loss of ALK1 function induces vascular hyperplasia and increases activity of the PI3K pathway.

Pharmacological inhibition of PI3K was able to eliminate vascular hyperplasia in mouse models.

Francesc Viñals, PhD, of Institut Catala d’Oncologia in Barcelona, Spain, and his colleagues described this research in Arteriosclerosis, Thrombosis and Vascular Biology.

“Our group has been working with endothelial cells for a long time, focusing on how they are affected by changes in the TGF-beta signaling pathway from a basic research perspective,” Dr Viñals noted.

The group was especially interested in ALK1, a receptor for the TGF-beta factor BMP9 that is expressed by endothelial cells. Mutations in ALK1 have been associated with HHT.

The researchers developed a model for the formation of blood vessels in the retina of mice that lacked a copy of the gene for the ALK1 receptor. These models exhibited an excess of endothelial cells and errors in the formation of blood vessels.

These results corresponded with the researchers’ theory. The team thought that, if members of the TGF-beta family usually act as a “brake” for cellular proliferation, mutations in one of the family’s components should lead to uncontrolled proliferation. The researchers replicated and confirmed their results in in vitro cultures.

Further investigation revealed the role of the PI3K pathway. The researchers found that stimulation of PI3K acts as an “accelerator” for endothelial cells to proliferate.

BMP9 (through ALK1) acts as a brake, inhibiting VEGF-mediated PI3K signaling by increasing PTEN activity. When ALK1 is mutated, there is no brake, and endothelial cells proliferate more thanks to the PI3K pathway.

The researchers discovered this mechanism via experiments in human umbilical vein endothelial cells. However, experiments in HHT2 patient samples supported these findings.

The team found that mutations in ALK1 increased endothelial cell proliferation in vessels from patients with HHT2. The researchers also found overexpression of genes linked to PI3K/AKT signaling in telangiectasial tissue from patients with HHT2, as compared to normal tissue from either HHT2 patients or healthy individuals.

Going back to murine experiments, the researchers found that loss of both PI3K and ALK1 function stabilizes the proliferation of endothelial cells.

The team tested LY294002, a pan-PI3K inhibitor, in mice and found that PI3K inhibition can reverse the vascular hyperplasia induced by loss of ALK1 function.

“Now, the next step is clear,” Dr Viñals said. “We have to assess the effects of PI3K inhibitors in patients. PI3K inhibitors are currently used in the treatment of patients with cancer or patients who require immunosuppression after organ transplantation, and it has been observed that, in patients with these pathologies and HHT, treatment results in a reduction of the issues caused by HHT, which is a very encouraging fact.”

Lab mouse

Preclinical research suggests PI3K inhibitors could treat hereditary hemorrhagic telangiectasia (HHT).

Experiments in mice and patient samples revealed that loss of ALK1 function induces vascular hyperplasia and increases activity of the PI3K pathway.

Pharmacological inhibition of PI3K was able to eliminate vascular hyperplasia in mouse models.

Francesc Viñals, PhD, of Institut Catala d’Oncologia in Barcelona, Spain, and his colleagues described this research in Arteriosclerosis, Thrombosis and Vascular Biology.

“Our group has been working with endothelial cells for a long time, focusing on how they are affected by changes in the TGF-beta signaling pathway from a basic research perspective,” Dr Viñals noted.

The group was especially interested in ALK1, a receptor for the TGF-beta factor BMP9 that is expressed by endothelial cells. Mutations in ALK1 have been associated with HHT.

The researchers developed a model for the formation of blood vessels in the retina of mice that lacked a copy of the gene for the ALK1 receptor. These models exhibited an excess of endothelial cells and errors in the formation of blood vessels.

These results corresponded with the researchers’ theory. The team thought that, if members of the TGF-beta family usually act as a “brake” for cellular proliferation, mutations in one of the family’s components should lead to uncontrolled proliferation. The researchers replicated and confirmed their results in in vitro cultures.

Further investigation revealed the role of the PI3K pathway. The researchers found that stimulation of PI3K acts as an “accelerator” for endothelial cells to proliferate.

BMP9 (through ALK1) acts as a brake, inhibiting VEGF-mediated PI3K signaling by increasing PTEN activity. When ALK1 is mutated, there is no brake, and endothelial cells proliferate more thanks to the PI3K pathway.

The researchers discovered this mechanism via experiments in human umbilical vein endothelial cells. However, experiments in HHT2 patient samples supported these findings.

The team found that mutations in ALK1 increased endothelial cell proliferation in vessels from patients with HHT2. The researchers also found overexpression of genes linked to PI3K/AKT signaling in telangiectasial tissue from patients with HHT2, as compared to normal tissue from either HHT2 patients or healthy individuals.

Going back to murine experiments, the researchers found that loss of both PI3K and ALK1 function stabilizes the proliferation of endothelial cells.

The team tested LY294002, a pan-PI3K inhibitor, in mice and found that PI3K inhibition can reverse the vascular hyperplasia induced by loss of ALK1 function.

“Now, the next step is clear,” Dr Viñals said. “We have to assess the effects of PI3K inhibitors in patients. PI3K inhibitors are currently used in the treatment of patients with cancer or patients who require immunosuppression after organ transplantation, and it has been observed that, in patients with these pathologies and HHT, treatment results in a reduction of the issues caused by HHT, which is a very encouraging fact.”

Lab mouse

Preclinical research suggests PI3K inhibitors could treat hereditary hemorrhagic telangiectasia (HHT).

Experiments in mice and patient samples revealed that loss of ALK1 function induces vascular hyperplasia and increases activity of the PI3K pathway.

Pharmacological inhibition of PI3K was able to eliminate vascular hyperplasia in mouse models.

Francesc Viñals, PhD, of Institut Catala d’Oncologia in Barcelona, Spain, and his colleagues described this research in Arteriosclerosis, Thrombosis and Vascular Biology.

“Our group has been working with endothelial cells for a long time, focusing on how they are affected by changes in the TGF-beta signaling pathway from a basic research perspective,” Dr Viñals noted.

The group was especially interested in ALK1, a receptor for the TGF-beta factor BMP9 that is expressed by endothelial cells. Mutations in ALK1 have been associated with HHT.

The researchers developed a model for the formation of blood vessels in the retina of mice that lacked a copy of the gene for the ALK1 receptor. These models exhibited an excess of endothelial cells and errors in the formation of blood vessels.

These results corresponded with the researchers’ theory. The team thought that, if members of the TGF-beta family usually act as a “brake” for cellular proliferation, mutations in one of the family’s components should lead to uncontrolled proliferation. The researchers replicated and confirmed their results in in vitro cultures.

Further investigation revealed the role of the PI3K pathway. The researchers found that stimulation of PI3K acts as an “accelerator” for endothelial cells to proliferate.

BMP9 (through ALK1) acts as a brake, inhibiting VEGF-mediated PI3K signaling by increasing PTEN activity. When ALK1 is mutated, there is no brake, and endothelial cells proliferate more thanks to the PI3K pathway.

The researchers discovered this mechanism via experiments in human umbilical vein endothelial cells. However, experiments in HHT2 patient samples supported these findings.

The team found that mutations in ALK1 increased endothelial cell proliferation in vessels from patients with HHT2. The researchers also found overexpression of genes linked to PI3K/AKT signaling in telangiectasial tissue from patients with HHT2, as compared to normal tissue from either HHT2 patients or healthy individuals.

Going back to murine experiments, the researchers found that loss of both PI3K and ALK1 function stabilizes the proliferation of endothelial cells.

The team tested LY294002, a pan-PI3K inhibitor, in mice and found that PI3K inhibition can reverse the vascular hyperplasia induced by loss of ALK1 function.

“Now, the next step is clear,” Dr Viñals said. “We have to assess the effects of PI3K inhibitors in patients. PI3K inhibitors are currently used in the treatment of patients with cancer or patients who require immunosuppression after organ transplantation, and it has been observed that, in patients with these pathologies and HHT, treatment results in a reduction of the issues caused by HHT, which is a very encouraging fact.”

Gun violence in America is a cancer—a metastasis that must be eradicated. As a nation, we continually mourn an ever-rising toll of victims and question why this senseless, tragic loss of life is repeated year after year. What is the reason for the increasing frequency of mass shootings? How is it that we are unable to stem the spread of this plague of gun-related deaths? When will we put an end to the massacres?

All good questions. And they have once again become the hue and cry of many people in the wake of the shooting at Marjory Stoneman Douglas High School in Parkland, Florida. This particular tragedy marked the 30th mass shooting in 2018—in other words, the latest in a line of tragedies that “should have” been preventable.¹

Whatever your political stance on the issue of guns, surely we can all agree that it is a problem that more than 549,000 acts of gun violence occur each year.² In 2015 (the most recent year for which a National Vital Statistics Report is available), there were 36,252 firearm-related deaths in the US—a rate of 11.1 deaths per 100,000 population. From 2012 to 2014, nearly 1,300 children died each year from a firearm-related injury.³ These statistics support the need to change our thinking about guns and gun violence.

Thus far, the discussion about gun control has tended to focus on passing and enforcing laws. We know that the US, compared to other countries, has fairly lenient restrictions for who can buy a gun and what kinds of guns can be purchased.⁴ In fact, many Americans can buy a gun in less than an hour, while in some countries, the process takes months.⁴ Furthermore, across the nation, there is no systematic fashion of gun regulation or ownership.

The challenge of how to balance gun safety and gun rights is an ongoing, yet one-focus, approach. The debate needs to be broadened; it’s time we stop talking about just the gun. We need to address the problem of firearm injuries in the context of a public health issue.⁵

A common assumption is that mental illness or high stress levels trigger gun violence. According to data from the Sandy Hook Promise organization, most criminal gun violence is committed by individuals who lack mental wellness (ie, coping skills, anger management, and other social/emotional skills).⁶ But other statistics contradict that notion. For example, a 2011 report in The Atlantic did not support mental illness as a causative factor in gun violence.⁷ And evidence presented by the Consortium for Risk-Based Firearm Policy indicates that the majority of people with mental illness do not engage in violence against others.⁸ The Consortium noted, however, that a small group of individuals with serious mental illness does have a propensity toward violence. It is this—the risk for dangerous behavior, rather than mental illness alone—that must be the focus for preventing gun violence.

Dangerous behaviors are those that carry a high risk for harm or injury to oneself or others.⁹ Emotional problems, social conflicts, access to weapons, and altered states of mind (via alcohol and drugs) all contribute to violent and homicidal behavior in adolescents.¹⁰ A worrisome fact: A nationwide study of mass shootings from 2009 to 2016 revealed that in at least 42% of these incidents there was documentation that the attacker exhibited dangerous warning signs before the shooting.¹¹ So, in many cases of violent behavior, the perpetrator threatens others or his own life before actually carrying out his plan.¹² But surely we must be able to do more than sit and watch for warning signs.

Continue to: Might tighter gun control laws...

Might tighter gun control laws help to mitigate this crisis? Perhaps; but we must also consider the importance of mental health care reform. In order to prevent gun violence, we need to understand (and address) the cause. We therefore need funding for mental health services to assist those who are at risk for harming themselves and others.

Instead of solely viewing gun control as a yes-or-no issue, we need to examine the intersection between mental health and violence. While our mental health care system is not equipped to help everyone, we need to acknowledge that gun-related deaths are preventable—and we need to make the choice to invest in that prevention.

Thus far, the ongoing debate about gun safety has largely centered around the Second Amendment, which has a two-fold obligation: the right of US citizens to be protected from violence and the right of the people to bear arms. Proponents on both sides of this polarizing issue have rallied to support their position; this often takes the form of shouting and counter-shouting (and sometimes threats)—and we make no progress on the core issue, which is that too many people in this country die because of gun violence.

We stand at the crossroads of realizing that something must be done. Share your reasoned suggestions (no rants, please!) for how we, as a nation, can combat gun violence and gun-related deaths with me at [email protected].

Gun violence in America is a cancer—a metastasis that must be eradicated. As a nation, we continually mourn an ever-rising toll of victims and question why this senseless, tragic loss of life is repeated year after year. What is the reason for the increasing frequency of mass shootings? How is it that we are unable to stem the spread of this plague of gun-related deaths? When will we put an end to the massacres?

All good questions. And they have once again become the hue and cry of many people in the wake of the shooting at Marjory Stoneman Douglas High School in Parkland, Florida. This particular tragedy marked the 30th mass shooting in 2018—in other words, the latest in a line of tragedies that “should have” been preventable.¹

Whatever your political stance on the issue of guns, surely we can all agree that it is a problem that more than 549,000 acts of gun violence occur each year.² In 2015 (the most recent year for which a National Vital Statistics Report is available), there were 36,252 firearm-related deaths in the US—a rate of 11.1 deaths per 100,000 population. From 2012 to 2014, nearly 1,300 children died each year from a firearm-related injury.³ These statistics support the need to change our thinking about guns and gun violence.

Thus far, the discussion about gun control has tended to focus on passing and enforcing laws. We know that the US, compared to other countries, has fairly lenient restrictions for who can buy a gun and what kinds of guns can be purchased.⁴ In fact, many Americans can buy a gun in less than an hour, while in some countries, the process takes months.⁴ Furthermore, across the nation, there is no systematic fashion of gun regulation or ownership.

The challenge of how to balance gun safety and gun rights is an ongoing, yet one-focus, approach. The debate needs to be broadened; it’s time we stop talking about just the gun. We need to address the problem of firearm injuries in the context of a public health issue.⁵

A common assumption is that mental illness or high stress levels trigger gun violence. According to data from the Sandy Hook Promise organization, most criminal gun violence is committed by individuals who lack mental wellness (ie, coping skills, anger management, and other social/emotional skills).⁶ But other statistics contradict that notion. For example, a 2011 report in The Atlantic did not support mental illness as a causative factor in gun violence.⁷ And evidence presented by the Consortium for Risk-Based Firearm Policy indicates that the majority of people with mental illness do not engage in violence against others.⁸ The Consortium noted, however, that a small group of individuals with serious mental illness does have a propensity toward violence. It is this—the risk for dangerous behavior, rather than mental illness alone—that must be the focus for preventing gun violence.

Dangerous behaviors are those that carry a high risk for harm or injury to oneself or others.⁹ Emotional problems, social conflicts, access to weapons, and altered states of mind (via alcohol and drugs) all contribute to violent and homicidal behavior in adolescents.¹⁰ A worrisome fact: A nationwide study of mass shootings from 2009 to 2016 revealed that in at least 42% of these incidents there was documentation that the attacker exhibited dangerous warning signs before the shooting.¹¹ So, in many cases of violent behavior, the perpetrator threatens others or his own life before actually carrying out his plan.¹² But surely we must be able to do more than sit and watch for warning signs.

Continue to: Might tighter gun control laws...

Might tighter gun control laws help to mitigate this crisis? Perhaps; but we must also consider the importance of mental health care reform. In order to prevent gun violence, we need to understand (and address) the cause. We therefore need funding for mental health services to assist those who are at risk for harming themselves and others.

Instead of solely viewing gun control as a yes-or-no issue, we need to examine the intersection between mental health and violence. While our mental health care system is not equipped to help everyone, we need to acknowledge that gun-related deaths are preventable—and we need to make the choice to invest in that prevention.

Thus far, the ongoing debate about gun safety has largely centered around the Second Amendment, which has a two-fold obligation: the right of US citizens to be protected from violence and the right of the people to bear arms. Proponents on both sides of this polarizing issue have rallied to support their position; this often takes the form of shouting and counter-shouting (and sometimes threats)—and we make no progress on the core issue, which is that too many people in this country die because of gun violence.

We stand at the crossroads of realizing that something must be done. Share your reasoned suggestions (no rants, please!) for how we, as a nation, can combat gun violence and gun-related deaths with me at [email protected].

Gun violence in America is a cancer—a metastasis that must be eradicated. As a nation, we continually mourn an ever-rising toll of victims and question why this senseless, tragic loss of life is repeated year after year. What is the reason for the increasing frequency of mass shootings? How is it that we are unable to stem the spread of this plague of gun-related deaths? When will we put an end to the massacres?

All good questions. And they have once again become the hue and cry of many people in the wake of the shooting at Marjory Stoneman Douglas High School in Parkland, Florida. This particular tragedy marked the 30th mass shooting in 2018—in other words, the latest in a line of tragedies that “should have” been preventable.¹

Whatever your political stance on the issue of guns, surely we can all agree that it is a problem that more than 549,000 acts of gun violence occur each year.² In 2015 (the most recent year for which a National Vital Statistics Report is available), there were 36,252 firearm-related deaths in the US—a rate of 11.1 deaths per 100,000 population. From 2012 to 2014, nearly 1,300 children died each year from a firearm-related injury.³ These statistics support the need to change our thinking about guns and gun violence.

Thus far, the discussion about gun control has tended to focus on passing and enforcing laws. We know that the US, compared to other countries, has fairly lenient restrictions for who can buy a gun and what kinds of guns can be purchased.⁴ In fact, many Americans can buy a gun in less than an hour, while in some countries, the process takes months.⁴ Furthermore, across the nation, there is no systematic fashion of gun regulation or ownership.

The challenge of how to balance gun safety and gun rights is an ongoing, yet one-focus, approach. The debate needs to be broadened; it’s time we stop talking about just the gun. We need to address the problem of firearm injuries in the context of a public health issue.⁵

A common assumption is that mental illness or high stress levels trigger gun violence. According to data from the Sandy Hook Promise organization, most criminal gun violence is committed by individuals who lack mental wellness (ie, coping skills, anger management, and other social/emotional skills).⁶ But other statistics contradict that notion. For example, a 2011 report in The Atlantic did not support mental illness as a causative factor in gun violence.⁷ And evidence presented by the Consortium for Risk-Based Firearm Policy indicates that the majority of people with mental illness do not engage in violence against others.⁸ The Consortium noted, however, that a small group of individuals with serious mental illness does have a propensity toward violence. It is this—the risk for dangerous behavior, rather than mental illness alone—that must be the focus for preventing gun violence.

Dangerous behaviors are those that carry a high risk for harm or injury to oneself or others.⁹ Emotional problems, social conflicts, access to weapons, and altered states of mind (via alcohol and drugs) all contribute to violent and homicidal behavior in adolescents.¹⁰ A worrisome fact: A nationwide study of mass shootings from 2009 to 2016 revealed that in at least 42% of these incidents there was documentation that the attacker exhibited dangerous warning signs before the shooting.¹¹ So, in many cases of violent behavior, the perpetrator threatens others or his own life before actually carrying out his plan.¹² But surely we must be able to do more than sit and watch for warning signs.

Continue to: Might tighter gun control laws...

Might tighter gun control laws help to mitigate this crisis? Perhaps; but we must also consider the importance of mental health care reform. In order to prevent gun violence, we need to understand (and address) the cause. We therefore need funding for mental health services to assist those who are at risk for harming themselves and others.

Instead of solely viewing gun control as a yes-or-no issue, we need to examine the intersection between mental health and violence. While our mental health care system is not equipped to help everyone, we need to acknowledge that gun-related deaths are preventable—and we need to make the choice to invest in that prevention.

Thus far, the ongoing debate about gun safety has largely centered around the Second Amendment, which has a two-fold obligation: the right of US citizens to be protected from violence and the right of the people to bear arms. Proponents on both sides of this polarizing issue have rallied to support their position; this often takes the form of shouting and counter-shouting (and sometimes threats)—and we make no progress on the core issue, which is that too many people in this country die because of gun violence.

We stand at the crossroads of realizing that something must be done. Share your reasoned suggestions (no rants, please!) for how we, as a nation, can combat gun violence and gun-related deaths with me at [email protected].

The opioid epidemic continues to devastate the United States across demographic and socioeconomic groups; two-thirds of the 63,632 Americans who died of drug overdoses¹ in 2016 died of prescription or illicit opioids.

In 2015, Theodore J. Cicero, PhD, professor of psychiatry at Washington University, St. Louis, reported on a fundamental change in the nature of the ongoing opioid epidemic: What started as prescription opioid overprescribing, leading to diversion, abuse, and opioid addiction, was transitioning to illicit heroin distribution and consumption. Prescription opioids, namely, extended-release oxycodone (Oxycontin), were perceived initially as pure and safe, as they were specifically dosed and physician prescribed. In addition, filling a prescription for opioids was not associated with the shame or stigma of buying illicit drugs off the street. Because those drugs were seen as therapeutic and pharmacologically “legitimate,” many clinicians and the lay public alike were surprised to see the surge of opioid addiction and overdoses.

Dr. Cicero and others noted² that prescription opioids, whether taken originally for analgesic or recreational purposes, became a “gateway” to heroin, which already was making its way into the United States from Mexico,³ as heroin was cheap and becoming cheaper, easier to find, easy to use, and “pure.” Prescription opioids, on the other hand, were becoming more expensive, and physicians were facing increased regulations in prescribing them. Thus, as prescription opioid use became more and more stigmatized, heroin use was seen, paradoxically, as a more practical alternative. The amount of opioids prescribed in the United States has peaked; physicians are prescribing opioids less often; and the averaged dose has dropped as well, according to the Centers for Disease Control and Prevention.⁴ The first wave of deaths was attributable to prescription opioids, and the second was tied to illicitly obtained potent fentanyl analogs (manufactured in China and smuggled primarily through Mexico), which is added to heroin and sold in the United States.⁵

Many addiction experts and health policy leaders were not surprised by the increases in HIV, TB, and hepatitis B and C that followed the increasing use of intravenous opioids. However, few had experience with previous opioid epidemics in the United States, the most recent being the heroin epidemic occurring in the 1960s-1970s in the aftermath of the Vietnam War. At that time, the notion that heroin was contaminated with other psychoactive drugs, medications, fillers, and other adulterants was a foregone conclusion – though in public health and treatment discussions, this issue is hardly ever raised. We believe this to be a significant lapse in policy and planning. Surveillance by the Drug Enforcement Administration shows that acetyl fentanyl–laced heroin costs a little more on the street than regular heroin. Yet it sells, because users believe its extreme potency produces a better high, thus worth the extra cost. This phenomenon underscores an important point: Opioid addicts often are in search of a better high and will go to any lengths – even risking their lives – to get it.

The “cutting” or “adulteration” of street drugs is common practice in the manufacturing, distribution, and selling of illicit drugs, and the motive is to increase profit. The term “adulterant” generally refers to addition of substances with some psychoactive effects, such as caffeine, ephedra, or even paracetamol. These substances are cheaper than the main substance, have similar or complementary effects when added, and thus help conceal the fact that the desired substance has been cut or diluted. Substances without psychoactive properties such as lactose, other sugars, or talc, are added to a drug primarily to increase the bulk or weight of the illicit substance, or for aesthetic purposes to fool the user. Some adulterants simply are the result of the particular manufacturing process used to make the drug. For example, illicitly manufactured methamphetamine frequently is contaminated by nonstimulant impurities such as lead or mercury (extremely toxic heavy metals), or from carcinogenic solvents used in the synthesis. The local anesthetic lidocaine often is added to cocaine, and the reasons are intuitive: Both drugs are fast-acting local anesthetics.

More intriguing is the story of the antiparasitic medication levamisole. The DEA has estimated that 60%-89% of the seized street cocaine contains levamisole. Levamisole appears to be partly metabolized into an amphetamine-like compound, which could increase dopamine concentration in the reward pathway and thus activate endogenous opioids: It can mimic the effects of cocaine at a fraction of the cost. Levamisole is associated with several types of severe blood disorders, including leukopenia, agranulocytosis, multifocal inflammatory leukoencephalopathy, and neutropenia; a common presentation is vasculitis resulting in loss of limbs. Thus, a real danger in adulterants such as levamisole is their toxicity beyond those of the drug to which they are added, causing numerous medical consequences – including death.

Dr. Gold is the 17th Distinguished Alumni Professor at the University of Florida, Gainesville, and professor of psychiatry (adjunct) at Washington University in St. Louis. He also serves as chairman of the scientific advisory boards for RiverMend Health. Dr. Srivastava is a fourth-year resident in the department of psychiatry at Washington University.

References

1 NCHS Data Brief. No. 294. December 2017.

2 N Engl J Med. 2015;373:1789-90.

3 DEA Strategic Intelligence Section. 2017 National Drug Threat Assessment: Drug Enforcement Administration, U.S. Department of Justice, 2017.

4 Centers for Disease Control and Prevention, press release. Mar 29, 2018.

5 MMWR. 2018. Mar 30;67(12):349-58.

6 Am J Public Health. 2017 Mar;107(3):430-2.

7 “Q&A: Thomas Kosten, MD: Anti-drug vaccines.” RiverMend Health.

8 “Q&A: Stacy Seikel, MD. Opioid addiction.” RiverMend Health.

9 N Engl J Med. 2018 Apr 26;378:1567-9. doi: 10.1056/NEJMp1801417.

10 Innov Clin Neurosci. 2014 Sep;11(9-10):182-90.

11 Am J Psychiatry. 187 May;144(5):563-7.

The opioid epidemic continues to devastate the United States across demographic and socioeconomic groups; two-thirds of the 63,632 Americans who died of drug overdoses¹ in 2016 died of prescription or illicit opioids.

In 2015, Theodore J. Cicero, PhD, professor of psychiatry at Washington University, St. Louis, reported on a fundamental change in the nature of the ongoing opioid epidemic: What started as prescription opioid overprescribing, leading to diversion, abuse, and opioid addiction, was transitioning to illicit heroin distribution and consumption. Prescription opioids, namely, extended-release oxycodone (Oxycontin), were perceived initially as pure and safe, as they were specifically dosed and physician prescribed. In addition, filling a prescription for opioids was not associated with the shame or stigma of buying illicit drugs off the street. Because those drugs were seen as therapeutic and pharmacologically “legitimate,” many clinicians and the lay public alike were surprised to see the surge of opioid addiction and overdoses.

Dr. Cicero and others noted² that prescription opioids, whether taken originally for analgesic or recreational purposes, became a “gateway” to heroin, which already was making its way into the United States from Mexico,³ as heroin was cheap and becoming cheaper, easier to find, easy to use, and “pure.” Prescription opioids, on the other hand, were becoming more expensive, and physicians were facing increased regulations in prescribing them. Thus, as prescription opioid use became more and more stigmatized, heroin use was seen, paradoxically, as a more practical alternative. The amount of opioids prescribed in the United States has peaked; physicians are prescribing opioids less often; and the averaged dose has dropped as well, according to the Centers for Disease Control and Prevention.⁴ The first wave of deaths was attributable to prescription opioids, and the second was tied to illicitly obtained potent fentanyl analogs (manufactured in China and smuggled primarily through Mexico), which is added to heroin and sold in the United States.⁵

Many addiction experts and health policy leaders were not surprised by the increases in HIV, TB, and hepatitis B and C that followed the increasing use of intravenous opioids. However, few had experience with previous opioid epidemics in the United States, the most recent being the heroin epidemic occurring in the 1960s-1970s in the aftermath of the Vietnam War. At that time, the notion that heroin was contaminated with other psychoactive drugs, medications, fillers, and other adulterants was a foregone conclusion – though in public health and treatment discussions, this issue is hardly ever raised. We believe this to be a significant lapse in policy and planning. Surveillance by the Drug Enforcement Administration shows that acetyl fentanyl–laced heroin costs a little more on the street than regular heroin. Yet it sells, because users believe its extreme potency produces a better high, thus worth the extra cost. This phenomenon underscores an important point: Opioid addicts often are in search of a better high and will go to any lengths – even risking their lives – to get it.

The “cutting” or “adulteration” of street drugs is common practice in the manufacturing, distribution, and selling of illicit drugs, and the motive is to increase profit. The term “adulterant” generally refers to addition of substances with some psychoactive effects, such as caffeine, ephedra, or even paracetamol. These substances are cheaper than the main substance, have similar or complementary effects when added, and thus help conceal the fact that the desired substance has been cut or diluted. Substances without psychoactive properties such as lactose, other sugars, or talc, are added to a drug primarily to increase the bulk or weight of the illicit substance, or for aesthetic purposes to fool the user. Some adulterants simply are the result of the particular manufacturing process used to make the drug. For example, illicitly manufactured methamphetamine frequently is contaminated by nonstimulant impurities such as lead or mercury (extremely toxic heavy metals), or from carcinogenic solvents used in the synthesis. The local anesthetic lidocaine often is added to cocaine, and the reasons are intuitive: Both drugs are fast-acting local anesthetics.

More intriguing is the story of the antiparasitic medication levamisole. The DEA has estimated that 60%-89% of the seized street cocaine contains levamisole. Levamisole appears to be partly metabolized into an amphetamine-like compound, which could increase dopamine concentration in the reward pathway and thus activate endogenous opioids: It can mimic the effects of cocaine at a fraction of the cost. Levamisole is associated with several types of severe blood disorders, including leukopenia, agranulocytosis, multifocal inflammatory leukoencephalopathy, and neutropenia; a common presentation is vasculitis resulting in loss of limbs. Thus, a real danger in adulterants such as levamisole is their toxicity beyond those of the drug to which they are added, causing numerous medical consequences – including death.

Dr. Gold is the 17th Distinguished Alumni Professor at the University of Florida, Gainesville, and professor of psychiatry (adjunct) at Washington University in St. Louis. He also serves as chairman of the scientific advisory boards for RiverMend Health. Dr. Srivastava is a fourth-year resident in the department of psychiatry at Washington University.

References

1 NCHS Data Brief. No. 294. December 2017.

2 N Engl J Med. 2015;373:1789-90.

3 DEA Strategic Intelligence Section. 2017 National Drug Threat Assessment: Drug Enforcement Administration, U.S. Department of Justice, 2017.

4 Centers for Disease Control and Prevention, press release. Mar 29, 2018.

5 MMWR. 2018. Mar 30;67(12):349-58.

6 Am J Public Health. 2017 Mar;107(3):430-2.

7 “Q&A: Thomas Kosten, MD: Anti-drug vaccines.” RiverMend Health.

8 “Q&A: Stacy Seikel, MD. Opioid addiction.” RiverMend Health.

9 N Engl J Med. 2018 Apr 26;378:1567-9. doi: 10.1056/NEJMp1801417.

10 Innov Clin Neurosci. 2014 Sep;11(9-10):182-90.

11 Am J Psychiatry. 187 May;144(5):563-7.

The opioid epidemic continues to devastate the United States across demographic and socioeconomic groups; two-thirds of the 63,632 Americans who died of drug overdoses¹ in 2016 died of prescription or illicit opioids.

In 2015, Theodore J. Cicero, PhD, professor of psychiatry at Washington University, St. Louis, reported on a fundamental change in the nature of the ongoing opioid epidemic: What started as prescription opioid overprescribing, leading to diversion, abuse, and opioid addiction, was transitioning to illicit heroin distribution and consumption. Prescription opioids, namely, extended-release oxycodone (Oxycontin), were perceived initially as pure and safe, as they were specifically dosed and physician prescribed. In addition, filling a prescription for opioids was not associated with the shame or stigma of buying illicit drugs off the street. Because those drugs were seen as therapeutic and pharmacologically “legitimate,” many clinicians and the lay public alike were surprised to see the surge of opioid addiction and overdoses.

Dr. Cicero and others noted² that prescription opioids, whether taken originally for analgesic or recreational purposes, became a “gateway” to heroin, which already was making its way into the United States from Mexico,³ as heroin was cheap and becoming cheaper, easier to find, easy to use, and “pure.” Prescription opioids, on the other hand, were becoming more expensive, and physicians were facing increased regulations in prescribing them. Thus, as prescription opioid use became more and more stigmatized, heroin use was seen, paradoxically, as a more practical alternative. The amount of opioids prescribed in the United States has peaked; physicians are prescribing opioids less often; and the averaged dose has dropped as well, according to the Centers for Disease Control and Prevention.⁴ The first wave of deaths was attributable to prescription opioids, and the second was tied to illicitly obtained potent fentanyl analogs (manufactured in China and smuggled primarily through Mexico), which is added to heroin and sold in the United States.⁵

Many addiction experts and health policy leaders were not surprised by the increases in HIV, TB, and hepatitis B and C that followed the increasing use of intravenous opioids. However, few had experience with previous opioid epidemics in the United States, the most recent being the heroin epidemic occurring in the 1960s-1970s in the aftermath of the Vietnam War. At that time, the notion that heroin was contaminated with other psychoactive drugs, medications, fillers, and other adulterants was a foregone conclusion – though in public health and treatment discussions, this issue is hardly ever raised. We believe this to be a significant lapse in policy and planning. Surveillance by the Drug Enforcement Administration shows that acetyl fentanyl–laced heroin costs a little more on the street than regular heroin. Yet it sells, because users believe its extreme potency produces a better high, thus worth the extra cost. This phenomenon underscores an important point: Opioid addicts often are in search of a better high and will go to any lengths – even risking their lives – to get it.

The “cutting” or “adulteration” of street drugs is common practice in the manufacturing, distribution, and selling of illicit drugs, and the motive is to increase profit. The term “adulterant” generally refers to addition of substances with some psychoactive effects, such as caffeine, ephedra, or even paracetamol. These substances are cheaper than the main substance, have similar or complementary effects when added, and thus help conceal the fact that the desired substance has been cut or diluted. Substances without psychoactive properties such as lactose, other sugars, or talc, are added to a drug primarily to increase the bulk or weight of the illicit substance, or for aesthetic purposes to fool the user. Some adulterants simply are the result of the particular manufacturing process used to make the drug. For example, illicitly manufactured methamphetamine frequently is contaminated by nonstimulant impurities such as lead or mercury (extremely toxic heavy metals), or from carcinogenic solvents used in the synthesis. The local anesthetic lidocaine often is added to cocaine, and the reasons are intuitive: Both drugs are fast-acting local anesthetics.

More intriguing is the story of the antiparasitic medication levamisole. The DEA has estimated that 60%-89% of the seized street cocaine contains levamisole. Levamisole appears to be partly metabolized into an amphetamine-like compound, which could increase dopamine concentration in the reward pathway and thus activate endogenous opioids: It can mimic the effects of cocaine at a fraction of the cost. Levamisole is associated with several types of severe blood disorders, including leukopenia, agranulocytosis, multifocal inflammatory leukoencephalopathy, and neutropenia; a common presentation is vasculitis resulting in loss of limbs. Thus, a real danger in adulterants such as levamisole is their toxicity beyond those of the drug to which they are added, causing numerous medical consequences – including death.

Dr. Gold is the 17th Distinguished Alumni Professor at the University of Florida, Gainesville, and professor of psychiatry (adjunct) at Washington University in St. Louis. He also serves as chairman of the scientific advisory boards for RiverMend Health. Dr. Srivastava is a fourth-year resident in the department of psychiatry at Washington University.

References

1 NCHS Data Brief. No. 294. December 2017.

2 N Engl J Med. 2015;373:1789-90.

3 DEA Strategic Intelligence Section. 2017 National Drug Threat Assessment: Drug Enforcement Administration, U.S. Department of Justice, 2017.

4 Centers for Disease Control and Prevention, press release. Mar 29, 2018.

5 MMWR. 2018. Mar 30;67(12):349-58.

6 Am J Public Health. 2017 Mar;107(3):430-2.

7 “Q&A: Thomas Kosten, MD: Anti-drug vaccines.” RiverMend Health.

8 “Q&A: Stacy Seikel, MD. Opioid addiction.” RiverMend Health.

9 N Engl J Med. 2018 Apr 26;378:1567-9. doi: 10.1056/NEJMp1801417.

10 Innov Clin Neurosci. 2014 Sep;11(9-10):182-90.

11 Am J Psychiatry. 187 May;144(5):563-7.

The controversy over psychiatry’s “Goldwater Rule,” specifically as it applies to discussion of President Donald Trump, shows no signs¹ of abating any time soon. In an earlier commentary, we considered the problematic practice of citing a “duty to warn” about the president’s mental state to justify professional assessment from afar. We argued that the Tarasoff principle² presupposes a doctor-patient relationship in which the therapist must break confidentiality to avert imminent harm. Claiming a duty to protect against a politician’s public conduct and utterances is the proverbial square peg in a round hole.

While misapplication of the Tarasoff doctrine persists,³ some outspoken and eminent critics within the psychiatric community have since pursued another line of reasoning: that the Goldwater Rule covers only formal diagnoses and anything short of that is fair game. Here, we consider the argument that applying psychiatric labels to individuals for public consumption, absent examination and authorization, is ethically supportable so long as a definitive diagnosis is avoided. Ultimately, this justification fares no better than the misplaced duty to warn.
 

Explanation or expansion?

Nonetheless, several prominent psychiatrists charge⁵ that the APA has impermissibly broadened the Goldwater Rule since President Trump’s inauguration. These critics⁵ are referring not to any modification of Section 7.3 itself, but to an APA Ethics Committee opinion issued in March 2017 that clarified what constitutes a “professional opinion.”⁶ According to this guidance, a professional opinion includes but is not limited to a diagnosis: “... when a psychiatrist renders an opinion about the affect, behavior, speech, or other presentation of an individual that draws on the skills, training, expertise, and/or knowledge inherent in the practice of psychiatry, the opinion is a professional one.” In an accompanying statement,⁷ then-APA President Maria A. Oquendo, MD, PhD, confirmed that the Goldwater Rule “applies to all professional opinions offered by psychiatrists, not just diagnoses.”

Among psychiatrists and other mental health professionals questioning⁸ President Trump’s fitness for office, the reaction to the ethics interpretation was swift and emphatic. Leonard L. Glass, MD, MPH, resigned from the APA in protest after more than four decades of membership. He and Bandy X. Lee, MD, MDiv, editor of a book assessing the president’s purported instability, wrote in Politico: “By fiat of the APA, the Goldwater Rule has effectively turned into a gag rule.”⁹ Dr. Glass and Dr. Lee reiterated their critique in the Boston Globe,¹⁰ and hinted that the APA’s “federal funding” should be jeopardized as a result. Meanwhile, in a New England Journal of Medicine article, Claire L. Pouncey, MD, PhD, called the APA’s interpretation a silencing mechanism whereby “psychiatrists are the only members of the citizenry who may not express concern about the mental health of the president using psychiatric diagnostic terminology.”¹¹

In light of such heated rhetoric, it is worth taking a step back to consider what, if anything, has changed. A brief historical inquiry shows that the answer is not much. Allen R. Dyer, MD, PhD, a psychiatrist and ethicist who helped draft the Goldwater Rule – and whom one of us (LHK) counts as a professional mentor – recalls originally suggesting the term “professional opinion” instead of “psychiatric diagnosis” in order “to reflect the place of ethics in defining a profession.”¹² What Dr. Dyer meant is that standards of conduct, which are the hallmark of any profession, are not intended to be legal rules, but rather normative guidelines for ethical practice.

A distinction without a difference

Putting aside the historical record, what is the substantive dispute with the APA’s ethics interpretation? In essence, the dissenters contend that even if it remains unethical to offer armchair diagnoses, it should be perfectly acceptable to call someone unstable and dangerous, and to do so as a self-identified psychiatric expert. Dr. Glass and Dr. Lee profess to be “mystified by the lack of recognition” that they aren’t formally diagnosing President Trump.¹³ Instead, they view their actions as performing a public service by illuminating the president’s dangerous psyche.

Yet legalistic parsing cannot delineate ethical boundaries for a profession. Without even addressing the issue of predictive validity when it comes to dangerousness or violence risk, it is clear to many that labeling someone as “dangerous” can be just as, if not more, hurtful than offering an unsolicited diagnosis.¹⁴ Whereas opponents of the Goldwater Rule tend to frame it as organized psychiatry’s response to professional embarrassment,¹⁵ other ethical issues are at play, the foremost being¹⁶ respect for human beings. In other words, psychiatric speculation can cause “real harm to real people.”¹⁷

As Richard A. Friedman, MD, explained long before President Trump emerged as a serious contender on the political scene, the problem with the Goldwater fiasco was not just that psychiatrists offered diagnoses, but that they gave “very specific and damaging psychiatric opinions, using the language and art of their profession, about a man whom they had not examined and who surely would not have consented to such statements.”¹⁸ Indeed, Sen. Barry Goldwater later testified to the toll that psychiatrists’ published comments about his masculinity took on his personal interactions.¹⁹

It is instructive that the survey Fact magazine sent to psychiatrists in 1964 asked20 not for diagnoses, but whether Sen. Goldwater was “psychologically fit” to be president. This question – to which nearly 2,000 psychiatrists replied in the negative – is almost exactly what some members of the profession are asking and answering about President Trump today. There is room for nuanced²¹ debate about what types of pronouncements the Goldwater Rule should cover, but there is nothing nuanced about mounting the pedestal of medical authority to brand someone as unsafe, unfit, and unstable. Doing so is disparaging to the individual and stigmatizing of mental illness in general. Ethical standards cannot condone stopping just short of malfeasance and then claiming to have clean hands.

Education vs. stigmatization

The Goldwater Rule is designed as a caveat, not a prohibition. Section 7 of the APA code affirms that psychiatrists, like all physicians,²² have a responsibility to contribute to the common good. A principal way of doing this is through civic education about mental health and illness. 


The Goldwater Rule is embedded in Section 7 as one of several qualifications for psychiatrists to consider when making public forays. For example, psychiatrists should clarify whether they are speaking for themselves or an organization, avoid blanket statements on behalf of the entire profession, and differentiate between their roles as citizen and physician. Viewed in light of these other less-controversial proscriptions, it should become clear that the Goldwater Rule creates minimal barriers to public education.

Specifically, the Goldwater principle is concerned only with psychiatrists’ statements that are professional, public, and individualized. It has nothing to say about opinions that are political, private, or general.¹⁴ As an APA commentary explains, “a general discussion of relevant psychiatric topics – rather than offering opinions about that specific person – is the best means of facilitating public education.”²³ This is not a gag order but a prescription for maintaining professional integrity when exposed to the media limelight.

There are valid reasons to critique the Goldwater Rule, but they require an honest reckoning. Psychiatrists who feel compelled to assess public figures could argue that it is a matter of etiquette, not ethics, and should be left to personal discretion.²⁴

So far, the morphing rationales for contravening the Goldwater Rule fall short, because they elide the real issues at stake. Ethical behavior cannot hinge on artificial distinctions. Whereas invoking a duty to warn about presidential fitness was dubious, differentiating between a diagnosis and a professional opinion is specious.

Lt. Col. Kels practices health and disability law in the U.S. Air Force. Dr. Kels teaches and practices psychiatry at the University of the Incarnate Word School of Osteopathic Medicine in San Antonio. Opinions expressed in this article are those of the authors alone and do not necessarily reflect those of the Air Force or Department of Defense.

References

1. Psychiatric Times. Mar 19, 2018.

2. Tarasoff v. Regents of University of California, 551 P2d 334 (Cal 1976).

3.The Boston Globe. Jan 2, 2018.

4. APA Principles of Medical Ethics, 2013 ed. [7.3].

5. Psychiatric Times. Jul 20, 2017.

6. APA Opinions of the Ethics Committee. 2017 ed. [Q.7b].

7. American Psychiatric Association (APA). “APA remains committed to supporting Goldwater Rule,” Mar 17, 2017.

8. The New York Times. Feb 13, 2017.

9. Politico. Jan 10, 2018.

10. The Boston Globe. Feb 26, 2018.

11. N Engl J Med. 2018;378[5]:405-7.

12. Allen R. Dyer, MD, PhD. “Evolution of the so-called ‘Goldwater rule’: An ethical analysis,” revised Sep 23, 2017.

13. The Boston Globe. Jan 10, 2018.

14. Psychiatric Times. Feb 16, 2018.

15. J Am Acad Psychiatry Law. 2016;44[2]:226-35.

16. Psychiatric Times. Jul 20, 2017.

17. J Am Acad Psychiatry Law. 2016;45[2]:228-32.

18. The New York Times. May 24, 2011.

19. Am J Psychiatry. 2015 Aug 1;172[8]:729-30.

20. Fact. Sep-Oct 1964.

21. Psychiatric Times. Oct 7, 2016.

22. AMA Principles of Medical Ethics. 2016 ed. [VII].

23. APA Commentary on Ethics in Practice, 2015 ed. [3.4.7].

24. J Am Acad Psychiatry Law. 2016;44[2]:226-35.

The controversy over psychiatry’s “Goldwater Rule,” specifically as it applies to discussion of President Donald Trump, shows no signs¹ of abating any time soon. In an earlier commentary, we considered the problematic practice of citing a “duty to warn” about the president’s mental state to justify professional assessment from afar. We argued that the Tarasoff principle² presupposes a doctor-patient relationship in which the therapist must break confidentiality to avert imminent harm. Claiming a duty to protect against a politician’s public conduct and utterances is the proverbial square peg in a round hole.

While misapplication of the Tarasoff doctrine persists,³ some outspoken and eminent critics within the psychiatric community have since pursued another line of reasoning: that the Goldwater Rule covers only formal diagnoses and anything short of that is fair game. Here, we consider the argument that applying psychiatric labels to individuals for public consumption, absent examination and authorization, is ethically supportable so long as a definitive diagnosis is avoided. Ultimately, this justification fares no better than the misplaced duty to warn.
 

Explanation or expansion?

Nonetheless, several prominent psychiatrists charge⁵ that the APA has impermissibly broadened the Goldwater Rule since President Trump’s inauguration. These critics⁵ are referring not to any modification of Section 7.3 itself, but to an APA Ethics Committee opinion issued in March 2017 that clarified what constitutes a “professional opinion.”⁶ According to this guidance, a professional opinion includes but is not limited to a diagnosis: “... when a psychiatrist renders an opinion about the affect, behavior, speech, or other presentation of an individual that draws on the skills, training, expertise, and/or knowledge inherent in the practice of psychiatry, the opinion is a professional one.” In an accompanying statement,⁷ then-APA President Maria A. Oquendo, MD, PhD, confirmed that the Goldwater Rule “applies to all professional opinions offered by psychiatrists, not just diagnoses.”

Among psychiatrists and other mental health professionals questioning⁸ President Trump’s fitness for office, the reaction to the ethics interpretation was swift and emphatic. Leonard L. Glass, MD, MPH, resigned from the APA in protest after more than four decades of membership. He and Bandy X. Lee, MD, MDiv, editor of a book assessing the president’s purported instability, wrote in Politico: “By fiat of the APA, the Goldwater Rule has effectively turned into a gag rule.”⁹ Dr. Glass and Dr. Lee reiterated their critique in the Boston Globe,¹⁰ and hinted that the APA’s “federal funding” should be jeopardized as a result. Meanwhile, in a New England Journal of Medicine article, Claire L. Pouncey, MD, PhD, called the APA’s interpretation a silencing mechanism whereby “psychiatrists are the only members of the citizenry who may not express concern about the mental health of the president using psychiatric diagnostic terminology.”¹¹

In light of such heated rhetoric, it is worth taking a step back to consider what, if anything, has changed. A brief historical inquiry shows that the answer is not much. Allen R. Dyer, MD, PhD, a psychiatrist and ethicist who helped draft the Goldwater Rule – and whom one of us (LHK) counts as a professional mentor – recalls originally suggesting the term “professional opinion” instead of “psychiatric diagnosis” in order “to reflect the place of ethics in defining a profession.”¹² What Dr. Dyer meant is that standards of conduct, which are the hallmark of any profession, are not intended to be legal rules, but rather normative guidelines for ethical practice.

A distinction without a difference

Putting aside the historical record, what is the substantive dispute with the APA’s ethics interpretation? In essence, the dissenters contend that even if it remains unethical to offer armchair diagnoses, it should be perfectly acceptable to call someone unstable and dangerous, and to do so as a self-identified psychiatric expert. Dr. Glass and Dr. Lee profess to be “mystified by the lack of recognition” that they aren’t formally diagnosing President Trump.¹³ Instead, they view their actions as performing a public service by illuminating the president’s dangerous psyche.

Yet legalistic parsing cannot delineate ethical boundaries for a profession. Without even addressing the issue of predictive validity when it comes to dangerousness or violence risk, it is clear to many that labeling someone as “dangerous” can be just as, if not more, hurtful than offering an unsolicited diagnosis.¹⁴ Whereas opponents of the Goldwater Rule tend to frame it as organized psychiatry’s response to professional embarrassment,¹⁵ other ethical issues are at play, the foremost being¹⁶ respect for human beings. In other words, psychiatric speculation can cause “real harm to real people.”¹⁷

As Richard A. Friedman, MD, explained long before President Trump emerged as a serious contender on the political scene, the problem with the Goldwater fiasco was not just that psychiatrists offered diagnoses, but that they gave “very specific and damaging psychiatric opinions, using the language and art of their profession, about a man whom they had not examined and who surely would not have consented to such statements.”¹⁸ Indeed, Sen. Barry Goldwater later testified to the toll that psychiatrists’ published comments about his masculinity took on his personal interactions.¹⁹

It is instructive that the survey Fact magazine sent to psychiatrists in 1964 asked20 not for diagnoses, but whether Sen. Goldwater was “psychologically fit” to be president. This question – to which nearly 2,000 psychiatrists replied in the negative – is almost exactly what some members of the profession are asking and answering about President Trump today. There is room for nuanced²¹ debate about what types of pronouncements the Goldwater Rule should cover, but there is nothing nuanced about mounting the pedestal of medical authority to brand someone as unsafe, unfit, and unstable. Doing so is disparaging to the individual and stigmatizing of mental illness in general. Ethical standards cannot condone stopping just short of malfeasance and then claiming to have clean hands.

Education vs. stigmatization

The Goldwater Rule is designed as a caveat, not a prohibition. Section 7 of the APA code affirms that psychiatrists, like all physicians,²² have a responsibility to contribute to the common good. A principal way of doing this is through civic education about mental health and illness. 


The Goldwater Rule is embedded in Section 7 as one of several qualifications for psychiatrists to consider when making public forays. For example, psychiatrists should clarify whether they are speaking for themselves or an organization, avoid blanket statements on behalf of the entire profession, and differentiate between their roles as citizen and physician. Viewed in light of these other less-controversial proscriptions, it should become clear that the Goldwater Rule creates minimal barriers to public education.

Specifically, the Goldwater principle is concerned only with psychiatrists’ statements that are professional, public, and individualized. It has nothing to say about opinions that are political, private, or general.¹⁴ As an APA commentary explains, “a general discussion of relevant psychiatric topics – rather than offering opinions about that specific person – is the best means of facilitating public education.”²³ This is not a gag order but a prescription for maintaining professional integrity when exposed to the media limelight.

There are valid reasons to critique the Goldwater Rule, but they require an honest reckoning. Psychiatrists who feel compelled to assess public figures could argue that it is a matter of etiquette, not ethics, and should be left to personal discretion.²⁴

So far, the morphing rationales for contravening the Goldwater Rule fall short, because they elide the real issues at stake. Ethical behavior cannot hinge on artificial distinctions. Whereas invoking a duty to warn about presidential fitness was dubious, differentiating between a diagnosis and a professional opinion is specious.

Lt. Col. Kels practices health and disability law in the U.S. Air Force. Dr. Kels teaches and practices psychiatry at the University of the Incarnate Word School of Osteopathic Medicine in San Antonio. Opinions expressed in this article are those of the authors alone and do not necessarily reflect those of the Air Force or Department of Defense.

References

1. Psychiatric Times. Mar 19, 2018.

2. Tarasoff v. Regents of University of California, 551 P2d 334 (Cal 1976).

3.The Boston Globe. Jan 2, 2018.

4. APA Principles of Medical Ethics, 2013 ed. [7.3].

5. Psychiatric Times. Jul 20, 2017.

6. APA Opinions of the Ethics Committee. 2017 ed. [Q.7b].

7. American Psychiatric Association (APA). “APA remains committed to supporting Goldwater Rule,” Mar 17, 2017.

8. The New York Times. Feb 13, 2017.

9. Politico. Jan 10, 2018.

10. The Boston Globe. Feb 26, 2018.

11. N Engl J Med. 2018;378[5]:405-7.

12. Allen R. Dyer, MD, PhD. “Evolution of the so-called ‘Goldwater rule’: An ethical analysis,” revised Sep 23, 2017.

13. The Boston Globe. Jan 10, 2018.

14. Psychiatric Times. Feb 16, 2018.

15. J Am Acad Psychiatry Law. 2016;44[2]:226-35.

16. Psychiatric Times. Jul 20, 2017.

17. J Am Acad Psychiatry Law. 2016;45[2]:228-32.

18. The New York Times. May 24, 2011.

19. Am J Psychiatry. 2015 Aug 1;172[8]:729-30.

20. Fact. Sep-Oct 1964.

21. Psychiatric Times. Oct 7, 2016.

22. AMA Principles of Medical Ethics. 2016 ed. [VII].

23. APA Commentary on Ethics in Practice, 2015 ed. [3.4.7].

24. J Am Acad Psychiatry Law. 2016;44[2]:226-35.

The controversy over psychiatry’s “Goldwater Rule,” specifically as it applies to discussion of President Donald Trump, shows no signs¹ of abating any time soon. In an earlier commentary, we considered the problematic practice of citing a “duty to warn” about the president’s mental state to justify professional assessment from afar. We argued that the Tarasoff principle² presupposes a doctor-patient relationship in which the therapist must break confidentiality to avert imminent harm. Claiming a duty to protect against a politician’s public conduct and utterances is the proverbial square peg in a round hole.

While misapplication of the Tarasoff doctrine persists,³ some outspoken and eminent critics within the psychiatric community have since pursued another line of reasoning: that the Goldwater Rule covers only formal diagnoses and anything short of that is fair game. Here, we consider the argument that applying psychiatric labels to individuals for public consumption, absent examination and authorization, is ethically supportable so long as a definitive diagnosis is avoided. Ultimately, this justification fares no better than the misplaced duty to warn.
 

Explanation or expansion?

Nonetheless, several prominent psychiatrists charge⁵ that the APA has impermissibly broadened the Goldwater Rule since President Trump’s inauguration. These critics⁵ are referring not to any modification of Section 7.3 itself, but to an APA Ethics Committee opinion issued in March 2017 that clarified what constitutes a “professional opinion.”⁶ According to this guidance, a professional opinion includes but is not limited to a diagnosis: “... when a psychiatrist renders an opinion about the affect, behavior, speech, or other presentation of an individual that draws on the skills, training, expertise, and/or knowledge inherent in the practice of psychiatry, the opinion is a professional one.” In an accompanying statement,⁷ then-APA President Maria A. Oquendo, MD, PhD, confirmed that the Goldwater Rule “applies to all professional opinions offered by psychiatrists, not just diagnoses.”

Among psychiatrists and other mental health professionals questioning⁸ President Trump’s fitness for office, the reaction to the ethics interpretation was swift and emphatic. Leonard L. Glass, MD, MPH, resigned from the APA in protest after more than four decades of membership. He and Bandy X. Lee, MD, MDiv, editor of a book assessing the president’s purported instability, wrote in Politico: “By fiat of the APA, the Goldwater Rule has effectively turned into a gag rule.”⁹ Dr. Glass and Dr. Lee reiterated their critique in the Boston Globe,¹⁰ and hinted that the APA’s “federal funding” should be jeopardized as a result. Meanwhile, in a New England Journal of Medicine article, Claire L. Pouncey, MD, PhD, called the APA’s interpretation a silencing mechanism whereby “psychiatrists are the only members of the citizenry who may not express concern about the mental health of the president using psychiatric diagnostic terminology.”¹¹

In light of such heated rhetoric, it is worth taking a step back to consider what, if anything, has changed. A brief historical inquiry shows that the answer is not much. Allen R. Dyer, MD, PhD, a psychiatrist and ethicist who helped draft the Goldwater Rule – and whom one of us (LHK) counts as a professional mentor – recalls originally suggesting the term “professional opinion” instead of “psychiatric diagnosis” in order “to reflect the place of ethics in defining a profession.”¹² What Dr. Dyer meant is that standards of conduct, which are the hallmark of any profession, are not intended to be legal rules, but rather normative guidelines for ethical practice.

A distinction without a difference

Putting aside the historical record, what is the substantive dispute with the APA’s ethics interpretation? In essence, the dissenters contend that even if it remains unethical to offer armchair diagnoses, it should be perfectly acceptable to call someone unstable and dangerous, and to do so as a self-identified psychiatric expert. Dr. Glass and Dr. Lee profess to be “mystified by the lack of recognition” that they aren’t formally diagnosing President Trump.¹³ Instead, they view their actions as performing a public service by illuminating the president’s dangerous psyche.

Yet legalistic parsing cannot delineate ethical boundaries for a profession. Without even addressing the issue of predictive validity when it comes to dangerousness or violence risk, it is clear to many that labeling someone as “dangerous” can be just as, if not more, hurtful than offering an unsolicited diagnosis.¹⁴ Whereas opponents of the Goldwater Rule tend to frame it as organized psychiatry’s response to professional embarrassment,¹⁵ other ethical issues are at play, the foremost being¹⁶ respect for human beings. In other words, psychiatric speculation can cause “real harm to real people.”¹⁷

As Richard A. Friedman, MD, explained long before President Trump emerged as a serious contender on the political scene, the problem with the Goldwater fiasco was not just that psychiatrists offered diagnoses, but that they gave “very specific and damaging psychiatric opinions, using the language and art of their profession, about a man whom they had not examined and who surely would not have consented to such statements.”¹⁸ Indeed, Sen. Barry Goldwater later testified to the toll that psychiatrists’ published comments about his masculinity took on his personal interactions.¹⁹

It is instructive that the survey Fact magazine sent to psychiatrists in 1964 asked20 not for diagnoses, but whether Sen. Goldwater was “psychologically fit” to be president. This question – to which nearly 2,000 psychiatrists replied in the negative – is almost exactly what some members of the profession are asking and answering about President Trump today. There is room for nuanced²¹ debate about what types of pronouncements the Goldwater Rule should cover, but there is nothing nuanced about mounting the pedestal of medical authority to brand someone as unsafe, unfit, and unstable. Doing so is disparaging to the individual and stigmatizing of mental illness in general. Ethical standards cannot condone stopping just short of malfeasance and then claiming to have clean hands.

Education vs. stigmatization

The Goldwater Rule is designed as a caveat, not a prohibition. Section 7 of the APA code affirms that psychiatrists, like all physicians,²² have a responsibility to contribute to the common good. A principal way of doing this is through civic education about mental health and illness. 


The Goldwater Rule is embedded in Section 7 as one of several qualifications for psychiatrists to consider when making public forays. For example, psychiatrists should clarify whether they are speaking for themselves or an organization, avoid blanket statements on behalf of the entire profession, and differentiate between their roles as citizen and physician. Viewed in light of these other less-controversial proscriptions, it should become clear that the Goldwater Rule creates minimal barriers to public education.

Specifically, the Goldwater principle is concerned only with psychiatrists’ statements that are professional, public, and individualized. It has nothing to say about opinions that are political, private, or general.¹⁴ As an APA commentary explains, “a general discussion of relevant psychiatric topics – rather than offering opinions about that specific person – is the best means of facilitating public education.”²³ This is not a gag order but a prescription for maintaining professional integrity when exposed to the media limelight.

There are valid reasons to critique the Goldwater Rule, but they require an honest reckoning. Psychiatrists who feel compelled to assess public figures could argue that it is a matter of etiquette, not ethics, and should be left to personal discretion.²⁴

So far, the morphing rationales for contravening the Goldwater Rule fall short, because they elide the real issues at stake. Ethical behavior cannot hinge on artificial distinctions. Whereas invoking a duty to warn about presidential fitness was dubious, differentiating between a diagnosis and a professional opinion is specious.

Lt. Col. Kels practices health and disability law in the U.S. Air Force. Dr. Kels teaches and practices psychiatry at the University of the Incarnate Word School of Osteopathic Medicine in San Antonio. Opinions expressed in this article are those of the authors alone and do not necessarily reflect those of the Air Force or Department of Defense.

References

1. Psychiatric Times. Mar 19, 2018.

2. Tarasoff v. Regents of University of California, 551 P2d 334 (Cal 1976).

3.The Boston Globe. Jan 2, 2018.

4. APA Principles of Medical Ethics, 2013 ed. [7.3].

5. Psychiatric Times. Jul 20, 2017.

6. APA Opinions of the Ethics Committee. 2017 ed. [Q.7b].

7. American Psychiatric Association (APA). “APA remains committed to supporting Goldwater Rule,” Mar 17, 2017.

8. The New York Times. Feb 13, 2017.

9. Politico. Jan 10, 2018.

10. The Boston Globe. Feb 26, 2018.

11. N Engl J Med. 2018;378[5]:405-7.

12. Allen R. Dyer, MD, PhD. “Evolution of the so-called ‘Goldwater rule’: An ethical analysis,” revised Sep 23, 2017.

13. The Boston Globe. Jan 10, 2018.

14. Psychiatric Times. Feb 16, 2018.

15. J Am Acad Psychiatry Law. 2016;44[2]:226-35.

16. Psychiatric Times. Jul 20, 2017.

17. J Am Acad Psychiatry Law. 2016;45[2]:228-32.

18. The New York Times. May 24, 2011.

19. Am J Psychiatry. 2015 Aug 1;172[8]:729-30.

20. Fact. Sep-Oct 1964.

21. Psychiatric Times. Oct 7, 2016.

22. AMA Principles of Medical Ethics. 2016 ed. [VII].

23. APA Commentary on Ethics in Practice, 2015 ed. [3.4.7].

24. J Am Acad Psychiatry Law. 2016;44[2]:226-35.

Presenter

Andrew J. Hale, MD
University of Vermont Medical Center, Burlington

Session summary

With rising temperatures from climate change, tick territory – and therefore tick-borne illnesses – are being seen with increasing frequency.

Lyme disease manifests as early-localized, early-disseminated, and late disease. The diagnosis of Lyme can be challenging and the pretest probability is key (geographic distribution, time of year, consistent symptoms). Do not send serologies unless the pretest probability is high, since the sensitivity of the test is generally low.

Concerning early-localized disease, 20% of patients will not develop the classic “bullseye” erythema migrans rash. Only 25% of patients recall even getting a tick bite. Not everyone with a rash will have a classic appearance (prepare for heterogeneity).

Neurologic symptoms can appear early or late in Lyme disease (usually weeks to months, but sometimes in days). The manifestations can include lymphocytic meningitis (which can be hard to separate from viral meningitis), radiculopathies, and cranial nerve palsies.

Lyme carditis happens early in the disseminated phase with a variety of disease (palpitations, conduction abnormalities, pericarditis, myocarditis, left ventricular failure). For those who develop a high-grade atrioventricular block, a temporary pacer may be needed; a permanent pacemaker is unnecessary because patients often do well with a course of antibiotics.

Late Lyme develops months to years after infection. It often presents as arthritis of the knee, although other large joints such as the shoulders, ankles, and elbows can also be affected. Chronic neurologic effects such as peripheral neuropathy and encephalitis can also occur.

Treatment depends on how the disease manifests. If one has arthritis or mild carditis, 28 days of doxycycline is appropriate; for neurologic disease or “bad” carditis, give ceftriaxone for 28 days; for everything else, 14-21 days of doxycycline. Amoxicillin can be used for patients who cannot tolerate doxycycline.

Borrelia miyamotoi and B. mayonii are emerging infections. Compared with Lyme, B. miyamotoi will present with more joint pain and less rash. B. mayonii has a more diffuse rash, but is otherwise similar to Lyme. Serologies for Lyme for both will be negative, but they are treated the same as Lyme disease.

Anaplasma presents as a flu-like illness and can be difficult to distinguish from Lyme. Ehrlichia is similar, but has more headache and CNS findings. Diagnosis during the first week is best with a blood smear (looking for morulae) and polymerase chain reaction; in week 2, serology is a bit better; after 3 weeks, serologies are very sensitive. Treatment for both is doxycycline for 7-14 days. Rifampin is second-line treatment, but does not treat Lyme (both can happen simultaneously).

Babesia is found in the same distribution as Lyme disease. Incubation is 1-12 weeks. Mild disease consists of parasitemia of less than 4% while severe disease is greater than 4%. Being asplenic, having HIV, receiving tumor necrosis factor alpha blockers or rituximab increases risk for severe disease. A blood smear is sufficient to diagnose Babesia, but polymerase chain reaction is also available. Treatment is atovaquone and azithromycin for 7 days for mild disease; clindamycin and quinine for 7-10 days for severe. Exchange transfusion can also be done especially for those with high parasitemia or severe symptoms.

Powassan virus is seen in the northeastern United States and the Minnesota/Wisconsin region. It has a fatality rate of 10%. About 50% of patients have long-term neurologic sequelae. Heartland virus has symptoms similar to other tick-borne illnesses, but can be associated with nausea, headache, diarrhea, myalgias, arthralgias, and renal failure. Bourbon virus also behaves like most tick-borne illnesses, but patients can develop a rapid sepsis picture.

Key takeaways for HM

• Lyme disease can be seen in inpatient settings with cardiac, neurologic, and musculoskeletal manifestations.
• Several emerging tick-borne infections (tularemia, STARI [southern tick-associated rash illness]), relapsing fever (B. hermsii), B. miyamotoi, and B. mayonii should also be on clinicians’ radar.
• Ticks can also spread viruses that can have particularly deadly consequences such as Powassan, Heartland, and Bourbon.
• Climate change is good for ticks, but bad for humans.

Dr. Kim is assistant professor of medicine in the division of hospital medicine at Emory University, Atlanta.

Presenter

Andrew J. Hale, MD
University of Vermont Medical Center, Burlington

Session summary

With rising temperatures from climate change, tick territory – and therefore tick-borne illnesses – are being seen with increasing frequency.

Lyme disease manifests as early-localized, early-disseminated, and late disease. The diagnosis of Lyme can be challenging and the pretest probability is key (geographic distribution, time of year, consistent symptoms). Do not send serologies unless the pretest probability is high, since the sensitivity of the test is generally low.

Concerning early-localized disease, 20% of patients will not develop the classic “bullseye” erythema migrans rash. Only 25% of patients recall even getting a tick bite. Not everyone with a rash will have a classic appearance (prepare for heterogeneity).

Neurologic symptoms can appear early or late in Lyme disease (usually weeks to months, but sometimes in days). The manifestations can include lymphocytic meningitis (which can be hard to separate from viral meningitis), radiculopathies, and cranial nerve palsies.

Lyme carditis happens early in the disseminated phase with a variety of disease (palpitations, conduction abnormalities, pericarditis, myocarditis, left ventricular failure). For those who develop a high-grade atrioventricular block, a temporary pacer may be needed; a permanent pacemaker is unnecessary because patients often do well with a course of antibiotics.

Late Lyme develops months to years after infection. It often presents as arthritis of the knee, although other large joints such as the shoulders, ankles, and elbows can also be affected. Chronic neurologic effects such as peripheral neuropathy and encephalitis can also occur.

Treatment depends on how the disease manifests. If one has arthritis or mild carditis, 28 days of doxycycline is appropriate; for neurologic disease or “bad” carditis, give ceftriaxone for 28 days; for everything else, 14-21 days of doxycycline. Amoxicillin can be used for patients who cannot tolerate doxycycline.

Borrelia miyamotoi and B. mayonii are emerging infections. Compared with Lyme, B. miyamotoi will present with more joint pain and less rash. B. mayonii has a more diffuse rash, but is otherwise similar to Lyme. Serologies for Lyme for both will be negative, but they are treated the same as Lyme disease.

Anaplasma presents as a flu-like illness and can be difficult to distinguish from Lyme. Ehrlichia is similar, but has more headache and CNS findings. Diagnosis during the first week is best with a blood smear (looking for morulae) and polymerase chain reaction; in week 2, serology is a bit better; after 3 weeks, serologies are very sensitive. Treatment for both is doxycycline for 7-14 days. Rifampin is second-line treatment, but does not treat Lyme (both can happen simultaneously).

Babesia is found in the same distribution as Lyme disease. Incubation is 1-12 weeks. Mild disease consists of parasitemia of less than 4% while severe disease is greater than 4%. Being asplenic, having HIV, receiving tumor necrosis factor alpha blockers or rituximab increases risk for severe disease. A blood smear is sufficient to diagnose Babesia, but polymerase chain reaction is also available. Treatment is atovaquone and azithromycin for 7 days for mild disease; clindamycin and quinine for 7-10 days for severe. Exchange transfusion can also be done especially for those with high parasitemia or severe symptoms.

Powassan virus is seen in the northeastern United States and the Minnesota/Wisconsin region. It has a fatality rate of 10%. About 50% of patients have long-term neurologic sequelae. Heartland virus has symptoms similar to other tick-borne illnesses, but can be associated with nausea, headache, diarrhea, myalgias, arthralgias, and renal failure. Bourbon virus also behaves like most tick-borne illnesses, but patients can develop a rapid sepsis picture.

Key takeaways for HM

• Lyme disease can be seen in inpatient settings with cardiac, neurologic, and musculoskeletal manifestations.
• Several emerging tick-borne infections (tularemia, STARI [southern tick-associated rash illness]), relapsing fever (B. hermsii), B. miyamotoi, and B. mayonii should also be on clinicians’ radar.
• Ticks can also spread viruses that can have particularly deadly consequences such as Powassan, Heartland, and Bourbon.
• Climate change is good for ticks, but bad for humans.

Dr. Kim is assistant professor of medicine in the division of hospital medicine at Emory University, Atlanta.

Presenter

Andrew J. Hale, MD
University of Vermont Medical Center, Burlington

Session summary

With rising temperatures from climate change, tick territory – and therefore tick-borne illnesses – are being seen with increasing frequency.

Lyme disease manifests as early-localized, early-disseminated, and late disease. The diagnosis of Lyme can be challenging and the pretest probability is key (geographic distribution, time of year, consistent symptoms). Do not send serologies unless the pretest probability is high, since the sensitivity of the test is generally low.

Concerning early-localized disease, 20% of patients will not develop the classic “bullseye” erythema migrans rash. Only 25% of patients recall even getting a tick bite. Not everyone with a rash will have a classic appearance (prepare for heterogeneity).

Neurologic symptoms can appear early or late in Lyme disease (usually weeks to months, but sometimes in days). The manifestations can include lymphocytic meningitis (which can be hard to separate from viral meningitis), radiculopathies, and cranial nerve palsies.

Lyme carditis happens early in the disseminated phase with a variety of disease (palpitations, conduction abnormalities, pericarditis, myocarditis, left ventricular failure). For those who develop a high-grade atrioventricular block, a temporary pacer may be needed; a permanent pacemaker is unnecessary because patients often do well with a course of antibiotics.

Late Lyme develops months to years after infection. It often presents as arthritis of the knee, although other large joints such as the shoulders, ankles, and elbows can also be affected. Chronic neurologic effects such as peripheral neuropathy and encephalitis can also occur.

Treatment depends on how the disease manifests. If one has arthritis or mild carditis, 28 days of doxycycline is appropriate; for neurologic disease or “bad” carditis, give ceftriaxone for 28 days; for everything else, 14-21 days of doxycycline. Amoxicillin can be used for patients who cannot tolerate doxycycline.

Borrelia miyamotoi and B. mayonii are emerging infections. Compared with Lyme, B. miyamotoi will present with more joint pain and less rash. B. mayonii has a more diffuse rash, but is otherwise similar to Lyme. Serologies for Lyme for both will be negative, but they are treated the same as Lyme disease.

Anaplasma presents as a flu-like illness and can be difficult to distinguish from Lyme. Ehrlichia is similar, but has more headache and CNS findings. Diagnosis during the first week is best with a blood smear (looking for morulae) and polymerase chain reaction; in week 2, serology is a bit better; after 3 weeks, serologies are very sensitive. Treatment for both is doxycycline for 7-14 days. Rifampin is second-line treatment, but does not treat Lyme (both can happen simultaneously).

Babesia is found in the same distribution as Lyme disease. Incubation is 1-12 weeks. Mild disease consists of parasitemia of less than 4% while severe disease is greater than 4%. Being asplenic, having HIV, receiving tumor necrosis factor alpha blockers or rituximab increases risk for severe disease. A blood smear is sufficient to diagnose Babesia, but polymerase chain reaction is also available. Treatment is atovaquone and azithromycin for 7 days for mild disease; clindamycin and quinine for 7-10 days for severe. Exchange transfusion can also be done especially for those with high parasitemia or severe symptoms.

Powassan virus is seen in the northeastern United States and the Minnesota/Wisconsin region. It has a fatality rate of 10%. About 50% of patients have long-term neurologic sequelae. Heartland virus has symptoms similar to other tick-borne illnesses, but can be associated with nausea, headache, diarrhea, myalgias, arthralgias, and renal failure. Bourbon virus also behaves like most tick-borne illnesses, but patients can develop a rapid sepsis picture.

Key takeaways for HM

• Lyme disease can be seen in inpatient settings with cardiac, neurologic, and musculoskeletal manifestations.
• Several emerging tick-borne infections (tularemia, STARI [southern tick-associated rash illness]), relapsing fever (B. hermsii), B. miyamotoi, and B. mayonii should also be on clinicians’ radar.
• Ticks can also spread viruses that can have particularly deadly consequences such as Powassan, Heartland, and Bourbon.
• Climate change is good for ticks, but bad for humans.

Dr. Kim is assistant professor of medicine in the division of hospital medicine at Emory University, Atlanta.

Significant depressive symptoms affect approximately one in four adults with type 1 and type 2 diabetes while a formal diagnosis of depressive disorders is made in approximately 10%-15% of individuals with diabetes.¹ The combination of diabetes and depression presents a major clinical challenge because the outcomes of each condition is worsened by the presence of the other, which results in worsened quality of life, impaired diabetes self-management, and poor clinical outcomes.¹ While the costs of treatment are high for both individual patients and health economies, these costs do not necessarily result in significant improvements in disease or quality of life outcomes.¹ This raises the question, “What is the best approach to managing patients with comorbid depression and diabetes?”

• Three part-time registered nurses who had diabetes education training (certified diabetes educators), as well as training on depression management, behavioral strategies, and glycemic, hypertension, and lipid control.
• Combined support for self-care with pharmacotherapy to control depression, hyperglycemia, hypertension, and hyperlipidemia with algorithm guidance.
• Motivational and encouraging coaching for problem-solving and adherence to self-care.
• Weekly nurse supervision with a psychiatrist, primary care physician, and psychologist, with a nurse communicating recommendations back to the primary care team.

An endocrinologist/diabetologist was also incorporated for consultation when needed. After 12 months, patients in the intervention group had greater reduction in hemoglobin A_1c (0.58%), LDL cholesterol (6.9 mg/dL), systolic blood pressure (5.1 mm Hg), and depression scores than did those in the usual care group. Patients in the intervention group were also more likely to have adjustments made to insulin, antihypertensive medications, and antidepressants.

The success of this intervention, known as TEAMCare, highlights the critical need to incorporate mental health care into primary care and endocrinology practice. Currently, psychiatric and psychological care are largely administered separately from medical care for diabetes, despite evidence showing the success of an integrated care delivery model. In order to address the important interaction between mental health disorders, such as depression, and diabetes, it is critical that evaluation and treatment of mental health be integrated into medical practice.

What can we – endocrinologists and psychiatrists – do to facilitate adoption of such models? First, we can lobby our health systems to support reorganization of our health care delivery approach for patients with comorbid depression and diabetes so that endocrinologists, psychiatrists, and behavioral specialists are incorporated into primary care practices. This will facilitate better alignment of specialists and primary care providers and also enable patients to receive care in a clinical environment where they are most comfortable and have established relationships. Instead of the primary care physician referring the patient separately to psychiatry and endocrinology and awaiting feedback, which can sometimes take several weeks, the psychiatrist and endocrinologist would meet weekly with the primary care physician and nurse case manager team to review the entire patient panel, make timely adjustments in diabetes and antidepressant medications, and recommend behavioral therapy. This population health strategy would enable our two specialties to make a greater impact on a larger number of patients than we can in a half-day clinic session.

Second, our other critical role is to collaborate with payers to develop a sustainable financial reimbursement model to support the psychiatrist and endocrinologist in this novel health care delivery approach, which departs from the traditional fee-for-service model.

Dr. Golden is the Hugh P. McCormick Family Professor of Endocrinology and Metabolism and executive vice-chair of the department of medicine at Johns Hopkins University, Baltimore.

References

1. Holt RIG et al. Current Diabetes Reports. 2014;14(6):491.

2. Shojania KG et al. JAMA. 2006;296(4):427-40.

3. Katon WJ et al. N Eng J Med. 2010;363(27):2611-20.

Significant depressive symptoms affect approximately one in four adults with type 1 and type 2 diabetes while a formal diagnosis of depressive disorders is made in approximately 10%-15% of individuals with diabetes.¹ The combination of diabetes and depression presents a major clinical challenge because the outcomes of each condition is worsened by the presence of the other, which results in worsened quality of life, impaired diabetes self-management, and poor clinical outcomes.¹ While the costs of treatment are high for both individual patients and health economies, these costs do not necessarily result in significant improvements in disease or quality of life outcomes.¹ This raises the question, “What is the best approach to managing patients with comorbid depression and diabetes?”

• Three part-time registered nurses who had diabetes education training (certified diabetes educators), as well as training on depression management, behavioral strategies, and glycemic, hypertension, and lipid control.
• Combined support for self-care with pharmacotherapy to control depression, hyperglycemia, hypertension, and hyperlipidemia with algorithm guidance.
• Motivational and encouraging coaching for problem-solving and adherence to self-care.
• Weekly nurse supervision with a psychiatrist, primary care physician, and psychologist, with a nurse communicating recommendations back to the primary care team.

An endocrinologist/diabetologist was also incorporated for consultation when needed. After 12 months, patients in the intervention group had greater reduction in hemoglobin A_1c (0.58%), LDL cholesterol (6.9 mg/dL), systolic blood pressure (5.1 mm Hg), and depression scores than did those in the usual care group. Patients in the intervention group were also more likely to have adjustments made to insulin, antihypertensive medications, and antidepressants.

The success of this intervention, known as TEAMCare, highlights the critical need to incorporate mental health care into primary care and endocrinology practice. Currently, psychiatric and psychological care are largely administered separately from medical care for diabetes, despite evidence showing the success of an integrated care delivery model. In order to address the important interaction between mental health disorders, such as depression, and diabetes, it is critical that evaluation and treatment of mental health be integrated into medical practice.

What can we – endocrinologists and psychiatrists – do to facilitate adoption of such models? First, we can lobby our health systems to support reorganization of our health care delivery approach for patients with comorbid depression and diabetes so that endocrinologists, psychiatrists, and behavioral specialists are incorporated into primary care practices. This will facilitate better alignment of specialists and primary care providers and also enable patients to receive care in a clinical environment where they are most comfortable and have established relationships. Instead of the primary care physician referring the patient separately to psychiatry and endocrinology and awaiting feedback, which can sometimes take several weeks, the psychiatrist and endocrinologist would meet weekly with the primary care physician and nurse case manager team to review the entire patient panel, make timely adjustments in diabetes and antidepressant medications, and recommend behavioral therapy. This population health strategy would enable our two specialties to make a greater impact on a larger number of patients than we can in a half-day clinic session.

Second, our other critical role is to collaborate with payers to develop a sustainable financial reimbursement model to support the psychiatrist and endocrinologist in this novel health care delivery approach, which departs from the traditional fee-for-service model.

Dr. Golden is the Hugh P. McCormick Family Professor of Endocrinology and Metabolism and executive vice-chair of the department of medicine at Johns Hopkins University, Baltimore.

References

1. Holt RIG et al. Current Diabetes Reports. 2014;14(6):491.

2. Shojania KG et al. JAMA. 2006;296(4):427-40.

3. Katon WJ et al. N Eng J Med. 2010;363(27):2611-20.

Significant depressive symptoms affect approximately one in four adults with type 1 and type 2 diabetes while a formal diagnosis of depressive disorders is made in approximately 10%-15% of individuals with diabetes.¹ The combination of diabetes and depression presents a major clinical challenge because the outcomes of each condition is worsened by the presence of the other, which results in worsened quality of life, impaired diabetes self-management, and poor clinical outcomes.¹ While the costs of treatment are high for both individual patients and health economies, these costs do not necessarily result in significant improvements in disease or quality of life outcomes.¹ This raises the question, “What is the best approach to managing patients with comorbid depression and diabetes?”

• Three part-time registered nurses who had diabetes education training (certified diabetes educators), as well as training on depression management, behavioral strategies, and glycemic, hypertension, and lipid control.
• Combined support for self-care with pharmacotherapy to control depression, hyperglycemia, hypertension, and hyperlipidemia with algorithm guidance.
• Motivational and encouraging coaching for problem-solving and adherence to self-care.
• Weekly nurse supervision with a psychiatrist, primary care physician, and psychologist, with a nurse communicating recommendations back to the primary care team.

An endocrinologist/diabetologist was also incorporated for consultation when needed. After 12 months, patients in the intervention group had greater reduction in hemoglobin A_1c (0.58%), LDL cholesterol (6.9 mg/dL), systolic blood pressure (5.1 mm Hg), and depression scores than did those in the usual care group. Patients in the intervention group were also more likely to have adjustments made to insulin, antihypertensive medications, and antidepressants.

The success of this intervention, known as TEAMCare, highlights the critical need to incorporate mental health care into primary care and endocrinology practice. Currently, psychiatric and psychological care are largely administered separately from medical care for diabetes, despite evidence showing the success of an integrated care delivery model. In order to address the important interaction between mental health disorders, such as depression, and diabetes, it is critical that evaluation and treatment of mental health be integrated into medical practice.

What can we – endocrinologists and psychiatrists – do to facilitate adoption of such models? First, we can lobby our health systems to support reorganization of our health care delivery approach for patients with comorbid depression and diabetes so that endocrinologists, psychiatrists, and behavioral specialists are incorporated into primary care practices. This will facilitate better alignment of specialists and primary care providers and also enable patients to receive care in a clinical environment where they are most comfortable and have established relationships. Instead of the primary care physician referring the patient separately to psychiatry and endocrinology and awaiting feedback, which can sometimes take several weeks, the psychiatrist and endocrinologist would meet weekly with the primary care physician and nurse case manager team to review the entire patient panel, make timely adjustments in diabetes and antidepressant medications, and recommend behavioral therapy. This population health strategy would enable our two specialties to make a greater impact on a larger number of patients than we can in a half-day clinic session.

Second, our other critical role is to collaborate with payers to develop a sustainable financial reimbursement model to support the psychiatrist and endocrinologist in this novel health care delivery approach, which departs from the traditional fee-for-service model.

Dr. Golden is the Hugh P. McCormick Family Professor of Endocrinology and Metabolism and executive vice-chair of the department of medicine at Johns Hopkins University, Baltimore.

References

1. Holt RIG et al. Current Diabetes Reports. 2014;14(6):491.

2. Shojania KG et al. JAMA. 2006;296(4):427-40.

3. Katon WJ et al. N Eng J Med. 2010;363(27):2611-20.

Sait Ashina, MD; Kimberly Sackheim, DO; Christopher Gharibo, MD

Dr. Ashina is Clinical Associate Professor, Department of Neurology, and Director of the Headache Center at NYU Langone Medical Center, New York, NY

Dr. Sackheim is Clinical Assistant Professor, Department of Rehabilitation Medicine, NYU Langone Medical Center, New York, NY

Dr. Gharibo is Associate Professor, Department of Anesthesiology, Perioperative Care, and Pain Medicine, NYU Langone Medical Center, New York, NY

Pain is one of the most prevalent medical complaints and one of the most common reasons people seek medical attention in the United States. Chronic pain has an enormous impact on the individual and is associated with high societal costs. Because of these facts, it is considered a major health problem in the United States. The pathophysiologic mechanisms of acute and chronic pain are not fully understood, and chronic pain remains poorly recognized and undertreated. However, in the past 25 years, there have been major advances in our understanding of pain. New agents, medications, and techniques for the treatment of acute and chronic pain have emerged.

Recognizing the undertreatment of pain, the Agency for Health Care Policy and Research at the US Department of Health and Human Services issued the Acute Pain Management: Operative or Medical Procedures and Trauma guidelines in 1992.¹ Subsequent years have witnessed increasing use of patient-controlled analgesia, postoperative analgesia, continuous peripheral nerve blocks, and development of new therapeutic and pharmacologic modalities. The recognition of pain medicine as a subspecialty in medicine across multiple specialties is one of the field’s major achievements. The first pain medicine fellowships were accredited in 1993. The number of programs increased to almost 100 by 1999,² and more programs are being accredited now.

References

1. Acute pain management: operative or medical procedures and trauma, part 2. Agency for Health Care Policy and Research. Clin Pharm. 1992;11(5):391-414.

2. Fishman SM, Ballantyne JC, Rathmell JP, eds. Bonica’s Management of Pain. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009.

3. Woolf CJ, Salter MW. Neuronal plasticity: increasing the gain in pain. Science. 2000;288(5472):1765-1769.

4. Kissin I. The development of new analgesics over the past 50 years: a lack of real breakthrough drugs. Anesth Analg. 2010;110(3):780-789.

5. Slavin KV. Peripheral nerve stimulation for neuropathic pain. Neurotherapeutics. 2008;5(1):100-106.

6. Bicket MC, Dunn RY, Ahmed SU. High-frequency spinal cord stimulation for chronic pain: pre-clinical overview and systematic review of controlled trials. Pain Med. 2016;17(12):2326-2336.

7. Gereau RW 4th, Sluka KA, Maixner W, et al. A pain research agenda for the 21st century. J Pain. 2014;15(12):1203-1214.

8. Schou WS, Ashina S, Amin FM, et al. Calcitonin gene-related peptide and pain: a systematic review. J Headache Pain. 2017;18(1):34.

Sait Ashina, MD; Kimberly Sackheim, DO; Christopher Gharibo, MD

Dr. Ashina is Clinical Associate Professor, Department of Neurology, and Director of the Headache Center at NYU Langone Medical Center, New York, NY

Dr. Sackheim is Clinical Assistant Professor, Department of Rehabilitation Medicine, NYU Langone Medical Center, New York, NY

Dr. Gharibo is Associate Professor, Department of Anesthesiology, Perioperative Care, and Pain Medicine, NYU Langone Medical Center, New York, NY

Pain is one of the most prevalent medical complaints and one of the most common reasons people seek medical attention in the United States. Chronic pain has an enormous impact on the individual and is associated with high societal costs. Because of these facts, it is considered a major health problem in the United States. The pathophysiologic mechanisms of acute and chronic pain are not fully understood, and chronic pain remains poorly recognized and undertreated. However, in the past 25 years, there have been major advances in our understanding of pain. New agents, medications, and techniques for the treatment of acute and chronic pain have emerged.

Recognizing the undertreatment of pain, the Agency for Health Care Policy and Research at the US Department of Health and Human Services issued the Acute Pain Management: Operative or Medical Procedures and Trauma guidelines in 1992.¹ Subsequent years have witnessed increasing use of patient-controlled analgesia, postoperative analgesia, continuous peripheral nerve blocks, and development of new therapeutic and pharmacologic modalities. The recognition of pain medicine as a subspecialty in medicine across multiple specialties is one of the field’s major achievements. The first pain medicine fellowships were accredited in 1993. The number of programs increased to almost 100 by 1999,² and more programs are being accredited now.

References

1. Acute pain management: operative or medical procedures and trauma, part 2. Agency for Health Care Policy and Research. Clin Pharm. 1992;11(5):391-414.

2. Fishman SM, Ballantyne JC, Rathmell JP, eds. Bonica’s Management of Pain. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009.

3. Woolf CJ, Salter MW. Neuronal plasticity: increasing the gain in pain. Science. 2000;288(5472):1765-1769.

4. Kissin I. The development of new analgesics over the past 50 years: a lack of real breakthrough drugs. Anesth Analg. 2010;110(3):780-789.

5. Slavin KV. Peripheral nerve stimulation for neuropathic pain. Neurotherapeutics. 2008;5(1):100-106.

6. Bicket MC, Dunn RY, Ahmed SU. High-frequency spinal cord stimulation for chronic pain: pre-clinical overview and systematic review of controlled trials. Pain Med. 2016;17(12):2326-2336.

7. Gereau RW 4th, Sluka KA, Maixner W, et al. A pain research agenda for the 21st century. J Pain. 2014;15(12):1203-1214.

8. Schou WS, Ashina S, Amin FM, et al. Calcitonin gene-related peptide and pain: a systematic review. J Headache Pain. 2017;18(1):34.

Sait Ashina, MD; Kimberly Sackheim, DO; Christopher Gharibo, MD

Dr. Ashina is Clinical Associate Professor, Department of Neurology, and Director of the Headache Center at NYU Langone Medical Center, New York, NY

Dr. Sackheim is Clinical Assistant Professor, Department of Rehabilitation Medicine, NYU Langone Medical Center, New York, NY

Dr. Gharibo is Associate Professor, Department of Anesthesiology, Perioperative Care, and Pain Medicine, NYU Langone Medical Center, New York, NY

Pain is one of the most prevalent medical complaints and one of the most common reasons people seek medical attention in the United States. Chronic pain has an enormous impact on the individual and is associated with high societal costs. Because of these facts, it is considered a major health problem in the United States. The pathophysiologic mechanisms of acute and chronic pain are not fully understood, and chronic pain remains poorly recognized and undertreated. However, in the past 25 years, there have been major advances in our understanding of pain. New agents, medications, and techniques for the treatment of acute and chronic pain have emerged.

Recognizing the undertreatment of pain, the Agency for Health Care Policy and Research at the US Department of Health and Human Services issued the Acute Pain Management: Operative or Medical Procedures and Trauma guidelines in 1992.¹ Subsequent years have witnessed increasing use of patient-controlled analgesia, postoperative analgesia, continuous peripheral nerve blocks, and development of new therapeutic and pharmacologic modalities. The recognition of pain medicine as a subspecialty in medicine across multiple specialties is one of the field’s major achievements. The first pain medicine fellowships were accredited in 1993. The number of programs increased to almost 100 by 1999,² and more programs are being accredited now.

References

1. Acute pain management: operative or medical procedures and trauma, part 2. Agency for Health Care Policy and Research. Clin Pharm. 1992;11(5):391-414.

2. Fishman SM, Ballantyne JC, Rathmell JP, eds. Bonica’s Management of Pain. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009.

3. Woolf CJ, Salter MW. Neuronal plasticity: increasing the gain in pain. Science. 2000;288(5472):1765-1769.

4. Kissin I. The development of new analgesics over the past 50 years: a lack of real breakthrough drugs. Anesth Analg. 2010;110(3):780-789.

5. Slavin KV. Peripheral nerve stimulation for neuropathic pain. Neurotherapeutics. 2008;5(1):100-106.

6. Bicket MC, Dunn RY, Ahmed SU. High-frequency spinal cord stimulation for chronic pain: pre-clinical overview and systematic review of controlled trials. Pain Med. 2016;17(12):2326-2336.

7. Gereau RW 4th, Sluka KA, Maixner W, et al. A pain research agenda for the 21st century. J Pain. 2014;15(12):1203-1214.

8. Schou WS, Ashina S, Amin FM, et al. Calcitonin gene-related peptide and pain: a systematic review. J Headache Pain. 2017;18(1):34.

DALLAS – An investigational dermal microexcisional device is an effective treatment for facial rejuvenation without the use of thermal energy and without scarring, according to preliminary results from an ongoing study.

“This differs from laser treatment in the sense that there’s no thermal injury and it takes a deep core approach, along the lines of what you might expect from a punch biopsy,” lead study author Roy G. Geronemus, MD, said at the annual conference of the American Society for Laser Medicine and Surgery. “The device causes microscale excisions below the size that causes scar. It’s mechanical only, without the use of any thermal energy. There is quantitative and directional reduction in area of skin. This leads to wrinkle improvement, tightening, smoothing of lax skin, and skin rejuvenation.”

DALLAS – An investigational dermal microexcisional device is an effective treatment for facial rejuvenation without the use of thermal energy and without scarring, according to preliminary results from an ongoing study.

“This differs from laser treatment in the sense that there’s no thermal injury and it takes a deep core approach, along the lines of what you might expect from a punch biopsy,” lead study author Roy G. Geronemus, MD, said at the annual conference of the American Society for Laser Medicine and Surgery. “The device causes microscale excisions below the size that causes scar. It’s mechanical only, without the use of any thermal energy. There is quantitative and directional reduction in area of skin. This leads to wrinkle improvement, tightening, smoothing of lax skin, and skin rejuvenation.”

DALLAS – An investigational dermal microexcisional device is an effective treatment for facial rejuvenation without the use of thermal energy and without scarring, according to preliminary results from an ongoing study.

“This differs from laser treatment in the sense that there’s no thermal injury and it takes a deep core approach, along the lines of what you might expect from a punch biopsy,” lead study author Roy G. Geronemus, MD, said at the annual conference of the American Society for Laser Medicine and Surgery. “The device causes microscale excisions below the size that causes scar. It’s mechanical only, without the use of any thermal energy. There is quantitative and directional reduction in area of skin. This leads to wrinkle improvement, tightening, smoothing of lax skin, and skin rejuvenation.”