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VIDEO: Ketamine, Botox, and SAMe: What will be approved for depression?
CHICAGO – Research continues into whether the anesthetic ketamine will deliver on what some see as its potential to be a notably effective treatment for refractory depression, but other medical treatments are also under review.
Dr. James Jefferson scanned the depression treatment horizon in a presentation at Psychiatry Update 2014, sponsored by Current Psychiatry and the American Academy of Clinical Psychiatrists. In a video interview, Dr. Jefferson of the University of Wisconsin, Madison, forecasts what he thinks will – or won’t – enter the armamentarium. Might that include Botox? And how promising is the nutritional supplement SAMe?
Dr. Jefferson shares his thoughts on these and other contenders, and he considers when atypical antipsychotics are appropriate for treating depression. He also delivers stern words to clinicians who do not read the package inserts in the medications they prescribe.
Current Psychiatry and this news organization are owned by the same parent company.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
On Twitter @whitneymcknight
CHICAGO – Research continues into whether the anesthetic ketamine will deliver on what some see as its potential to be a notably effective treatment for refractory depression, but other medical treatments are also under review.
Dr. James Jefferson scanned the depression treatment horizon in a presentation at Psychiatry Update 2014, sponsored by Current Psychiatry and the American Academy of Clinical Psychiatrists. In a video interview, Dr. Jefferson of the University of Wisconsin, Madison, forecasts what he thinks will – or won’t – enter the armamentarium. Might that include Botox? And how promising is the nutritional supplement SAMe?
Dr. Jefferson shares his thoughts on these and other contenders, and he considers when atypical antipsychotics are appropriate for treating depression. He also delivers stern words to clinicians who do not read the package inserts in the medications they prescribe.
Current Psychiatry and this news organization are owned by the same parent company.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
On Twitter @whitneymcknight
CHICAGO – Research continues into whether the anesthetic ketamine will deliver on what some see as its potential to be a notably effective treatment for refractory depression, but other medical treatments are also under review.
Dr. James Jefferson scanned the depression treatment horizon in a presentation at Psychiatry Update 2014, sponsored by Current Psychiatry and the American Academy of Clinical Psychiatrists. In a video interview, Dr. Jefferson of the University of Wisconsin, Madison, forecasts what he thinks will – or won’t – enter the armamentarium. Might that include Botox? And how promising is the nutritional supplement SAMe?
Dr. Jefferson shares his thoughts on these and other contenders, and he considers when atypical antipsychotics are appropriate for treating depression. He also delivers stern words to clinicians who do not read the package inserts in the medications they prescribe.
Current Psychiatry and this news organization are owned by the same parent company.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
On Twitter @whitneymcknight
EXPERT ANALYSIS FROM PSYCHIATRY UPDATE 2014
AUDIO: Despite low efficacy in OCD, adjunct antipsychotics still prescribed
CHICAGO – At best, only a third of adults treated with selective serotonin reuptake inhibitors for obsessive-compulsive disorder respond to adjunctive therapy with the second-generation antipsychotic risperidone.
That’s according to Dr. H. Blair Simpson, professor of psychiatry at Columbia University and the director of the Center for Obsessive-Compulsive and Related Disorders and the Anxiety and Related Disorders Clinic at the New York State Psychiatric Institute/Columbia University.
"And if they do, typically you will know within about 4 weeks," said Dr. Simpson at the annual conference of the Anxiety and Depression Association of America.
So, why do so many patients with OCD – even pediatric ones for whom there are even fewer efficacy data – receive the second-generation antipsychotic (SGA) instead of cognitive-behavioral therapy, which does have more efficacy data? And for patients who do respond, what is the best way to titrate them off the SGA?
In an interview, Dr. Simpson and her colleague Dr. Moira Rynn, director of the Child and Adolescent Psychiatric Evaluation Service at the New York State Psychiatric Institute/Columbia University, explore the answers to these questions, as well as discuss whether two standards of mental health care are developing by default – and if so, why, as academic centers offer a wider range of treatments for refractory cases of OCD than do community-based clinicians.
CHICAGO – At best, only a third of adults treated with selective serotonin reuptake inhibitors for obsessive-compulsive disorder respond to adjunctive therapy with the second-generation antipsychotic risperidone.
That’s according to Dr. H. Blair Simpson, professor of psychiatry at Columbia University and the director of the Center for Obsessive-Compulsive and Related Disorders and the Anxiety and Related Disorders Clinic at the New York State Psychiatric Institute/Columbia University.
"And if they do, typically you will know within about 4 weeks," said Dr. Simpson at the annual conference of the Anxiety and Depression Association of America.
So, why do so many patients with OCD – even pediatric ones for whom there are even fewer efficacy data – receive the second-generation antipsychotic (SGA) instead of cognitive-behavioral therapy, which does have more efficacy data? And for patients who do respond, what is the best way to titrate them off the SGA?
In an interview, Dr. Simpson and her colleague Dr. Moira Rynn, director of the Child and Adolescent Psychiatric Evaluation Service at the New York State Psychiatric Institute/Columbia University, explore the answers to these questions, as well as discuss whether two standards of mental health care are developing by default – and if so, why, as academic centers offer a wider range of treatments for refractory cases of OCD than do community-based clinicians.
CHICAGO – At best, only a third of adults treated with selective serotonin reuptake inhibitors for obsessive-compulsive disorder respond to adjunctive therapy with the second-generation antipsychotic risperidone.
That’s according to Dr. H. Blair Simpson, professor of psychiatry at Columbia University and the director of the Center for Obsessive-Compulsive and Related Disorders and the Anxiety and Related Disorders Clinic at the New York State Psychiatric Institute/Columbia University.
"And if they do, typically you will know within about 4 weeks," said Dr. Simpson at the annual conference of the Anxiety and Depression Association of America.
So, why do so many patients with OCD – even pediatric ones for whom there are even fewer efficacy data – receive the second-generation antipsychotic (SGA) instead of cognitive-behavioral therapy, which does have more efficacy data? And for patients who do respond, what is the best way to titrate them off the SGA?
In an interview, Dr. Simpson and her colleague Dr. Moira Rynn, director of the Child and Adolescent Psychiatric Evaluation Service at the New York State Psychiatric Institute/Columbia University, explore the answers to these questions, as well as discuss whether two standards of mental health care are developing by default – and if so, why, as academic centers offer a wider range of treatments for refractory cases of OCD than do community-based clinicians.
EXPERT ANALYSIS FROM THE AADA ANNUAL CONFERENCE
Olokizumab showed promise for RA patients nonresponsive to antitumor necrosis factor therapies
Olokizumab, a humanized monoclonal antibody specific for the interleukin-6 cytokine, showed promise for patients with rheumatoid arthritis who had an inadequate response to antitumor necrosis factor therapies in a 12-week, phase II trial.
Olokizumab showed comparable efficacy to tocilizumab in this patient population and at doses in line with this class of drug. Treatment-related adverse events and laboratory profiles in the trial also were consistent with the use of an IL-6 targeted therapy in patients with moderate to severe rheumatoid arthritis.
The randomized, double-blind, placebo- and active-controlled multicenter trial of 221 patients measured changes in 28-joint and C-reactive protein Disease Activity Score (DAS28-CRP) at week 12 as its primary endpoint. Secondary endpoints included the American College of Rheumatology (ACR) 20, ACR50, and ACR70 response rates at week 12. The patients were randomly assigned to one of nine treatment arms, receiving either an intravenous subcutaneous injection of the trial drug or placebo every 2 weeks or every 4 weeks in dosages of 60 mg, 120 mg, or 240 mg, or an 8 mg/kg infusion of tocilizumab (Actemra) every 4 weeks. Patients who were not randomized to tocilizumab also received a placebo infusion every 4 weeks (Ann. Rheum. Dis. 2014 March 18 [doi:10.1136/annrheumdis-2013-204760]).
First author Dr. Mark C. Genovese of Stanford (Calif.) University and his associates found that at week 12, olokizumab produced greater reductions in baseline DAS28-CRP scores than did placebo (P less than .001), regardless of the dose tested. ACR20 and ACR50 responses were numerically higher in the test group than in placebo, but the trial was not powered to detect between-group differences in ACR endpoints. The investigators recorded ACR20 responses in 32.5%-60.7% of olokizumab-treated patients and in 17.1%-29.9% of placebo-treated patients. ACR50 responses occurred in 11.5%-33.2% of patients who received olokizumab, compared with 1.3%-4.9% of placebo patients. Few patients in any treatment arm were ACR70 responders.
Regardless of dose, olokizumab demonstrated comparable efficacy to tocilizumab across multiple endpoints. Most adverse events, such as upper respiratory infection or gastrointestinal disorders, were mild to moderate, and did not vary significantly between the two drug treatment groups.
Funding for the study was provided by UCB Pharma. Dr. Genovese disclosed he receives funding from UCB beyond the scope of this study. The other researchers involved in this study disclosed an extensive list of industry relationships.
Olokizumab, a humanized monoclonal antibody specific for the interleukin-6 cytokine, showed promise for patients with rheumatoid arthritis who had an inadequate response to antitumor necrosis factor therapies in a 12-week, phase II trial.
Olokizumab showed comparable efficacy to tocilizumab in this patient population and at doses in line with this class of drug. Treatment-related adverse events and laboratory profiles in the trial also were consistent with the use of an IL-6 targeted therapy in patients with moderate to severe rheumatoid arthritis.
The randomized, double-blind, placebo- and active-controlled multicenter trial of 221 patients measured changes in 28-joint and C-reactive protein Disease Activity Score (DAS28-CRP) at week 12 as its primary endpoint. Secondary endpoints included the American College of Rheumatology (ACR) 20, ACR50, and ACR70 response rates at week 12. The patients were randomly assigned to one of nine treatment arms, receiving either an intravenous subcutaneous injection of the trial drug or placebo every 2 weeks or every 4 weeks in dosages of 60 mg, 120 mg, or 240 mg, or an 8 mg/kg infusion of tocilizumab (Actemra) every 4 weeks. Patients who were not randomized to tocilizumab also received a placebo infusion every 4 weeks (Ann. Rheum. Dis. 2014 March 18 [doi:10.1136/annrheumdis-2013-204760]).
First author Dr. Mark C. Genovese of Stanford (Calif.) University and his associates found that at week 12, olokizumab produced greater reductions in baseline DAS28-CRP scores than did placebo (P less than .001), regardless of the dose tested. ACR20 and ACR50 responses were numerically higher in the test group than in placebo, but the trial was not powered to detect between-group differences in ACR endpoints. The investigators recorded ACR20 responses in 32.5%-60.7% of olokizumab-treated patients and in 17.1%-29.9% of placebo-treated patients. ACR50 responses occurred in 11.5%-33.2% of patients who received olokizumab, compared with 1.3%-4.9% of placebo patients. Few patients in any treatment arm were ACR70 responders.
Regardless of dose, olokizumab demonstrated comparable efficacy to tocilizumab across multiple endpoints. Most adverse events, such as upper respiratory infection or gastrointestinal disorders, were mild to moderate, and did not vary significantly between the two drug treatment groups.
Funding for the study was provided by UCB Pharma. Dr. Genovese disclosed he receives funding from UCB beyond the scope of this study. The other researchers involved in this study disclosed an extensive list of industry relationships.
Olokizumab, a humanized monoclonal antibody specific for the interleukin-6 cytokine, showed promise for patients with rheumatoid arthritis who had an inadequate response to antitumor necrosis factor therapies in a 12-week, phase II trial.
Olokizumab showed comparable efficacy to tocilizumab in this patient population and at doses in line with this class of drug. Treatment-related adverse events and laboratory profiles in the trial also were consistent with the use of an IL-6 targeted therapy in patients with moderate to severe rheumatoid arthritis.
The randomized, double-blind, placebo- and active-controlled multicenter trial of 221 patients measured changes in 28-joint and C-reactive protein Disease Activity Score (DAS28-CRP) at week 12 as its primary endpoint. Secondary endpoints included the American College of Rheumatology (ACR) 20, ACR50, and ACR70 response rates at week 12. The patients were randomly assigned to one of nine treatment arms, receiving either an intravenous subcutaneous injection of the trial drug or placebo every 2 weeks or every 4 weeks in dosages of 60 mg, 120 mg, or 240 mg, or an 8 mg/kg infusion of tocilizumab (Actemra) every 4 weeks. Patients who were not randomized to tocilizumab also received a placebo infusion every 4 weeks (Ann. Rheum. Dis. 2014 March 18 [doi:10.1136/annrheumdis-2013-204760]).
First author Dr. Mark C. Genovese of Stanford (Calif.) University and his associates found that at week 12, olokizumab produced greater reductions in baseline DAS28-CRP scores than did placebo (P less than .001), regardless of the dose tested. ACR20 and ACR50 responses were numerically higher in the test group than in placebo, but the trial was not powered to detect between-group differences in ACR endpoints. The investigators recorded ACR20 responses in 32.5%-60.7% of olokizumab-treated patients and in 17.1%-29.9% of placebo-treated patients. ACR50 responses occurred in 11.5%-33.2% of patients who received olokizumab, compared with 1.3%-4.9% of placebo patients. Few patients in any treatment arm were ACR70 responders.
Regardless of dose, olokizumab demonstrated comparable efficacy to tocilizumab across multiple endpoints. Most adverse events, such as upper respiratory infection or gastrointestinal disorders, were mild to moderate, and did not vary significantly between the two drug treatment groups.
Funding for the study was provided by UCB Pharma. Dr. Genovese disclosed he receives funding from UCB beyond the scope of this study. The other researchers involved in this study disclosed an extensive list of industry relationships.
FROM ANNALS OF THE RHEUMATIC DISEASES
Major finding: Olokizumab at all dose levels produced a greater reduction in DAS28-CRP than did placebo (P less than .001).
Data source: A phase II, randomized, double-blind, placebo- and active-controlled multicenter trial of 221 patients with moderate to severe RA who previously did not respond to antitumor necrosis factor therapies.
Disclosures: Funding for the study was provided by UCB Pharma. Dr. Genovese disclosed he receives funding from UCB beyond the scope of this study. The other researchers involved in this study disclosed an extensive list of industry relationships.
Evidence needed on obesity definition, treatment, AACE declares
WASHINGTON – Obesity requires a medical definition that goes beyond gauging a person’s body mass index if cost-effective care is to be delivered in an integrated fashion, according to a consensus statement issued by the American Association of Clinical Endocrinologists and the American College of Endocrinology.
"The definition of obesity as a disease is not perfect," Dr. W. Timothy Garvey, who chaired the AACE/ACE Obesity Consensus Conference, said in a media briefing. "We rely upon an [anthropometric] measure of body mass index, which is a measure of height versus weight, and there was consensus that this was ... divorced from the impact of weight gain on the health of the individual. This imprecision in our diagnosis of obesity was constraining us."
In 2013, the American Medical Association officially recognized obesity as a disease. Better codification of what actually constitutes "obesity, the disease," will allow a more integrated and effective approach to treating it, said Dr. Garvey, professor of medicine and chair of the department of nutrition sciences at the University of Alabama at Birmingham. To do so, the AACE/ACE held an intensive, 2-day session that largely featured spontaneous discussions between panelists and audience members representing four specific obesity "pillars": biomedical, government and regulation, health industry and economics, and research and education sectors.
A constant theme across the sectors was the need for a definition of obesity that accounts for cultural differences, ethnicity, and the presence or absence of cardiometabolic markers of disease in persons who are overweight or obese.
The conference’s multidisciplined approach informed the consensus statement that obesity is a chronic disease that should be treated with the established AACE/ACE obesity algorithm and met with lifestyle interventions. The consensus statement also addressed our current "obesogenic" environment, which many participants said was created in part by the abundance of nonnutritious foods.
In an interview, Dr. Susan Kansagra, deputy commissioner of the New York City Department of Health and Mental Hygiene, said that by working with local vendors and their suppliers, among other actions, her agency is focused on increasing access to more nutritious foods in neighborhoods across the city as a way to shape the food environment. "It’s not people who’ve changed over the past 30 years; it’s the environment," Dr. Kansagra said at the conference.
Also addressed by the consensus statement was the need for preventive care, particularly at the pediatric level, and more cohesive public awareness campaigns that could affect how private payers develop their reimbursement strategies. Audience member Dr. Robert Silverman, medical director of CIGNA Healthcare, said that payers would respond to the need for obesity care, but that what currently is missing is "a tie between the evidence and the complications [of obesity]."
"We learned that different stakeholders require different levels of evidence," AACE President Jeffrey I. Mechanick said in the media briefing. "So, we’re going to be able come up with a more efficient way to make recommendations about research so that private insurance carriers, the Centers for Medicare & Medicaid Services, or regulatory agencies have the type of data they require to facilitate the action [they need]."
These differences were brought to light during the conference as various audience members representing the Centers for Disease Control and Prevention, the Food and Drug Administration, the CMS, the National Institutes of Health, and others involved in research and policy making, addressed the panel to either explain or defend why their agency operates as it does.
In the case of the CMS, a statutory organization, it can apply coverage only according to what the agency is mandated to do, said Dr. Elizabeth Koller of the CMS. The level of evidence the agency looks for, she said, includes "hard endpoints of clinical relevance, like reductions in sleep apnea and degenerative joint disease." The CMS is also concerned about the lack of long-term data on interventions, the durability of interventions, and which characteristics are common in people who relapse in their disease, said Dr. Koller, who addressed the group as an audience member.
"Hearing from the CMS was incredibly helpful. We learned so much," said Dr. Mechanick, director of metabolic support at the Mt. Sinai School of Medicine in New York, in an interview.
Dr. Mechanick also said this was the first of three meetings, the next to be held in about a year, where the ultimate goal would be to use the evidence base they will have created to develop recommendations for all involved in delivering obesity care.
The talk was "polite," Dr. John Morton, chief of bariatric surgery at Stanford (Calif.) University and president of the American Society of Bariatric and Metabolic Surgery, said in an interview, but he said he thinks there is bias against people with obesity. "We wouldn’t be having this discussion if it were about cancer," he said in the interview. "Sometimes we think the consequences of obesity are the result of a personal decision, and that may skew people in a direction where they don’t necessarily want to provide help."
Regardless, Dr. Garvey said at the briefing, "the ‘old world’ thinking that obesity is a lifestyle choice has failed us."
Dr. Mechanick is a consultant for Abbott Nutrition. Dr. Garvey has multiple industry relationships, including with Merck, Vivus, and Eisai.
WASHINGTON – Obesity requires a medical definition that goes beyond gauging a person’s body mass index if cost-effective care is to be delivered in an integrated fashion, according to a consensus statement issued by the American Association of Clinical Endocrinologists and the American College of Endocrinology.
"The definition of obesity as a disease is not perfect," Dr. W. Timothy Garvey, who chaired the AACE/ACE Obesity Consensus Conference, said in a media briefing. "We rely upon an [anthropometric] measure of body mass index, which is a measure of height versus weight, and there was consensus that this was ... divorced from the impact of weight gain on the health of the individual. This imprecision in our diagnosis of obesity was constraining us."
In 2013, the American Medical Association officially recognized obesity as a disease. Better codification of what actually constitutes "obesity, the disease," will allow a more integrated and effective approach to treating it, said Dr. Garvey, professor of medicine and chair of the department of nutrition sciences at the University of Alabama at Birmingham. To do so, the AACE/ACE held an intensive, 2-day session that largely featured spontaneous discussions between panelists and audience members representing four specific obesity "pillars": biomedical, government and regulation, health industry and economics, and research and education sectors.
A constant theme across the sectors was the need for a definition of obesity that accounts for cultural differences, ethnicity, and the presence or absence of cardiometabolic markers of disease in persons who are overweight or obese.
The conference’s multidisciplined approach informed the consensus statement that obesity is a chronic disease that should be treated with the established AACE/ACE obesity algorithm and met with lifestyle interventions. The consensus statement also addressed our current "obesogenic" environment, which many participants said was created in part by the abundance of nonnutritious foods.
In an interview, Dr. Susan Kansagra, deputy commissioner of the New York City Department of Health and Mental Hygiene, said that by working with local vendors and their suppliers, among other actions, her agency is focused on increasing access to more nutritious foods in neighborhoods across the city as a way to shape the food environment. "It’s not people who’ve changed over the past 30 years; it’s the environment," Dr. Kansagra said at the conference.
Also addressed by the consensus statement was the need for preventive care, particularly at the pediatric level, and more cohesive public awareness campaigns that could affect how private payers develop their reimbursement strategies. Audience member Dr. Robert Silverman, medical director of CIGNA Healthcare, said that payers would respond to the need for obesity care, but that what currently is missing is "a tie between the evidence and the complications [of obesity]."
"We learned that different stakeholders require different levels of evidence," AACE President Jeffrey I. Mechanick said in the media briefing. "So, we’re going to be able come up with a more efficient way to make recommendations about research so that private insurance carriers, the Centers for Medicare & Medicaid Services, or regulatory agencies have the type of data they require to facilitate the action [they need]."
These differences were brought to light during the conference as various audience members representing the Centers for Disease Control and Prevention, the Food and Drug Administration, the CMS, the National Institutes of Health, and others involved in research and policy making, addressed the panel to either explain or defend why their agency operates as it does.
In the case of the CMS, a statutory organization, it can apply coverage only according to what the agency is mandated to do, said Dr. Elizabeth Koller of the CMS. The level of evidence the agency looks for, she said, includes "hard endpoints of clinical relevance, like reductions in sleep apnea and degenerative joint disease." The CMS is also concerned about the lack of long-term data on interventions, the durability of interventions, and which characteristics are common in people who relapse in their disease, said Dr. Koller, who addressed the group as an audience member.
"Hearing from the CMS was incredibly helpful. We learned so much," said Dr. Mechanick, director of metabolic support at the Mt. Sinai School of Medicine in New York, in an interview.
Dr. Mechanick also said this was the first of three meetings, the next to be held in about a year, where the ultimate goal would be to use the evidence base they will have created to develop recommendations for all involved in delivering obesity care.
The talk was "polite," Dr. John Morton, chief of bariatric surgery at Stanford (Calif.) University and president of the American Society of Bariatric and Metabolic Surgery, said in an interview, but he said he thinks there is bias against people with obesity. "We wouldn’t be having this discussion if it were about cancer," he said in the interview. "Sometimes we think the consequences of obesity are the result of a personal decision, and that may skew people in a direction where they don’t necessarily want to provide help."
Regardless, Dr. Garvey said at the briefing, "the ‘old world’ thinking that obesity is a lifestyle choice has failed us."
Dr. Mechanick is a consultant for Abbott Nutrition. Dr. Garvey has multiple industry relationships, including with Merck, Vivus, and Eisai.
WASHINGTON – Obesity requires a medical definition that goes beyond gauging a person’s body mass index if cost-effective care is to be delivered in an integrated fashion, according to a consensus statement issued by the American Association of Clinical Endocrinologists and the American College of Endocrinology.
"The definition of obesity as a disease is not perfect," Dr. W. Timothy Garvey, who chaired the AACE/ACE Obesity Consensus Conference, said in a media briefing. "We rely upon an [anthropometric] measure of body mass index, which is a measure of height versus weight, and there was consensus that this was ... divorced from the impact of weight gain on the health of the individual. This imprecision in our diagnosis of obesity was constraining us."
In 2013, the American Medical Association officially recognized obesity as a disease. Better codification of what actually constitutes "obesity, the disease," will allow a more integrated and effective approach to treating it, said Dr. Garvey, professor of medicine and chair of the department of nutrition sciences at the University of Alabama at Birmingham. To do so, the AACE/ACE held an intensive, 2-day session that largely featured spontaneous discussions between panelists and audience members representing four specific obesity "pillars": biomedical, government and regulation, health industry and economics, and research and education sectors.
A constant theme across the sectors was the need for a definition of obesity that accounts for cultural differences, ethnicity, and the presence or absence of cardiometabolic markers of disease in persons who are overweight or obese.
The conference’s multidisciplined approach informed the consensus statement that obesity is a chronic disease that should be treated with the established AACE/ACE obesity algorithm and met with lifestyle interventions. The consensus statement also addressed our current "obesogenic" environment, which many participants said was created in part by the abundance of nonnutritious foods.
In an interview, Dr. Susan Kansagra, deputy commissioner of the New York City Department of Health and Mental Hygiene, said that by working with local vendors and their suppliers, among other actions, her agency is focused on increasing access to more nutritious foods in neighborhoods across the city as a way to shape the food environment. "It’s not people who’ve changed over the past 30 years; it’s the environment," Dr. Kansagra said at the conference.
Also addressed by the consensus statement was the need for preventive care, particularly at the pediatric level, and more cohesive public awareness campaigns that could affect how private payers develop their reimbursement strategies. Audience member Dr. Robert Silverman, medical director of CIGNA Healthcare, said that payers would respond to the need for obesity care, but that what currently is missing is "a tie between the evidence and the complications [of obesity]."
"We learned that different stakeholders require different levels of evidence," AACE President Jeffrey I. Mechanick said in the media briefing. "So, we’re going to be able come up with a more efficient way to make recommendations about research so that private insurance carriers, the Centers for Medicare & Medicaid Services, or regulatory agencies have the type of data they require to facilitate the action [they need]."
These differences were brought to light during the conference as various audience members representing the Centers for Disease Control and Prevention, the Food and Drug Administration, the CMS, the National Institutes of Health, and others involved in research and policy making, addressed the panel to either explain or defend why their agency operates as it does.
In the case of the CMS, a statutory organization, it can apply coverage only according to what the agency is mandated to do, said Dr. Elizabeth Koller of the CMS. The level of evidence the agency looks for, she said, includes "hard endpoints of clinical relevance, like reductions in sleep apnea and degenerative joint disease." The CMS is also concerned about the lack of long-term data on interventions, the durability of interventions, and which characteristics are common in people who relapse in their disease, said Dr. Koller, who addressed the group as an audience member.
"Hearing from the CMS was incredibly helpful. We learned so much," said Dr. Mechanick, director of metabolic support at the Mt. Sinai School of Medicine in New York, in an interview.
Dr. Mechanick also said this was the first of three meetings, the next to be held in about a year, where the ultimate goal would be to use the evidence base they will have created to develop recommendations for all involved in delivering obesity care.
The talk was "polite," Dr. John Morton, chief of bariatric surgery at Stanford (Calif.) University and president of the American Society of Bariatric and Metabolic Surgery, said in an interview, but he said he thinks there is bias against people with obesity. "We wouldn’t be having this discussion if it were about cancer," he said in the interview. "Sometimes we think the consequences of obesity are the result of a personal decision, and that may skew people in a direction where they don’t necessarily want to provide help."
Regardless, Dr. Garvey said at the briefing, "the ‘old world’ thinking that obesity is a lifestyle choice has failed us."
Dr. Mechanick is a consultant for Abbott Nutrition. Dr. Garvey has multiple industry relationships, including with Merck, Vivus, and Eisai.
AT THE AACE/ACE CONSENSUS CONFERENCE ON OBESITY
VIDEO: Getting payers to cover obesity treatment
WASHINGTON – Payers will cover obesity treatment, people will suffer less from cardiometabolic disease, and the economy will be less burdened by the costs of untreated complications and lost productivity related to obesity. That’s the vision of Dr. Jeffrey I. Mechanick and his colleagues at the American Association of Clinical Endocrinologists and the American College of Endocrinology, who’ve jointly released a consensus statement on obesity treatment.
In a video interview, AACE president Dr. Mechanick, discusses why payers haven’t covered obesity treatment as a matter of course in the past, but why they may going forward, and how a growing impatience with a fractured approach to obesity care spurred the AACE and ACE to create a cross-disciplinary conference that also included members of the nonmedical professions involved in obesity care.
"By limiting the conference just to the biomedical model, we wouldn’t have access to this type of information," Dr. Mechanick also of the Icahn School of Medicine at Mount Sinai, New York, said in a press conference at the meeting. "We learned that different stakeholders require different levels of evidence."
The value of measuring body mass index is a controversial topic in obesity treatment. Dr. Mechanick explains why BMI will still be part of the developing ACCE/ACE standards of care and how it will be incorporated with other factors.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
WASHINGTON – Payers will cover obesity treatment, people will suffer less from cardiometabolic disease, and the economy will be less burdened by the costs of untreated complications and lost productivity related to obesity. That’s the vision of Dr. Jeffrey I. Mechanick and his colleagues at the American Association of Clinical Endocrinologists and the American College of Endocrinology, who’ve jointly released a consensus statement on obesity treatment.
In a video interview, AACE president Dr. Mechanick, discusses why payers haven’t covered obesity treatment as a matter of course in the past, but why they may going forward, and how a growing impatience with a fractured approach to obesity care spurred the AACE and ACE to create a cross-disciplinary conference that also included members of the nonmedical professions involved in obesity care.
"By limiting the conference just to the biomedical model, we wouldn’t have access to this type of information," Dr. Mechanick also of the Icahn School of Medicine at Mount Sinai, New York, said in a press conference at the meeting. "We learned that different stakeholders require different levels of evidence."
The value of measuring body mass index is a controversial topic in obesity treatment. Dr. Mechanick explains why BMI will still be part of the developing ACCE/ACE standards of care and how it will be incorporated with other factors.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
WASHINGTON – Payers will cover obesity treatment, people will suffer less from cardiometabolic disease, and the economy will be less burdened by the costs of untreated complications and lost productivity related to obesity. That’s the vision of Dr. Jeffrey I. Mechanick and his colleagues at the American Association of Clinical Endocrinologists and the American College of Endocrinology, who’ve jointly released a consensus statement on obesity treatment.
In a video interview, AACE president Dr. Mechanick, discusses why payers haven’t covered obesity treatment as a matter of course in the past, but why they may going forward, and how a growing impatience with a fractured approach to obesity care spurred the AACE and ACE to create a cross-disciplinary conference that also included members of the nonmedical professions involved in obesity care.
"By limiting the conference just to the biomedical model, we wouldn’t have access to this type of information," Dr. Mechanick also of the Icahn School of Medicine at Mount Sinai, New York, said in a press conference at the meeting. "We learned that different stakeholders require different levels of evidence."
The value of measuring body mass index is a controversial topic in obesity treatment. Dr. Mechanick explains why BMI will still be part of the developing ACCE/ACE standards of care and how it will be incorporated with other factors.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
AT THE AACE/ACE CONSENSUS CONFERENCE ON OBESITY
Is Bariatric Surgery the Right Treatment Model for Obesity?
WASHINGTON – Bariatric surgery has the greatest amount of data demonstrating its efficacy in reducing the comorbidities of obesity, as well as providing a long-term solution to the disease itself, according to Dr. John Morton, chief of bariatric surgery at Stanford (Calif.) University. Is it the model for obesity care that the nation needs to address the rising epidemic? If so, what stands in the way of its implementation? Dr. Morton offers a range of opinions in this audio interview.
WASHINGTON – Bariatric surgery has the greatest amount of data demonstrating its efficacy in reducing the comorbidities of obesity, as well as providing a long-term solution to the disease itself, according to Dr. John Morton, chief of bariatric surgery at Stanford (Calif.) University. Is it the model for obesity care that the nation needs to address the rising epidemic? If so, what stands in the way of its implementation? Dr. Morton offers a range of opinions in this audio interview.
WASHINGTON – Bariatric surgery has the greatest amount of data demonstrating its efficacy in reducing the comorbidities of obesity, as well as providing a long-term solution to the disease itself, according to Dr. John Morton, chief of bariatric surgery at Stanford (Calif.) University. Is it the model for obesity care that the nation needs to address the rising epidemic? If so, what stands in the way of its implementation? Dr. Morton offers a range of opinions in this audio interview.
EXPERT ANALYSIS FROM THE AACE/ACE CONSENSUS CONFERENCE ON OBESITY
Choice vs. regulation: the role of public policy in obesity management
WASHINGTON – It’s not people who’ve changed over the last 3 decades, but the environment around them that has brought on the obesity crisis, according to the deputy commissioner of the New York City Department of Health and Mental Hygiene, Dr. Susan M. Kansagra.
"The environment promotes people to consume more calories," Dr. Kansagra said in an audio interview during the American Association of Clinical Endocrinologists and American College of Endocrinology’s joint consensus conference on obesity. In this interview about the multifactorial nature of the disease, Dr. Kansagra discusses what role she sees as the role of public officials in shaping that environment.
WASHINGTON – It’s not people who’ve changed over the last 3 decades, but the environment around them that has brought on the obesity crisis, according to the deputy commissioner of the New York City Department of Health and Mental Hygiene, Dr. Susan M. Kansagra.
"The environment promotes people to consume more calories," Dr. Kansagra said in an audio interview during the American Association of Clinical Endocrinologists and American College of Endocrinology’s joint consensus conference on obesity. In this interview about the multifactorial nature of the disease, Dr. Kansagra discusses what role she sees as the role of public officials in shaping that environment.
WASHINGTON – It’s not people who’ve changed over the last 3 decades, but the environment around them that has brought on the obesity crisis, according to the deputy commissioner of the New York City Department of Health and Mental Hygiene, Dr. Susan M. Kansagra.
"The environment promotes people to consume more calories," Dr. Kansagra said in an audio interview during the American Association of Clinical Endocrinologists and American College of Endocrinology’s joint consensus conference on obesity. In this interview about the multifactorial nature of the disease, Dr. Kansagra discusses what role she sees as the role of public officials in shaping that environment.
EXPERT ANALYSIS FROM THE AACE/ACE CONSENSUS CONFERENCE ON OBESITY
What causes ‘weight fate,’ and is it really inevitable?
WASHINGTON – Young children who are overweight are four times more likely to become obese as they age. Is this a sign that we are fated from youth to be a burden on the health care system, or are their optimal points for intervention to change that fate?
In this audio interview, Solveig Cunningham, Ph.D., of Emory University, Atlanta, discusses the role of epigenetics, behavioral intervention, and maternal weight during gestation, along with other factors affecting pediatric obesity.
WASHINGTON – Young children who are overweight are four times more likely to become obese as they age. Is this a sign that we are fated from youth to be a burden on the health care system, or are their optimal points for intervention to change that fate?
In this audio interview, Solveig Cunningham, Ph.D., of Emory University, Atlanta, discusses the role of epigenetics, behavioral intervention, and maternal weight during gestation, along with other factors affecting pediatric obesity.
WASHINGTON – Young children who are overweight are four times more likely to become obese as they age. Is this a sign that we are fated from youth to be a burden on the health care system, or are their optimal points for intervention to change that fate?
In this audio interview, Solveig Cunningham, Ph.D., of Emory University, Atlanta, discusses the role of epigenetics, behavioral intervention, and maternal weight during gestation, along with other factors affecting pediatric obesity.
EXPERT ANALYSIS FROM THE AACE/ACE CONSENSUS CONFERENCE ON OBESITY
TNFR1 shown as marker for mortality risk in type 2 diabetes with kidney disease
Tumor necrosis factor receptor 1 is an effective marker for all-cause mortality in type 2 diabetes with kidney disease, according to results of a French study.
Additionally, TNFR1 was found to add clinical utility to the U.K. Prospective Diabetes Study (UKPDS) outcome equation for mortality.
"Our data showed a clear and graded relationship between concentrations of serum TNFR1 and risk of all-cause mortality," Pierre Jean Saulnier, Ph.D., of the University of Poitiers (France) and his colleagues wrote.
In a follow-up analysis of the SURDIAGENE study, designed to identify genetic and environmental causes of micro- and macrovascular complications in type 2 diabetes, investigators followed 522 patients with baseline urinary albumin to creatinine ratios (uACR) greater than 30 mg/mmol, an estimated glomerular filtration rate (eGFR) greater than 60 mL/min per 1.73 m2, or both. Patients with a history of myocardial infarction and/or stroke were considered to have cardiovascular disease at baseline (Diabetes Care 2014 March 12 [doi:10.2337/dc13-2580]).
The primary endpoint was all-cause mortality. The secondary endpoint was the occurrence of a composite renal outcome in patients who did not have end-stage renal disease at baseline. The median duration of the study was 48 months. In that time, 196 deaths occurred.
The increased rate of death correlated with increased levels of TNFR1 across quartiles: 4.7% patient years in the first quartile, 7.7% in the second, 9.3% in the third, and 15.9% in the fourth.
Of note, when the investigators ran a multivariate analysis using age, diabetes duration, hemoglobin A1c, uACR, and eGFR, they found that the risk of death tripled in patients in the fourth quartile (adjusted hazard ratio, 2.98), compared with patients in the first quartile.
When TNFR1 was combined with the UKDPS equation, which uses age, diabetes duration, sex, ethnicity, current smoking status, systolic blood pressure, HbA1c, body mass index, eGFR, heart rate, atrial fibrillation, albuminuria, and peripheral vascular disease, the predictive value for mortality improved significantly (P = .03).
TNFR1 is a proinflammatory marker that a growing body of literature indicates has prognostic value for cardiovascular disease in patients with diabetes. "Our current findings add to this literature," the researchers wrote, adding that while it was not the focus of their study, the data may contribute to understanding the role of TNFR1 in vasculopathy and diabetes-related events such as amputation.
None of the authors of this study reported any relevant disclosures. Funding was provided by the French Ministry of Health, among others.
Tumor necrosis factor receptor 1 is an effective marker for all-cause mortality in type 2 diabetes with kidney disease, according to results of a French study.
Additionally, TNFR1 was found to add clinical utility to the U.K. Prospective Diabetes Study (UKPDS) outcome equation for mortality.
"Our data showed a clear and graded relationship between concentrations of serum TNFR1 and risk of all-cause mortality," Pierre Jean Saulnier, Ph.D., of the University of Poitiers (France) and his colleagues wrote.
In a follow-up analysis of the SURDIAGENE study, designed to identify genetic and environmental causes of micro- and macrovascular complications in type 2 diabetes, investigators followed 522 patients with baseline urinary albumin to creatinine ratios (uACR) greater than 30 mg/mmol, an estimated glomerular filtration rate (eGFR) greater than 60 mL/min per 1.73 m2, or both. Patients with a history of myocardial infarction and/or stroke were considered to have cardiovascular disease at baseline (Diabetes Care 2014 March 12 [doi:10.2337/dc13-2580]).
The primary endpoint was all-cause mortality. The secondary endpoint was the occurrence of a composite renal outcome in patients who did not have end-stage renal disease at baseline. The median duration of the study was 48 months. In that time, 196 deaths occurred.
The increased rate of death correlated with increased levels of TNFR1 across quartiles: 4.7% patient years in the first quartile, 7.7% in the second, 9.3% in the third, and 15.9% in the fourth.
Of note, when the investigators ran a multivariate analysis using age, diabetes duration, hemoglobin A1c, uACR, and eGFR, they found that the risk of death tripled in patients in the fourth quartile (adjusted hazard ratio, 2.98), compared with patients in the first quartile.
When TNFR1 was combined with the UKDPS equation, which uses age, diabetes duration, sex, ethnicity, current smoking status, systolic blood pressure, HbA1c, body mass index, eGFR, heart rate, atrial fibrillation, albuminuria, and peripheral vascular disease, the predictive value for mortality improved significantly (P = .03).
TNFR1 is a proinflammatory marker that a growing body of literature indicates has prognostic value for cardiovascular disease in patients with diabetes. "Our current findings add to this literature," the researchers wrote, adding that while it was not the focus of their study, the data may contribute to understanding the role of TNFR1 in vasculopathy and diabetes-related events such as amputation.
None of the authors of this study reported any relevant disclosures. Funding was provided by the French Ministry of Health, among others.
Tumor necrosis factor receptor 1 is an effective marker for all-cause mortality in type 2 diabetes with kidney disease, according to results of a French study.
Additionally, TNFR1 was found to add clinical utility to the U.K. Prospective Diabetes Study (UKPDS) outcome equation for mortality.
"Our data showed a clear and graded relationship between concentrations of serum TNFR1 and risk of all-cause mortality," Pierre Jean Saulnier, Ph.D., of the University of Poitiers (France) and his colleagues wrote.
In a follow-up analysis of the SURDIAGENE study, designed to identify genetic and environmental causes of micro- and macrovascular complications in type 2 diabetes, investigators followed 522 patients with baseline urinary albumin to creatinine ratios (uACR) greater than 30 mg/mmol, an estimated glomerular filtration rate (eGFR) greater than 60 mL/min per 1.73 m2, or both. Patients with a history of myocardial infarction and/or stroke were considered to have cardiovascular disease at baseline (Diabetes Care 2014 March 12 [doi:10.2337/dc13-2580]).
The primary endpoint was all-cause mortality. The secondary endpoint was the occurrence of a composite renal outcome in patients who did not have end-stage renal disease at baseline. The median duration of the study was 48 months. In that time, 196 deaths occurred.
The increased rate of death correlated with increased levels of TNFR1 across quartiles: 4.7% patient years in the first quartile, 7.7% in the second, 9.3% in the third, and 15.9% in the fourth.
Of note, when the investigators ran a multivariate analysis using age, diabetes duration, hemoglobin A1c, uACR, and eGFR, they found that the risk of death tripled in patients in the fourth quartile (adjusted hazard ratio, 2.98), compared with patients in the first quartile.
When TNFR1 was combined with the UKDPS equation, which uses age, diabetes duration, sex, ethnicity, current smoking status, systolic blood pressure, HbA1c, body mass index, eGFR, heart rate, atrial fibrillation, albuminuria, and peripheral vascular disease, the predictive value for mortality improved significantly (P = .03).
TNFR1 is a proinflammatory marker that a growing body of literature indicates has prognostic value for cardiovascular disease in patients with diabetes. "Our current findings add to this literature," the researchers wrote, adding that while it was not the focus of their study, the data may contribute to understanding the role of TNFR1 in vasculopathy and diabetes-related events such as amputation.
None of the authors of this study reported any relevant disclosures. Funding was provided by the French Ministry of Health, among others.
FROM DIABETES CARE
Major finding: Increased rate of death correlated with increased rates of TNFR1 across quartiles: 4.7% patient years; 7.7%; 9.3%; 15.9%.
Data source: A prospective, single-center study of 522 patients.
Disclosures: None of the authors of this study reported any relevant disclosures. Funding was provided by the French Ministry of Health, among others.
New tanning bed technology no safer than the old
Tanning bed technology circa the year 2000, when the industry began using lamps that emit larger doses of long-wave ultraviolet A (between 335 and 400 nm), is no safer than tanning beds pre-2000, a meta-analysis of the association between melanoma and tanning beds has shown.
Globally, people who had been exposed to tanning beds were 16% more likely to have melanoma; in the United States, where tanning bed intensity is unrestricted, the risk from exposure is 23% higher than in the general population. In Europe and in Australia and New Zealand, where the intensity is limited to an ultraviolet index of 12 and 36 respectively, the increased risk was not significant, reported investigators in the March issue of the Journal of the American Academy of Dermatology (doi:10.1016/j.jaad.2013.11.050).
Further, tanning bed use before the age of 25 years additionally increased a person’s melanoma odds to 35% compared with 11% in those who had indoor tanning exposure after the age of 25 years. Sophia Colantonia of the University of Ottawa and her coauthors also found a threshold effect of 10 or more tanning bed sessions being associated with the highest risk of melanoma.
"Assessing and communicating health risk to patients in an easily understood metric based on number of tanning bed sessions could be helpful to clinical practice," wrote the investigators.
For the meta-analysis, the investigators searched Scopus, MEDLINE, and the Cumulative Index to Nursing and Allied Health Literature for studies published before Aug. 14, 2013. In all, 31 studies that included 14,956 cases of melanoma and 233,106 controls were analyzed. In those who had ever used a tanning bed, the odds ratio (OR) for melanoma was 1.16 (95% CI, 1.05-1.28). Tanning bed use after 2000 had an OR of 1.22 (95% CI, 1.03-1.45). For individuals who had used 10 or more tanning bed sessions, the OR was 1.34 (95% CI, 1.05-1.71). North Americans were found to have higher rates of melanoma (OR, 1.23; 95% CI, 1.03-1.47) vs. Europeans and Oceanianians for whom the OR was not significant. Ten or more tanning sessions in a lifetime was associated with the highest risk of melanoma (OR, 1.34; 95% CI, 1.05-1.71).
Limitations to the meta-analysis included that not all of the studies used the same age range for their study groups, and evidence quality ranged from mediocre to poor, the investigators noted.
The investigators reported that there were no funding sources, and no conflicts of interest were declared.
Tanning bed technology circa the year 2000, when the industry began using lamps that emit larger doses of long-wave ultraviolet A (between 335 and 400 nm), is no safer than tanning beds pre-2000, a meta-analysis of the association between melanoma and tanning beds has shown.
Globally, people who had been exposed to tanning beds were 16% more likely to have melanoma; in the United States, where tanning bed intensity is unrestricted, the risk from exposure is 23% higher than in the general population. In Europe and in Australia and New Zealand, where the intensity is limited to an ultraviolet index of 12 and 36 respectively, the increased risk was not significant, reported investigators in the March issue of the Journal of the American Academy of Dermatology (doi:10.1016/j.jaad.2013.11.050).
Further, tanning bed use before the age of 25 years additionally increased a person’s melanoma odds to 35% compared with 11% in those who had indoor tanning exposure after the age of 25 years. Sophia Colantonia of the University of Ottawa and her coauthors also found a threshold effect of 10 or more tanning bed sessions being associated with the highest risk of melanoma.
"Assessing and communicating health risk to patients in an easily understood metric based on number of tanning bed sessions could be helpful to clinical practice," wrote the investigators.
For the meta-analysis, the investigators searched Scopus, MEDLINE, and the Cumulative Index to Nursing and Allied Health Literature for studies published before Aug. 14, 2013. In all, 31 studies that included 14,956 cases of melanoma and 233,106 controls were analyzed. In those who had ever used a tanning bed, the odds ratio (OR) for melanoma was 1.16 (95% CI, 1.05-1.28). Tanning bed use after 2000 had an OR of 1.22 (95% CI, 1.03-1.45). For individuals who had used 10 or more tanning bed sessions, the OR was 1.34 (95% CI, 1.05-1.71). North Americans were found to have higher rates of melanoma (OR, 1.23; 95% CI, 1.03-1.47) vs. Europeans and Oceanianians for whom the OR was not significant. Ten or more tanning sessions in a lifetime was associated with the highest risk of melanoma (OR, 1.34; 95% CI, 1.05-1.71).
Limitations to the meta-analysis included that not all of the studies used the same age range for their study groups, and evidence quality ranged from mediocre to poor, the investigators noted.
The investigators reported that there were no funding sources, and no conflicts of interest were declared.
Tanning bed technology circa the year 2000, when the industry began using lamps that emit larger doses of long-wave ultraviolet A (between 335 and 400 nm), is no safer than tanning beds pre-2000, a meta-analysis of the association between melanoma and tanning beds has shown.
Globally, people who had been exposed to tanning beds were 16% more likely to have melanoma; in the United States, where tanning bed intensity is unrestricted, the risk from exposure is 23% higher than in the general population. In Europe and in Australia and New Zealand, where the intensity is limited to an ultraviolet index of 12 and 36 respectively, the increased risk was not significant, reported investigators in the March issue of the Journal of the American Academy of Dermatology (doi:10.1016/j.jaad.2013.11.050).
Further, tanning bed use before the age of 25 years additionally increased a person’s melanoma odds to 35% compared with 11% in those who had indoor tanning exposure after the age of 25 years. Sophia Colantonia of the University of Ottawa and her coauthors also found a threshold effect of 10 or more tanning bed sessions being associated with the highest risk of melanoma.
"Assessing and communicating health risk to patients in an easily understood metric based on number of tanning bed sessions could be helpful to clinical practice," wrote the investigators.
For the meta-analysis, the investigators searched Scopus, MEDLINE, and the Cumulative Index to Nursing and Allied Health Literature for studies published before Aug. 14, 2013. In all, 31 studies that included 14,956 cases of melanoma and 233,106 controls were analyzed. In those who had ever used a tanning bed, the odds ratio (OR) for melanoma was 1.16 (95% CI, 1.05-1.28). Tanning bed use after 2000 had an OR of 1.22 (95% CI, 1.03-1.45). For individuals who had used 10 or more tanning bed sessions, the OR was 1.34 (95% CI, 1.05-1.71). North Americans were found to have higher rates of melanoma (OR, 1.23; 95% CI, 1.03-1.47) vs. Europeans and Oceanianians for whom the OR was not significant. Ten or more tanning sessions in a lifetime was associated with the highest risk of melanoma (OR, 1.34; 95% CI, 1.05-1.71).
Limitations to the meta-analysis included that not all of the studies used the same age range for their study groups, and evidence quality ranged from mediocre to poor, the investigators noted.
The investigators reported that there were no funding sources, and no conflicts of interest were declared.
FROM JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY
Major finding: Exposure to tanning bed technology, new or old, led to a 16% increased risk of melanoma worldwide.
Data source: A meta-analysis of 31 studies with 14,956 melanoma cases and 233,106 controls.
Disclosures: The investigators reported that there were no funding sources, and no conflicts of interest were declared.