The Cutis Editorial Board is now accepting applications for the 2024 Resident Corner column. The Editorial Board will select 2 to 3 residents to serve as the Resident Corner columnists for 1 year. Articles are posted online only at www.mdedge.com/dermatology but will be referenced in Index Medicus. All applicants must be current residents and will be in residency throughout 2024.

For consideration, send your curriculum vitae along with a brief (not to exceed 500 words) statement of why you enjoy Cutis and what you can offer your fellow residents in contributing a monthly column.

A signed letter of recommendation from the Director of the dermatology residency program also should be supplied.

All materials should be submitted via email to Melissa Sears ([email protected]) by November 1. The residents who are selected to write the column for the upcoming year will be notified by November 15.

We look forward to continuing to educate dermatology residents on topics that are most important to them!

The Cutis Editorial Board is now accepting applications for the 2024 Resident Corner column. The Editorial Board will select 2 to 3 residents to serve as the Resident Corner columnists for 1 year. Articles are posted online only at www.mdedge.com/dermatology but will be referenced in Index Medicus. All applicants must be current residents and will be in residency throughout 2024.

For consideration, send your curriculum vitae along with a brief (not to exceed 500 words) statement of why you enjoy Cutis and what you can offer your fellow residents in contributing a monthly column.

A signed letter of recommendation from the Director of the dermatology residency program also should be supplied.

All materials should be submitted via email to Melissa Sears ([email protected]) by November 1. The residents who are selected to write the column for the upcoming year will be notified by November 15.

We look forward to continuing to educate dermatology residents on topics that are most important to them!

The Cutis Editorial Board is now accepting applications for the 2024 Resident Corner column. The Editorial Board will select 2 to 3 residents to serve as the Resident Corner columnists for 1 year. Articles are posted online only at www.mdedge.com/dermatology but will be referenced in Index Medicus. All applicants must be current residents and will be in residency throughout 2024.

For consideration, send your curriculum vitae along with a brief (not to exceed 500 words) statement of why you enjoy Cutis and what you can offer your fellow residents in contributing a monthly column.

A signed letter of recommendation from the Director of the dermatology residency program also should be supplied.

All materials should be submitted via email to Melissa Sears ([email protected]) by November 1. The residents who are selected to write the column for the upcoming year will be notified by November 15.

We look forward to continuing to educate dermatology residents on topics that are most important to them!

For comatose adult survivors of out-of-hospital cardiac arrest (OHCA), controlling body temperature to less than 37.5° C is a “reasonable and evidence-based approach,” a new American Heart Association (AHA) scientific advisory suggests.

On the basis of data from recent trials, the International Liaison Committee on Resuscitation and other organizations have altered their treatment recommendations for temperature management after cardiac arrest.

The AHA will present guidelines on this topic in a focused update to be published later in the year. Meanwhile, AHA’s Emergency Cardiovascular Care Committee convened a writing group to review the Hypothermia Versus Normothermia After Out-of-Hospital Cardiac Arrest (TTM2) trial in the context of other recent evidence and rendered an expert opinion on how the trial may influence clinical practice. These findings will be incorporated into the upcoming guidelines.

“Many centers have already moved toward controlled normothermia for post-arrest patients, so we think this guidance will be welcomed by many,” said Sarah Perman, MD, of the Yale University, and Kate Berg, MD, of Beth Israel Deaconess Medical Center, who are both members of the AHA Emergency Cardiovascular Care Committee that authored the advisory.

“For those who continue to favor temperatures in the 32° to 36° range for some or even all patients, the guidance that we have drafted leaves room for clinicians to make patient-centered decisions,” they told this news organization.

“Certainly, a finite guideline that recommends one temperature for all would be easier to apply,” the authors acknowledged. “However, cardiac arrest is a heterogeneous event and brain injury is variable, and definitive evidence that one temperature in the range of 32-37.5 is superior to another is lacking. We hope that clinicians find that this guidance supports and informs their practice.”

The advisory was published online in Circulation.
 

TTM2 key

The new guidance is based largely on findings from the TTM2 trial, a multicenter, randomized clinical trial of temperature management for neuroprotection after cardiac arrest that included 1,900 unresponsive adult patients successfully resuscitated from OHCA.

Patients were randomly assigned to receive hypothermia, defined as a target temperature of 33° C for 28 hours, followed by gradual rewarming to 37° C, or normothermia, defined as a target temperature < 37.8° C, with early treatment of fever.

No significant between-group difference was seen in the primary outcome of death at 6 months, nor were there any significant differences by subgroups of sex, age, time to return of spontaneous circulation, initial rhythm, or circulatory shock on admission.

Although it’s still not clear whether certain patients might benefit from lower target temperatures, the authors noted, major international organizations now suggest a target post–cardiac arrest temperature of less than 37.5° C.

By contrast, current AHA guidelines endorse targeting a temperature between 32° C and 36° C for 24 hours.

Between now and the forthcoming formal guidance in the “2023 American Heart Association Focused Update on Advanced Cardiovascular Life Support,” the scientific advisory writing group agreed: “For unresponsive post–cardiac arrest adult patients with characteristics similar to those of individuals included in the TTM2 trial (OHCA of cardiac or unknown cause, excluding those with unwitnessed asystole), controlling patient temperature to < 37.5° C is a reasonable and evidence-based approach.

“For the broader group of patients with in-hospital cardiac arrest or OHCA of noncardiac (other medical) cause, evidence for the ideal approach to temperature management after return of spontaneous circulation is less certain; whether some of these patients might benefit from temperature control at temperatures between 33° C and 37.5° C remains unclear.”

Unless a catastrophic brain injury results from OHCA, the group wrote, “strictly preventing fever with continuous temperature monitoring, providing comprehensive critical care support, and deploying multimodal evidence-based strategies for neuroprognostication at a minimum of 72 hours after normothermia remain essential ...”

Dr. Perman and Dr. Berg concluded, “We hope that this guidance continues to encourage aggressive post-arrest care that includes focus on temperature control as well as the other major contributors to post-arrest bundles of care including hemodynamic optimization and guideline concordant neuroprognostication.”

No funding was reported. Dr. Berg has received grant support from AHA/ILCOR, and Dr. Perman, from NIH/NHLBI.

A version of this article first appeared on Medscape.com.

For comatose adult survivors of out-of-hospital cardiac arrest (OHCA), controlling body temperature to less than 37.5° C is a “reasonable and evidence-based approach,” a new American Heart Association (AHA) scientific advisory suggests.

On the basis of data from recent trials, the International Liaison Committee on Resuscitation and other organizations have altered their treatment recommendations for temperature management after cardiac arrest.

The AHA will present guidelines on this topic in a focused update to be published later in the year. Meanwhile, AHA’s Emergency Cardiovascular Care Committee convened a writing group to review the Hypothermia Versus Normothermia After Out-of-Hospital Cardiac Arrest (TTM2) trial in the context of other recent evidence and rendered an expert opinion on how the trial may influence clinical practice. These findings will be incorporated into the upcoming guidelines.

“Many centers have already moved toward controlled normothermia for post-arrest patients, so we think this guidance will be welcomed by many,” said Sarah Perman, MD, of the Yale University, and Kate Berg, MD, of Beth Israel Deaconess Medical Center, who are both members of the AHA Emergency Cardiovascular Care Committee that authored the advisory.

“For those who continue to favor temperatures in the 32° to 36° range for some or even all patients, the guidance that we have drafted leaves room for clinicians to make patient-centered decisions,” they told this news organization.

“Certainly, a finite guideline that recommends one temperature for all would be easier to apply,” the authors acknowledged. “However, cardiac arrest is a heterogeneous event and brain injury is variable, and definitive evidence that one temperature in the range of 32-37.5 is superior to another is lacking. We hope that clinicians find that this guidance supports and informs their practice.”

The advisory was published online in Circulation.
 

TTM2 key

The new guidance is based largely on findings from the TTM2 trial, a multicenter, randomized clinical trial of temperature management for neuroprotection after cardiac arrest that included 1,900 unresponsive adult patients successfully resuscitated from OHCA.

Patients were randomly assigned to receive hypothermia, defined as a target temperature of 33° C for 28 hours, followed by gradual rewarming to 37° C, or normothermia, defined as a target temperature < 37.8° C, with early treatment of fever.

No significant between-group difference was seen in the primary outcome of death at 6 months, nor were there any significant differences by subgroups of sex, age, time to return of spontaneous circulation, initial rhythm, or circulatory shock on admission.

Although it’s still not clear whether certain patients might benefit from lower target temperatures, the authors noted, major international organizations now suggest a target post–cardiac arrest temperature of less than 37.5° C.

By contrast, current AHA guidelines endorse targeting a temperature between 32° C and 36° C for 24 hours.

Between now and the forthcoming formal guidance in the “2023 American Heart Association Focused Update on Advanced Cardiovascular Life Support,” the scientific advisory writing group agreed: “For unresponsive post–cardiac arrest adult patients with characteristics similar to those of individuals included in the TTM2 trial (OHCA of cardiac or unknown cause, excluding those with unwitnessed asystole), controlling patient temperature to < 37.5° C is a reasonable and evidence-based approach.

“For the broader group of patients with in-hospital cardiac arrest or OHCA of noncardiac (other medical) cause, evidence for the ideal approach to temperature management after return of spontaneous circulation is less certain; whether some of these patients might benefit from temperature control at temperatures between 33° C and 37.5° C remains unclear.”

Unless a catastrophic brain injury results from OHCA, the group wrote, “strictly preventing fever with continuous temperature monitoring, providing comprehensive critical care support, and deploying multimodal evidence-based strategies for neuroprognostication at a minimum of 72 hours after normothermia remain essential ...”

Dr. Perman and Dr. Berg concluded, “We hope that this guidance continues to encourage aggressive post-arrest care that includes focus on temperature control as well as the other major contributors to post-arrest bundles of care including hemodynamic optimization and guideline concordant neuroprognostication.”

No funding was reported. Dr. Berg has received grant support from AHA/ILCOR, and Dr. Perman, from NIH/NHLBI.

A version of this article first appeared on Medscape.com.

For comatose adult survivors of out-of-hospital cardiac arrest (OHCA), controlling body temperature to less than 37.5° C is a “reasonable and evidence-based approach,” a new American Heart Association (AHA) scientific advisory suggests.

On the basis of data from recent trials, the International Liaison Committee on Resuscitation and other organizations have altered their treatment recommendations for temperature management after cardiac arrest.

The AHA will present guidelines on this topic in a focused update to be published later in the year. Meanwhile, AHA’s Emergency Cardiovascular Care Committee convened a writing group to review the Hypothermia Versus Normothermia After Out-of-Hospital Cardiac Arrest (TTM2) trial in the context of other recent evidence and rendered an expert opinion on how the trial may influence clinical practice. These findings will be incorporated into the upcoming guidelines.

“Many centers have already moved toward controlled normothermia for post-arrest patients, so we think this guidance will be welcomed by many,” said Sarah Perman, MD, of the Yale University, and Kate Berg, MD, of Beth Israel Deaconess Medical Center, who are both members of the AHA Emergency Cardiovascular Care Committee that authored the advisory.

“For those who continue to favor temperatures in the 32° to 36° range for some or even all patients, the guidance that we have drafted leaves room for clinicians to make patient-centered decisions,” they told this news organization.

“Certainly, a finite guideline that recommends one temperature for all would be easier to apply,” the authors acknowledged. “However, cardiac arrest is a heterogeneous event and brain injury is variable, and definitive evidence that one temperature in the range of 32-37.5 is superior to another is lacking. We hope that clinicians find that this guidance supports and informs their practice.”

The advisory was published online in Circulation.
 

TTM2 key

The new guidance is based largely on findings from the TTM2 trial, a multicenter, randomized clinical trial of temperature management for neuroprotection after cardiac arrest that included 1,900 unresponsive adult patients successfully resuscitated from OHCA.

Patients were randomly assigned to receive hypothermia, defined as a target temperature of 33° C for 28 hours, followed by gradual rewarming to 37° C, or normothermia, defined as a target temperature < 37.8° C, with early treatment of fever.

No significant between-group difference was seen in the primary outcome of death at 6 months, nor were there any significant differences by subgroups of sex, age, time to return of spontaneous circulation, initial rhythm, or circulatory shock on admission.

Although it’s still not clear whether certain patients might benefit from lower target temperatures, the authors noted, major international organizations now suggest a target post–cardiac arrest temperature of less than 37.5° C.

By contrast, current AHA guidelines endorse targeting a temperature between 32° C and 36° C for 24 hours.

Between now and the forthcoming formal guidance in the “2023 American Heart Association Focused Update on Advanced Cardiovascular Life Support,” the scientific advisory writing group agreed: “For unresponsive post–cardiac arrest adult patients with characteristics similar to those of individuals included in the TTM2 trial (OHCA of cardiac or unknown cause, excluding those with unwitnessed asystole), controlling patient temperature to < 37.5° C is a reasonable and evidence-based approach.

“For the broader group of patients with in-hospital cardiac arrest or OHCA of noncardiac (other medical) cause, evidence for the ideal approach to temperature management after return of spontaneous circulation is less certain; whether some of these patients might benefit from temperature control at temperatures between 33° C and 37.5° C remains unclear.”

Unless a catastrophic brain injury results from OHCA, the group wrote, “strictly preventing fever with continuous temperature monitoring, providing comprehensive critical care support, and deploying multimodal evidence-based strategies for neuroprognostication at a minimum of 72 hours after normothermia remain essential ...”

Dr. Perman and Dr. Berg concluded, “We hope that this guidance continues to encourage aggressive post-arrest care that includes focus on temperature control as well as the other major contributors to post-arrest bundles of care including hemodynamic optimization and guideline concordant neuroprognostication.”

No funding was reported. Dr. Berg has received grant support from AHA/ILCOR, and Dr. Perman, from NIH/NHLBI.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

I’d like to present you today with a case that raised a large amount of discussion and debate. I got involved as an ethics consultant on the case. I think you’ll find it very interesting and I also think there are going to be some differences of opinion about how to manage the case. I’ll be looking forward to getting comments and feedback on this.

The case involved a 14-year-old boy who had been brought into the hospital by his parents, suffering from severe bouts of anxiety that were just almost overwhelming to him. When he was brought in, he was assigned a health care provider who had a West African last name. Prior to meeting the patient, I have to say that the father of this kid told the intake department nurse that he requested someone else. He saw the name – he hadn’t even met the provider – and he said he wanted someone who might be Catholic.

The parents are both from the Dominican Republic. They identified as White, but they appeared to be non-White Latinx to the nurse who was doing some of the initial intake. They got reassigned to a different provider in the department who identified as African American.

The first month of treatment for the young boy went very well, and he seemed to be getting along extremely well with his provider. He was reporting relief to both parents of some of his anxiety, and the provider felt very connected to the child. A good doctor-patient alliance had been formed.

Nevertheless, at the end of the first month, the father connected back to one of the administrators at the hospital and complained, saying he still wanted a different provider. When asked why, he said, “Well, I don’t really want to answer that,” but getting pressed, he basically said he wasn’t comfortable with having an African American doctor take care of his child. He eventually went back to the argument that what he wanted was someone with a Catholic background, although I don’t know that he knew whether this particular provider was religious – Catholic or anything else.

The issue became what to do in the face of these continued demands by the dad for a change. Some people felt that, as the father in charge of the child’s care, if we could accommodate what he wanted in terms of the parents being comfortable, then that’s something we should do. I absolutely did not agree.

My view is that in a situation where a strong provider-patient relationship has been established, where trust is going both ways, where there are no issues coming up between this 14-year-old and the provider, and when a serious mental health issue is being adequately addressed, the patient’s interest must come first.

Once that therapeutic alliance had been established and both the patient and the provider felt satisfied, I don’t think the father’s wishes made any sense. He may have been acting more out of bigotry or just discomfort about difference in terms of who the provider was. I don’t think that’s something that any health system should have to accommodate unless it is getting in the way of patient care.

I hope that we treat all physicians as properly trained to deal with all kinds of patients, regardless of their religion, ethnicity, or skin color. They should have the skills to manage and do well with any patient. There may be situations where it just doesn’t work or where people don’t get along. Yes, I think we then should try, perhaps, to shift the doctor, get a different nurse, or have a different person do an exam. That’s because of the inability to get the patient’s health interests addressed.

Listening to this dad about what he preferred in terms of religion or ethnicity seemed to me to be interfering with medical success. Could I stop him from moving this patient out entirely from the care setting? Probably not, but I think the way to manage this is to try to talk to him – and, by the way, to talk to the mother.

When we did bring the mom into the situation, she was very happy with the health care provider. She didn’t agree with the dad and wanted to have a meeting with the social worker, the dad, and her to get him to get over the worries, concerns, and maybe even biases he was bringing in about the kind of provider he wanted. That’s exactly what we did.

I know that there are many instances where patients may say, “I don’t want a particular doctor or a particular type.” My view is that we shouldn’t accommodate that. We should say that our doctors are trained to help and care for all manner of people. Unless we can think of some reason that there might be a gap or a problem in the actual delivery of the quality of care, we are not going to accommodate racism, bigotry, or bias.

We certainly shouldn’t be accommodating that once a successful therapeutic relationship is established. Even when it’s a child, I would argue that the patient’s best interest has to trump parental desires, parental worries, and parental concerns about the background, ethnicity, and religion of the provider.

Dr. Caplan is director of the division of medical ethics at NYU Langone Medical Center, New York. He disclosed a conflict of interest with Johnson & Johnson.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

I’d like to present you today with a case that raised a large amount of discussion and debate. I got involved as an ethics consultant on the case. I think you’ll find it very interesting and I also think there are going to be some differences of opinion about how to manage the case. I’ll be looking forward to getting comments and feedback on this.

The case involved a 14-year-old boy who had been brought into the hospital by his parents, suffering from severe bouts of anxiety that were just almost overwhelming to him. When he was brought in, he was assigned a health care provider who had a West African last name. Prior to meeting the patient, I have to say that the father of this kid told the intake department nurse that he requested someone else. He saw the name – he hadn’t even met the provider – and he said he wanted someone who might be Catholic.

The parents are both from the Dominican Republic. They identified as White, but they appeared to be non-White Latinx to the nurse who was doing some of the initial intake. They got reassigned to a different provider in the department who identified as African American.

The first month of treatment for the young boy went very well, and he seemed to be getting along extremely well with his provider. He was reporting relief to both parents of some of his anxiety, and the provider felt very connected to the child. A good doctor-patient alliance had been formed.

Nevertheless, at the end of the first month, the father connected back to one of the administrators at the hospital and complained, saying he still wanted a different provider. When asked why, he said, “Well, I don’t really want to answer that,” but getting pressed, he basically said he wasn’t comfortable with having an African American doctor take care of his child. He eventually went back to the argument that what he wanted was someone with a Catholic background, although I don’t know that he knew whether this particular provider was religious – Catholic or anything else.

The issue became what to do in the face of these continued demands by the dad for a change. Some people felt that, as the father in charge of the child’s care, if we could accommodate what he wanted in terms of the parents being comfortable, then that’s something we should do. I absolutely did not agree.

My view is that in a situation where a strong provider-patient relationship has been established, where trust is going both ways, where there are no issues coming up between this 14-year-old and the provider, and when a serious mental health issue is being adequately addressed, the patient’s interest must come first.

Once that therapeutic alliance had been established and both the patient and the provider felt satisfied, I don’t think the father’s wishes made any sense. He may have been acting more out of bigotry or just discomfort about difference in terms of who the provider was. I don’t think that’s something that any health system should have to accommodate unless it is getting in the way of patient care.

I hope that we treat all physicians as properly trained to deal with all kinds of patients, regardless of their religion, ethnicity, or skin color. They should have the skills to manage and do well with any patient. There may be situations where it just doesn’t work or where people don’t get along. Yes, I think we then should try, perhaps, to shift the doctor, get a different nurse, or have a different person do an exam. That’s because of the inability to get the patient’s health interests addressed.

Listening to this dad about what he preferred in terms of religion or ethnicity seemed to me to be interfering with medical success. Could I stop him from moving this patient out entirely from the care setting? Probably not, but I think the way to manage this is to try to talk to him – and, by the way, to talk to the mother.

When we did bring the mom into the situation, she was very happy with the health care provider. She didn’t agree with the dad and wanted to have a meeting with the social worker, the dad, and her to get him to get over the worries, concerns, and maybe even biases he was bringing in about the kind of provider he wanted. That’s exactly what we did.

I know that there are many instances where patients may say, “I don’t want a particular doctor or a particular type.” My view is that we shouldn’t accommodate that. We should say that our doctors are trained to help and care for all manner of people. Unless we can think of some reason that there might be a gap or a problem in the actual delivery of the quality of care, we are not going to accommodate racism, bigotry, or bias.

We certainly shouldn’t be accommodating that once a successful therapeutic relationship is established. Even when it’s a child, I would argue that the patient’s best interest has to trump parental desires, parental worries, and parental concerns about the background, ethnicity, and religion of the provider.

Dr. Caplan is director of the division of medical ethics at NYU Langone Medical Center, New York. He disclosed a conflict of interest with Johnson & Johnson.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

I’d like to present you today with a case that raised a large amount of discussion and debate. I got involved as an ethics consultant on the case. I think you’ll find it very interesting and I also think there are going to be some differences of opinion about how to manage the case. I’ll be looking forward to getting comments and feedback on this.

The case involved a 14-year-old boy who had been brought into the hospital by his parents, suffering from severe bouts of anxiety that were just almost overwhelming to him. When he was brought in, he was assigned a health care provider who had a West African last name. Prior to meeting the patient, I have to say that the father of this kid told the intake department nurse that he requested someone else. He saw the name – he hadn’t even met the provider – and he said he wanted someone who might be Catholic.

The parents are both from the Dominican Republic. They identified as White, but they appeared to be non-White Latinx to the nurse who was doing some of the initial intake. They got reassigned to a different provider in the department who identified as African American.

The first month of treatment for the young boy went very well, and he seemed to be getting along extremely well with his provider. He was reporting relief to both parents of some of his anxiety, and the provider felt very connected to the child. A good doctor-patient alliance had been formed.

Nevertheless, at the end of the first month, the father connected back to one of the administrators at the hospital and complained, saying he still wanted a different provider. When asked why, he said, “Well, I don’t really want to answer that,” but getting pressed, he basically said he wasn’t comfortable with having an African American doctor take care of his child. He eventually went back to the argument that what he wanted was someone with a Catholic background, although I don’t know that he knew whether this particular provider was religious – Catholic or anything else.

The issue became what to do in the face of these continued demands by the dad for a change. Some people felt that, as the father in charge of the child’s care, if we could accommodate what he wanted in terms of the parents being comfortable, then that’s something we should do. I absolutely did not agree.

My view is that in a situation where a strong provider-patient relationship has been established, where trust is going both ways, where there are no issues coming up between this 14-year-old and the provider, and when a serious mental health issue is being adequately addressed, the patient’s interest must come first.

Once that therapeutic alliance had been established and both the patient and the provider felt satisfied, I don’t think the father’s wishes made any sense. He may have been acting more out of bigotry or just discomfort about difference in terms of who the provider was. I don’t think that’s something that any health system should have to accommodate unless it is getting in the way of patient care.

I hope that we treat all physicians as properly trained to deal with all kinds of patients, regardless of their religion, ethnicity, or skin color. They should have the skills to manage and do well with any patient. There may be situations where it just doesn’t work or where people don’t get along. Yes, I think we then should try, perhaps, to shift the doctor, get a different nurse, or have a different person do an exam. That’s because of the inability to get the patient’s health interests addressed.

Listening to this dad about what he preferred in terms of religion or ethnicity seemed to me to be interfering with medical success. Could I stop him from moving this patient out entirely from the care setting? Probably not, but I think the way to manage this is to try to talk to him – and, by the way, to talk to the mother.

When we did bring the mom into the situation, she was very happy with the health care provider. She didn’t agree with the dad and wanted to have a meeting with the social worker, the dad, and her to get him to get over the worries, concerns, and maybe even biases he was bringing in about the kind of provider he wanted. That’s exactly what we did.

I know that there are many instances where patients may say, “I don’t want a particular doctor or a particular type.” My view is that we shouldn’t accommodate that. We should say that our doctors are trained to help and care for all manner of people. Unless we can think of some reason that there might be a gap or a problem in the actual delivery of the quality of care, we are not going to accommodate racism, bigotry, or bias.

We certainly shouldn’t be accommodating that once a successful therapeutic relationship is established. Even when it’s a child, I would argue that the patient’s best interest has to trump parental desires, parental worries, and parental concerns about the background, ethnicity, and religion of the provider.

Dr. Caplan is director of the division of medical ethics at NYU Langone Medical Center, New York. He disclosed a conflict of interest with Johnson & Johnson.

A version of this article first appeared on Medscape.com.

A scientific review by researchers in Spain confirms the negative influence of artificial sweeteners on several primary cardiovascular risk factors. It also shows evidence that these products are not beneficial for controlling excess weight. 

Francisco Gómez-Delgado, MD, PhD, and Pablo Pérez-Martínez, MD, PhD, are members of the Spanish Society of Arteriosclerosis and of the Spanish Society of Internal Medicine. They have coordinated an updated review of the leading scientific evidence surrounding artificial sweeteners: evidence showing that far from positively affecting our health, they have “negative effects for the cardiometabolic system.”

The paper, published in Current Opinion in Cardiology, delves into the consumption of these sweeteners and their negative influence on the development of obesity and of several of the most important cardiometabolic risk factors (hypertension, dyslipidemia, and diabetes).

Globalization and the increase in consumption of ultraprocessed foods have led to a need for greater knowledge on the health impacts of certain nutrients such as artificial sweeteners (nutritive and nonnutritive). This review aims to analyze their role and their effect on cardiometabolic and cardiovascular disease risk.
 

Cardiovascular risk

The detrimental effects of a high-calorie, high-sugar diet have been well established. For this reason, health authorities recommend limiting sugar consumption. The recommendation has led the food industry to develop different artificial sweeteners with specific properties, such as flavor and stability (nutritive artificial sweeteners), and others aimed at limiting sugar in the diet (nonnutritive artificial sweeteners). Recent evidence explores the influence of these two types of artificial sweeteners on cardiovascular disease risk through risk factors such as obesity and type 2 diabetes, among others.

Initially, the consumption of artificial sweeteners was presented as an alternative for reducing calorie intake in the diet as an option for people with excess weight and obesity. However, as this paper explains, the consumption of these artificial sweeteners favors weight gain because of neuroendocrine mechanisms related to satiety that are abnormally activated when artificial sweeteners are consumed.
 

Weight gain

On the other hand, evidence shows that consuming artificial sweeteners does not encourage weight loss. “Quite the contrary,” Dr. Pérez-Martínez, scientific director at the Maimonides Biomedical Research Institute and internist at the University Hospital Reina Sofia, both in Córdoba, told this news organization. “There is evidence showing weight gain resulting from the effect that artificial sweetener consumption has at the neurohormonal level by altering the mechanisms involved in regulating the feeling of satiety.”

However, on the basis of current evidence, sugar cannot be claimed to be less harmful. “What we do know is that in both cases, we should reduce or remove them from our diets and replace them with other healthier alternatives for weight management, such as eating plant-based products or being physically active.”
 

Confronting ignorance 

Nonetheless, these recommendations are conditional, “because the weight of the evidence is not extremely high, since there have not been a whole lot of studies. All nutritional studies must be viewed with caution,” Manuel Anguita, MD, PhD, said in an interview. Dr. Anguita is department head of clinical cardiology at the University Hospital Reina Sofia in Córdoba and past president of the Spanish Society of Cardiology.

“It’s something that should be included within the medical record when you’re assessing cardiovascular risk. In addition to identifying patients who use artificial sweeteners, it’s especially important to emphasize that it’s not an appropriate recommendation for weight management.” Healthier measures include moderate exercise and the Mediterranean diet.

Explaining why this research is valuable, he said, “It’s generally useful because there’s ignorance not only in the population but among physicians as well [about] these negative effects of sweeteners.”
 

Diabetes and metabolic syndrome

Artificial sweeteners cause significant disruptions in the endocrine system, leading our metabolism to function abnormally. The review revealed that consuming artificial sweeteners raises the risk for type 2 diabetes by between 18% and 24% and raises the risk for metabolic syndrome by up to 44%.

Dr. Gómez-Delgado, an internal medicine specialist at the University Hospital of Jaen in Spain and first author of the study, discussed the deleterious effects of sweeteners on metabolism. “On one hand, neurohormonal disorders impact appetite, and the feeling of satiety is abnormally delayed.” On the other hand, “they induce excessive insulin secretion in the pancreas,” which in the long run, encourages metabolic disorders that lead to diabetes. Ultimately, this process produces what we know as “dysbiosis, since our microbiota is unable to process these artificial sweeteners.” Dysbiosis triggers specific pathophysiologic processes that negatively affect cardiometabolic and cardiovascular systems.
 

No differences 

Regarding the type of sweetener, Dr. Gómez-Delgado noted that currently available studies assess the consumption of special dietary products that, in most cases, include various types of artificial sweeteners. “So, it’s not possible to define specific differences between them as to how they impact our health.” Additional studies are needed to confirm this effect at the cardiometabolic level and to analyze the different types of artificial sweeteners individually.

“There’s enough evidence to confirm that consuming artificial sweeteners negatively interferes with our metabolism – especially glucose metabolism – and increases the risk of developing diabetes,” said Dr. Gómez-Delgado.
 

High-sodium drinks

When it comes to the influence of artificial sweeteners on hypertension, “there is no single explanation. The World Health Organization already discussed this issue 4-5 years ago, not only due to their carcinogenic risk, but also due to this cardiovascular risk in terms of a lack of control of obesity, diabetes, and hypertension,” said Dr. Anguita.

Another important point “is that this is not in reference to the sweeteners themselves, but to soft drinks containing those components, which is where we have more studies,” he added. There are two factors explaining this increase in hypertension, which poses a problem at the population level, with medium- to long-term follow-up. “The sugary beverages that we mentioned have a higher sodium content. That is, the sweeteners add this element, which is a factor that’s directly linked to the increase in blood pressure levels.” Another factor that can influence blood pressure is “the increase in insulin secretion that has been described as resulting from sweeteners. In the medium and long term, this is associated with increased blood pressure levels.”
 

Cardiovascular risk factor?

Are artificial sweeteners considered to be a new cardiovascular risk factor? “What they really do is increase the incidence of the other classic risk factors,” including obesity, said Dr. Anguita. It has been shown that artificial sweeteners don’t reduce obesity when used continuously. Nonetheless, “there is still not enough evidence to view it in the same light as the classic risk factors,” added Dr. Anguita. However, it is a factor that can clearly worsen the control of the other factors. Therefore, “it’s appropriate to sound an alarm and explain that it’s not the best way to lose weight; there are many other healthier choices.”

“We need more robust evidence to take a clear position on the use of this type of sweetener and its detrimental effect on health. Meanwhile, it would be ideal to limit their consumption or even avoid adding artificial sweeteners to coffee or teas,” added Dr. Pérez-Martínez.
 

Regulate consumption 

Dr. Pérez-Martínez mentioned that the measures proposed to regulate the consumption of artificial sweeteners and to modify the current legislation must involve “minimizing the consumption of these special dietary products as much as possible and even avoiding adding these artificial sweeteners to the foods that we consume; for example, to coffee and tea.” On the other hand, “we must provide consumers with information that is as clear and simple as possible regarding the composition of the food they consume and how it impacts their health.”

However, “we need more evidence to be able to take a clear position on what type of sweeteners we can consume in our diet and also to what extent we should limit their presence in the foods we consume,” said Dr. Pérez-Martínez. 

Last, “most of the evidence is from short-term observational studies that assess frequencies and patterns of consumption of foods containing these artificial sweeteners.” Of course, “we need studies that specifically analyze their effects at the metabolic level as well as longer-term studies where the nutritional follow-up of participants is more accurate and rigorous, especially when it comes to the consumption of this type of food,” concluded Dr. Gómez-Delgado.

This article was translated from the Medscape Spanish Edition. A version appeared on Medscape.com.

A scientific review by researchers in Spain confirms the negative influence of artificial sweeteners on several primary cardiovascular risk factors. It also shows evidence that these products are not beneficial for controlling excess weight. 

Francisco Gómez-Delgado, MD, PhD, and Pablo Pérez-Martínez, MD, PhD, are members of the Spanish Society of Arteriosclerosis and of the Spanish Society of Internal Medicine. They have coordinated an updated review of the leading scientific evidence surrounding artificial sweeteners: evidence showing that far from positively affecting our health, they have “negative effects for the cardiometabolic system.”

The paper, published in Current Opinion in Cardiology, delves into the consumption of these sweeteners and their negative influence on the development of obesity and of several of the most important cardiometabolic risk factors (hypertension, dyslipidemia, and diabetes).

Globalization and the increase in consumption of ultraprocessed foods have led to a need for greater knowledge on the health impacts of certain nutrients such as artificial sweeteners (nutritive and nonnutritive). This review aims to analyze their role and their effect on cardiometabolic and cardiovascular disease risk.
 

Cardiovascular risk

The detrimental effects of a high-calorie, high-sugar diet have been well established. For this reason, health authorities recommend limiting sugar consumption. The recommendation has led the food industry to develop different artificial sweeteners with specific properties, such as flavor and stability (nutritive artificial sweeteners), and others aimed at limiting sugar in the diet (nonnutritive artificial sweeteners). Recent evidence explores the influence of these two types of artificial sweeteners on cardiovascular disease risk through risk factors such as obesity and type 2 diabetes, among others.

Initially, the consumption of artificial sweeteners was presented as an alternative for reducing calorie intake in the diet as an option for people with excess weight and obesity. However, as this paper explains, the consumption of these artificial sweeteners favors weight gain because of neuroendocrine mechanisms related to satiety that are abnormally activated when artificial sweeteners are consumed.
 

Weight gain

On the other hand, evidence shows that consuming artificial sweeteners does not encourage weight loss. “Quite the contrary,” Dr. Pérez-Martínez, scientific director at the Maimonides Biomedical Research Institute and internist at the University Hospital Reina Sofia, both in Córdoba, told this news organization. “There is evidence showing weight gain resulting from the effect that artificial sweetener consumption has at the neurohormonal level by altering the mechanisms involved in regulating the feeling of satiety.”

However, on the basis of current evidence, sugar cannot be claimed to be less harmful. “What we do know is that in both cases, we should reduce or remove them from our diets and replace them with other healthier alternatives for weight management, such as eating plant-based products or being physically active.”
 

Confronting ignorance 

Nonetheless, these recommendations are conditional, “because the weight of the evidence is not extremely high, since there have not been a whole lot of studies. All nutritional studies must be viewed with caution,” Manuel Anguita, MD, PhD, said in an interview. Dr. Anguita is department head of clinical cardiology at the University Hospital Reina Sofia in Córdoba and past president of the Spanish Society of Cardiology.

“It’s something that should be included within the medical record when you’re assessing cardiovascular risk. In addition to identifying patients who use artificial sweeteners, it’s especially important to emphasize that it’s not an appropriate recommendation for weight management.” Healthier measures include moderate exercise and the Mediterranean diet.

Explaining why this research is valuable, he said, “It’s generally useful because there’s ignorance not only in the population but among physicians as well [about] these negative effects of sweeteners.”
 

Diabetes and metabolic syndrome

Artificial sweeteners cause significant disruptions in the endocrine system, leading our metabolism to function abnormally. The review revealed that consuming artificial sweeteners raises the risk for type 2 diabetes by between 18% and 24% and raises the risk for metabolic syndrome by up to 44%.

Dr. Gómez-Delgado, an internal medicine specialist at the University Hospital of Jaen in Spain and first author of the study, discussed the deleterious effects of sweeteners on metabolism. “On one hand, neurohormonal disorders impact appetite, and the feeling of satiety is abnormally delayed.” On the other hand, “they induce excessive insulin secretion in the pancreas,” which in the long run, encourages metabolic disorders that lead to diabetes. Ultimately, this process produces what we know as “dysbiosis, since our microbiota is unable to process these artificial sweeteners.” Dysbiosis triggers specific pathophysiologic processes that negatively affect cardiometabolic and cardiovascular systems.
 

No differences 

Regarding the type of sweetener, Dr. Gómez-Delgado noted that currently available studies assess the consumption of special dietary products that, in most cases, include various types of artificial sweeteners. “So, it’s not possible to define specific differences between them as to how they impact our health.” Additional studies are needed to confirm this effect at the cardiometabolic level and to analyze the different types of artificial sweeteners individually.

“There’s enough evidence to confirm that consuming artificial sweeteners negatively interferes with our metabolism – especially glucose metabolism – and increases the risk of developing diabetes,” said Dr. Gómez-Delgado.
 

High-sodium drinks

When it comes to the influence of artificial sweeteners on hypertension, “there is no single explanation. The World Health Organization already discussed this issue 4-5 years ago, not only due to their carcinogenic risk, but also due to this cardiovascular risk in terms of a lack of control of obesity, diabetes, and hypertension,” said Dr. Anguita.

Another important point “is that this is not in reference to the sweeteners themselves, but to soft drinks containing those components, which is where we have more studies,” he added. There are two factors explaining this increase in hypertension, which poses a problem at the population level, with medium- to long-term follow-up. “The sugary beverages that we mentioned have a higher sodium content. That is, the sweeteners add this element, which is a factor that’s directly linked to the increase in blood pressure levels.” Another factor that can influence blood pressure is “the increase in insulin secretion that has been described as resulting from sweeteners. In the medium and long term, this is associated with increased blood pressure levels.”
 

Cardiovascular risk factor?

Are artificial sweeteners considered to be a new cardiovascular risk factor? “What they really do is increase the incidence of the other classic risk factors,” including obesity, said Dr. Anguita. It has been shown that artificial sweeteners don’t reduce obesity when used continuously. Nonetheless, “there is still not enough evidence to view it in the same light as the classic risk factors,” added Dr. Anguita. However, it is a factor that can clearly worsen the control of the other factors. Therefore, “it’s appropriate to sound an alarm and explain that it’s not the best way to lose weight; there are many other healthier choices.”

“We need more robust evidence to take a clear position on the use of this type of sweetener and its detrimental effect on health. Meanwhile, it would be ideal to limit their consumption or even avoid adding artificial sweeteners to coffee or teas,” added Dr. Pérez-Martínez.
 

Regulate consumption 

Dr. Pérez-Martínez mentioned that the measures proposed to regulate the consumption of artificial sweeteners and to modify the current legislation must involve “minimizing the consumption of these special dietary products as much as possible and even avoiding adding these artificial sweeteners to the foods that we consume; for example, to coffee and tea.” On the other hand, “we must provide consumers with information that is as clear and simple as possible regarding the composition of the food they consume and how it impacts their health.”

However, “we need more evidence to be able to take a clear position on what type of sweeteners we can consume in our diet and also to what extent we should limit their presence in the foods we consume,” said Dr. Pérez-Martínez. 

Last, “most of the evidence is from short-term observational studies that assess frequencies and patterns of consumption of foods containing these artificial sweeteners.” Of course, “we need studies that specifically analyze their effects at the metabolic level as well as longer-term studies where the nutritional follow-up of participants is more accurate and rigorous, especially when it comes to the consumption of this type of food,” concluded Dr. Gómez-Delgado.

This article was translated from the Medscape Spanish Edition. A version appeared on Medscape.com.

A scientific review by researchers in Spain confirms the negative influence of artificial sweeteners on several primary cardiovascular risk factors. It also shows evidence that these products are not beneficial for controlling excess weight. 

Francisco Gómez-Delgado, MD, PhD, and Pablo Pérez-Martínez, MD, PhD, are members of the Spanish Society of Arteriosclerosis and of the Spanish Society of Internal Medicine. They have coordinated an updated review of the leading scientific evidence surrounding artificial sweeteners: evidence showing that far from positively affecting our health, they have “negative effects for the cardiometabolic system.”

The paper, published in Current Opinion in Cardiology, delves into the consumption of these sweeteners and their negative influence on the development of obesity and of several of the most important cardiometabolic risk factors (hypertension, dyslipidemia, and diabetes).

Globalization and the increase in consumption of ultraprocessed foods have led to a need for greater knowledge on the health impacts of certain nutrients such as artificial sweeteners (nutritive and nonnutritive). This review aims to analyze their role and their effect on cardiometabolic and cardiovascular disease risk.
 

Cardiovascular risk

The detrimental effects of a high-calorie, high-sugar diet have been well established. For this reason, health authorities recommend limiting sugar consumption. The recommendation has led the food industry to develop different artificial sweeteners with specific properties, such as flavor and stability (nutritive artificial sweeteners), and others aimed at limiting sugar in the diet (nonnutritive artificial sweeteners). Recent evidence explores the influence of these two types of artificial sweeteners on cardiovascular disease risk through risk factors such as obesity and type 2 diabetes, among others.

Initially, the consumption of artificial sweeteners was presented as an alternative for reducing calorie intake in the diet as an option for people with excess weight and obesity. However, as this paper explains, the consumption of these artificial sweeteners favors weight gain because of neuroendocrine mechanisms related to satiety that are abnormally activated when artificial sweeteners are consumed.
 

Weight gain

On the other hand, evidence shows that consuming artificial sweeteners does not encourage weight loss. “Quite the contrary,” Dr. Pérez-Martínez, scientific director at the Maimonides Biomedical Research Institute and internist at the University Hospital Reina Sofia, both in Córdoba, told this news organization. “There is evidence showing weight gain resulting from the effect that artificial sweetener consumption has at the neurohormonal level by altering the mechanisms involved in regulating the feeling of satiety.”

However, on the basis of current evidence, sugar cannot be claimed to be less harmful. “What we do know is that in both cases, we should reduce or remove them from our diets and replace them with other healthier alternatives for weight management, such as eating plant-based products or being physically active.”
 

Confronting ignorance 

Nonetheless, these recommendations are conditional, “because the weight of the evidence is not extremely high, since there have not been a whole lot of studies. All nutritional studies must be viewed with caution,” Manuel Anguita, MD, PhD, said in an interview. Dr. Anguita is department head of clinical cardiology at the University Hospital Reina Sofia in Córdoba and past president of the Spanish Society of Cardiology.

“It’s something that should be included within the medical record when you’re assessing cardiovascular risk. In addition to identifying patients who use artificial sweeteners, it’s especially important to emphasize that it’s not an appropriate recommendation for weight management.” Healthier measures include moderate exercise and the Mediterranean diet.

Explaining why this research is valuable, he said, “It’s generally useful because there’s ignorance not only in the population but among physicians as well [about] these negative effects of sweeteners.”
 

Diabetes and metabolic syndrome

Artificial sweeteners cause significant disruptions in the endocrine system, leading our metabolism to function abnormally. The review revealed that consuming artificial sweeteners raises the risk for type 2 diabetes by between 18% and 24% and raises the risk for metabolic syndrome by up to 44%.

Dr. Gómez-Delgado, an internal medicine specialist at the University Hospital of Jaen in Spain and first author of the study, discussed the deleterious effects of sweeteners on metabolism. “On one hand, neurohormonal disorders impact appetite, and the feeling of satiety is abnormally delayed.” On the other hand, “they induce excessive insulin secretion in the pancreas,” which in the long run, encourages metabolic disorders that lead to diabetes. Ultimately, this process produces what we know as “dysbiosis, since our microbiota is unable to process these artificial sweeteners.” Dysbiosis triggers specific pathophysiologic processes that negatively affect cardiometabolic and cardiovascular systems.
 

No differences 

Regarding the type of sweetener, Dr. Gómez-Delgado noted that currently available studies assess the consumption of special dietary products that, in most cases, include various types of artificial sweeteners. “So, it’s not possible to define specific differences between them as to how they impact our health.” Additional studies are needed to confirm this effect at the cardiometabolic level and to analyze the different types of artificial sweeteners individually.

“There’s enough evidence to confirm that consuming artificial sweeteners negatively interferes with our metabolism – especially glucose metabolism – and increases the risk of developing diabetes,” said Dr. Gómez-Delgado.
 

High-sodium drinks

When it comes to the influence of artificial sweeteners on hypertension, “there is no single explanation. The World Health Organization already discussed this issue 4-5 years ago, not only due to their carcinogenic risk, but also due to this cardiovascular risk in terms of a lack of control of obesity, diabetes, and hypertension,” said Dr. Anguita.

Another important point “is that this is not in reference to the sweeteners themselves, but to soft drinks containing those components, which is where we have more studies,” he added. There are two factors explaining this increase in hypertension, which poses a problem at the population level, with medium- to long-term follow-up. “The sugary beverages that we mentioned have a higher sodium content. That is, the sweeteners add this element, which is a factor that’s directly linked to the increase in blood pressure levels.” Another factor that can influence blood pressure is “the increase in insulin secretion that has been described as resulting from sweeteners. In the medium and long term, this is associated with increased blood pressure levels.”
 

Cardiovascular risk factor?

Are artificial sweeteners considered to be a new cardiovascular risk factor? “What they really do is increase the incidence of the other classic risk factors,” including obesity, said Dr. Anguita. It has been shown that artificial sweeteners don’t reduce obesity when used continuously. Nonetheless, “there is still not enough evidence to view it in the same light as the classic risk factors,” added Dr. Anguita. However, it is a factor that can clearly worsen the control of the other factors. Therefore, “it’s appropriate to sound an alarm and explain that it’s not the best way to lose weight; there are many other healthier choices.”

“We need more robust evidence to take a clear position on the use of this type of sweetener and its detrimental effect on health. Meanwhile, it would be ideal to limit their consumption or even avoid adding artificial sweeteners to coffee or teas,” added Dr. Pérez-Martínez.
 

Regulate consumption 

Dr. Pérez-Martínez mentioned that the measures proposed to regulate the consumption of artificial sweeteners and to modify the current legislation must involve “minimizing the consumption of these special dietary products as much as possible and even avoiding adding these artificial sweeteners to the foods that we consume; for example, to coffee and tea.” On the other hand, “we must provide consumers with information that is as clear and simple as possible regarding the composition of the food they consume and how it impacts their health.”

However, “we need more evidence to be able to take a clear position on what type of sweeteners we can consume in our diet and also to what extent we should limit their presence in the foods we consume,” said Dr. Pérez-Martínez. 

Last, “most of the evidence is from short-term observational studies that assess frequencies and patterns of consumption of foods containing these artificial sweeteners.” Of course, “we need studies that specifically analyze their effects at the metabolic level as well as longer-term studies where the nutritional follow-up of participants is more accurate and rigorous, especially when it comes to the consumption of this type of food,” concluded Dr. Gómez-Delgado.

This article was translated from the Medscape Spanish Edition. A version appeared on Medscape.com.

An epidemiologic study of children aged 2 months to 5.5 years using data from the French national birth cohort (ELFE) reveals an increased risk of food allergies linked to a delayed introduction of major allergenic foods. These findings were published in Allergy.

Launched in April 2011, the French ELFE study aims to monitor children from birth to adulthood to better understand the factors from the intrauterine period to adolescence that affect their development, health, social skills, and school career. Thanks to this cohort, a team of scientists has reviewed the relationship between complementary feeding practices and allergies in French children.

The study focused on 6,662 children who had no signs of an allergic reaction before 2 months of age. Data on feeding practices were collected monthly from ages 3 months to 10 months. Their age at complementary feeding introduction was calculated, and a food diversity score was determined at 8 and 10 months. The number of major allergenic foods (out of eggs, fish, wheat, and dairy products) not introduced at 8 and 10 months was also determined. Allergic diseases (food allergy, eczema, asthma, and rhinoconjunctivitis) were reported by parents at 2 months and at 1, 2, 3.5, and 5.5 years.

Initially, scientists determined that just 62% of children began complementary feeding in the recommended age window, which is between ages 4 months and 6 months. They then closely studied the link between delayed introduction of major allergenic foods and the risk of food allergies. They saw that for 1 in 10 children, at least two major allergens, from eggs, fish, wheat, and dairy products, had still not been introduced into the diet of infants by the age of 10 months. Now, these children have a risk of developing a food allergy before the age of 5.5 years that is two times greater than that of children in whom the four major allergens were introduced before the age of 10 months.

These findings therefore confirm the importance of not delaying the introduction of major food allergens to prevent the occurrence of childhood allergic diseases. They provide convincing arguments in support of new recommendations made by the French pediatric and allergy societies as well as those issued by Public Health France.
 

ELFE: The first cohort to follow children from birth to adulthood

ELFE is the first longitudinal nationwide French study dedicated to monitoring children from birth to adulthood. More than 18,000 children born in metropolitan France in 2011 were included in this study, which represents 1 in 50 children born in 2011. From the time that researchers first met the families in the maternity ward, the parents who agreed to participate in this great scientific adventure have been questioned at regular intervals to better understand how environment, family members, and living conditions affect the development, health, and socialization of children.

This article was translated from the Medscape French Edition. A version of this article first appeared on Medscape.com.

An epidemiologic study of children aged 2 months to 5.5 years using data from the French national birth cohort (ELFE) reveals an increased risk of food allergies linked to a delayed introduction of major allergenic foods. These findings were published in Allergy.

Launched in April 2011, the French ELFE study aims to monitor children from birth to adulthood to better understand the factors from the intrauterine period to adolescence that affect their development, health, social skills, and school career. Thanks to this cohort, a team of scientists has reviewed the relationship between complementary feeding practices and allergies in French children.

The study focused on 6,662 children who had no signs of an allergic reaction before 2 months of age. Data on feeding practices were collected monthly from ages 3 months to 10 months. Their age at complementary feeding introduction was calculated, and a food diversity score was determined at 8 and 10 months. The number of major allergenic foods (out of eggs, fish, wheat, and dairy products) not introduced at 8 and 10 months was also determined. Allergic diseases (food allergy, eczema, asthma, and rhinoconjunctivitis) were reported by parents at 2 months and at 1, 2, 3.5, and 5.5 years.

Initially, scientists determined that just 62% of children began complementary feeding in the recommended age window, which is between ages 4 months and 6 months. They then closely studied the link between delayed introduction of major allergenic foods and the risk of food allergies. They saw that for 1 in 10 children, at least two major allergens, from eggs, fish, wheat, and dairy products, had still not been introduced into the diet of infants by the age of 10 months. Now, these children have a risk of developing a food allergy before the age of 5.5 years that is two times greater than that of children in whom the four major allergens were introduced before the age of 10 months.

These findings therefore confirm the importance of not delaying the introduction of major food allergens to prevent the occurrence of childhood allergic diseases. They provide convincing arguments in support of new recommendations made by the French pediatric and allergy societies as well as those issued by Public Health France.
 

ELFE: The first cohort to follow children from birth to adulthood

ELFE is the first longitudinal nationwide French study dedicated to monitoring children from birth to adulthood. More than 18,000 children born in metropolitan France in 2011 were included in this study, which represents 1 in 50 children born in 2011. From the time that researchers first met the families in the maternity ward, the parents who agreed to participate in this great scientific adventure have been questioned at regular intervals to better understand how environment, family members, and living conditions affect the development, health, and socialization of children.

This article was translated from the Medscape French Edition. A version of this article first appeared on Medscape.com.

An epidemiologic study of children aged 2 months to 5.5 years using data from the French national birth cohort (ELFE) reveals an increased risk of food allergies linked to a delayed introduction of major allergenic foods. These findings were published in Allergy.

Launched in April 2011, the French ELFE study aims to monitor children from birth to adulthood to better understand the factors from the intrauterine period to adolescence that affect their development, health, social skills, and school career. Thanks to this cohort, a team of scientists has reviewed the relationship between complementary feeding practices and allergies in French children.

The study focused on 6,662 children who had no signs of an allergic reaction before 2 months of age. Data on feeding practices were collected monthly from ages 3 months to 10 months. Their age at complementary feeding introduction was calculated, and a food diversity score was determined at 8 and 10 months. The number of major allergenic foods (out of eggs, fish, wheat, and dairy products) not introduced at 8 and 10 months was also determined. Allergic diseases (food allergy, eczema, asthma, and rhinoconjunctivitis) were reported by parents at 2 months and at 1, 2, 3.5, and 5.5 years.

Initially, scientists determined that just 62% of children began complementary feeding in the recommended age window, which is between ages 4 months and 6 months. They then closely studied the link between delayed introduction of major allergenic foods and the risk of food allergies. They saw that for 1 in 10 children, at least two major allergens, from eggs, fish, wheat, and dairy products, had still not been introduced into the diet of infants by the age of 10 months. Now, these children have a risk of developing a food allergy before the age of 5.5 years that is two times greater than that of children in whom the four major allergens were introduced before the age of 10 months.

These findings therefore confirm the importance of not delaying the introduction of major food allergens to prevent the occurrence of childhood allergic diseases. They provide convincing arguments in support of new recommendations made by the French pediatric and allergy societies as well as those issued by Public Health France.
 

ELFE: The first cohort to follow children from birth to adulthood

ELFE is the first longitudinal nationwide French study dedicated to monitoring children from birth to adulthood. More than 18,000 children born in metropolitan France in 2011 were included in this study, which represents 1 in 50 children born in 2011. From the time that researchers first met the families in the maternity ward, the parents who agreed to participate in this great scientific adventure have been questioned at regular intervals to better understand how environment, family members, and living conditions affect the development, health, and socialization of children.

This article was translated from the Medscape French Edition. A version of this article first appeared on Medscape.com.

The long-awaited vaccine for respiratory syncytial virus (RSV) that can be given during pregnancy has been approved by the Food and Drug Administration.

The vaccine, known as Abrysvo, can be given between weeks 32 and 36 of pregnancy and is designed to protect infants from the virus from birth to 6 months of age.

Administered as a single-dose, intramuscular injection, the FDA approved Abrysvo at the end of May for the prevention of lower respiratory tract illness caused by RSV in people aged 60 years and older.

However, “RSV is a common cause of illness in children, and infants are among those at highest risk for severe disease, which can lead to hospitalization,” Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research, pointed out in a news release. “This approval provides an option for health care providers and pregnant individuals to protect infants from this potentially life-threatening disease.”

Most children are infected with the contagious virus at least once by the time they reach age 2 years. Very young children are at particular risk of severe complications, such as pneumonia or bronchitis, and in clinical trials, the new vaccine reduced that risk by up to 82%.

Before the vaccine became available, up to 3% of infants infected with RSV needed to be hospitalized, according to the Centers for Disease Control and Prevention. In the hospital, treatment typically includes oxygen, intravenous fluids, and mechanical ventilation.

RSV often causes common cold symptoms, but the virus poses the risk of severe complications that can lead to death among young children and older people. The CDC estimates 100-300 deaths of children younger than 5 years and 6,000-10,000 deaths of people aged 65 years and older are linked to RSV annually.

This is also the first year that an antibody shot is available to be given after birth to prevent severe RSV in infants younger than 1 year.

In its approval announcement, the FDA pointed out that preeclampsia occurred in 1.8% of pregnancies after Abrysvo, compared with 1.4% of those who received placebo. The FDA also reported that, in infants, low birth weight and jaundice occurred at a higher rate among the pregnant Abrysvo recipients, compared with the placebo group.

Studies have also shown that pregnant vaccine recipients experienced preterm birth at a rate of 5.7%, compared with a rate of 4.7% among those who received placebo. The FDA called the difference “a numerical imbalance” but said in the approval announcement that a “causal relationship” could not be established.

The FDA also noted that people already at high risk of preterm birth were excluded from clinical trials and that Pfizer must conduct ongoing studies to monitor the risk of preeclampsia as well as preterm birth.

A version of this article first appeared on Medscape.com.

The long-awaited vaccine for respiratory syncytial virus (RSV) that can be given during pregnancy has been approved by the Food and Drug Administration.

The vaccine, known as Abrysvo, can be given between weeks 32 and 36 of pregnancy and is designed to protect infants from the virus from birth to 6 months of age.

Administered as a single-dose, intramuscular injection, the FDA approved Abrysvo at the end of May for the prevention of lower respiratory tract illness caused by RSV in people aged 60 years and older.

However, “RSV is a common cause of illness in children, and infants are among those at highest risk for severe disease, which can lead to hospitalization,” Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research, pointed out in a news release. “This approval provides an option for health care providers and pregnant individuals to protect infants from this potentially life-threatening disease.”

Most children are infected with the contagious virus at least once by the time they reach age 2 years. Very young children are at particular risk of severe complications, such as pneumonia or bronchitis, and in clinical trials, the new vaccine reduced that risk by up to 82%.

Before the vaccine became available, up to 3% of infants infected with RSV needed to be hospitalized, according to the Centers for Disease Control and Prevention. In the hospital, treatment typically includes oxygen, intravenous fluids, and mechanical ventilation.

RSV often causes common cold symptoms, but the virus poses the risk of severe complications that can lead to death among young children and older people. The CDC estimates 100-300 deaths of children younger than 5 years and 6,000-10,000 deaths of people aged 65 years and older are linked to RSV annually.

This is also the first year that an antibody shot is available to be given after birth to prevent severe RSV in infants younger than 1 year.

In its approval announcement, the FDA pointed out that preeclampsia occurred in 1.8% of pregnancies after Abrysvo, compared with 1.4% of those who received placebo. The FDA also reported that, in infants, low birth weight and jaundice occurred at a higher rate among the pregnant Abrysvo recipients, compared with the placebo group.

Studies have also shown that pregnant vaccine recipients experienced preterm birth at a rate of 5.7%, compared with a rate of 4.7% among those who received placebo. The FDA called the difference “a numerical imbalance” but said in the approval announcement that a “causal relationship” could not be established.

The FDA also noted that people already at high risk of preterm birth were excluded from clinical trials and that Pfizer must conduct ongoing studies to monitor the risk of preeclampsia as well as preterm birth.

A version of this article first appeared on Medscape.com.

The long-awaited vaccine for respiratory syncytial virus (RSV) that can be given during pregnancy has been approved by the Food and Drug Administration.

The vaccine, known as Abrysvo, can be given between weeks 32 and 36 of pregnancy and is designed to protect infants from the virus from birth to 6 months of age.

Administered as a single-dose, intramuscular injection, the FDA approved Abrysvo at the end of May for the prevention of lower respiratory tract illness caused by RSV in people aged 60 years and older.

However, “RSV is a common cause of illness in children, and infants are among those at highest risk for severe disease, which can lead to hospitalization,” Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research, pointed out in a news release. “This approval provides an option for health care providers and pregnant individuals to protect infants from this potentially life-threatening disease.”

Most children are infected with the contagious virus at least once by the time they reach age 2 years. Very young children are at particular risk of severe complications, such as pneumonia or bronchitis, and in clinical trials, the new vaccine reduced that risk by up to 82%.

Before the vaccine became available, up to 3% of infants infected with RSV needed to be hospitalized, according to the Centers for Disease Control and Prevention. In the hospital, treatment typically includes oxygen, intravenous fluids, and mechanical ventilation.

RSV often causes common cold symptoms, but the virus poses the risk of severe complications that can lead to death among young children and older people. The CDC estimates 100-300 deaths of children younger than 5 years and 6,000-10,000 deaths of people aged 65 years and older are linked to RSV annually.

This is also the first year that an antibody shot is available to be given after birth to prevent severe RSV in infants younger than 1 year.

In its approval announcement, the FDA pointed out that preeclampsia occurred in 1.8% of pregnancies after Abrysvo, compared with 1.4% of those who received placebo. The FDA also reported that, in infants, low birth weight and jaundice occurred at a higher rate among the pregnant Abrysvo recipients, compared with the placebo group.

Studies have also shown that pregnant vaccine recipients experienced preterm birth at a rate of 5.7%, compared with a rate of 4.7% among those who received placebo. The FDA called the difference “a numerical imbalance” but said in the approval announcement that a “causal relationship” could not be established.

The FDA also noted that people already at high risk of preterm birth were excluded from clinical trials and that Pfizer must conduct ongoing studies to monitor the risk of preeclampsia as well as preterm birth.

A version of this article first appeared on Medscape.com.

A type of gene therapy that reboots the brain’s reward system could curb drinking in those with severe alcohol use disorder. 

Researchers from Oregon Health & Science University, Portland implanted the therapy directly into the brains of rhesus monkeys that had been conditioned to drink 8-10 alcoholic drinks a day. A harmless virus that carried a specific gene was placed in the region of the brain that regulates dopamine, which provides feelings of reward and pleasure. 

“We wanted to see if we could normalize the dopamine in these motivational areas – if, indeed, motivation to overdrink or drink heavily would be mitigated,” said study author Kathleen Grant, PhD, a professor and chief of the division of neuroscience at the university’s Oregon National Primate Research Center.

The need for new alcohol use disorder treatments may be more dire than ever. Alcohol-related deaths in the United States increased dramatically between 2007 and 2020, especially in women, according to research published in the journal  JAMA Network Open. The next year, they spiked again, to 108,791 alcohol-related deaths in 2021 alone, according to the National Institutes of Health. That’s slightly more than the number of drug overdoses recorded in 2021.

For the 29.5 million Americans with alcohol use disorder, also known as alcohol abuse or dependence, the road to recovery can be challenging. One reason is that the reward systems in their brains are working against them. 

At the first taste of alcohol, the body releases dopamine. But if a person drinks too much for too long, the brain reduces dopamine production and even more alcohol is needed to feel good again.

The gene researchers placed in the monkeys’ brains is called glial-derived neurotrophic factor. It is a growth factor, stimulating cells to multiply. It may help improve function of brain cells that synthesize dopamine, effectively resetting the whole system and reducing the urge to drink. 

The study was surprisingly successful. Compared with primates that received a placebo, those that received the growth factor gene decreased their drinking by about 90%. They basically quit drinking, while the primates that got the placebo resumed their habit. 

A similar procedure is already used in patients with Parkinson’s disease. But more animal studies, and human clinical trials, would be needed before this therapy could be used in humans with alcohol use disorder. This invasive treatment involves brain surgery, which has risks, so it would likely be reserved for those with the most severe, dangerous drinking habits.

“I think it’d be appropriate for individuals where other treatment modalities just weren’t effective, and they’re worried for their lives,” Dr. Grant said.
 

Alcohol use disorder treatments

Today, treatment for alcohol use disorder ranges from a brief conversation with a health care provider, in mild cases, to psychiatric treatment or medication in moderate or severe cases.

There are four Food and Drug Administration–approved treatments for alcohol use disorder and a few more medications that health care providers can prescribe off label.

“They’re not widely used,” said Henry Kranzler, MD, a professor of psychiatry and director of the Center for Studies of Addiction at the University of Pennsylvania, Philadelphia. “They’re shockingly underutilized.”

One reason: Just 4.6% of people with alcohol use disorder seek treatment each year, according to NIH data. 

“Some of the issues include the ubiquity of alcohol, and its acceptance in American culture – and the fact that that makes it difficult for people to acknowledge that they have a problem with alcohol,” said Dr. Kranzler.

But another problem is that many health care professionals don’t recognize and treat alcohol use disorder in patients who do seek care. Those seeking treatment for alcohol use disorder can find a qualified provider at the American Academy of Addiction Psychiatry or American Society of Addiction Medicine directories.
 

The future of treatment

Ongoing research could lead to more treatments, and make them more available and more appealing.

Unlike many other drugs that work on a single receptor in the body – like opioids that target opioid receptors, or nicotine, which targets choline receptors – alcohol affects many different receptors, said Robert Swift, MD, PhD, a professor of psychiatry and human behavior at Brown University, Providence, R.I. It also penetrates cells at high doses.

“There are so many different effects of alcohol, which makes it very hard to treat,” he said. “But on the other hand, it gives us an advantage, and there are probably different points that we can attack.”

Other exciting developments are underway, although more research, including clinical trials in humans, is needed before they arrive.

Some of the most promising:

• Hallucinogens. In the 1950s, before they became illegal, these drugs helped people drink less. Even Bill Wilson, cofounder of Alcoholics Anonymous, used hallucinogenic treatment in his recovery; it helped him envision overcoming a challenge. Today, there is renewed interest in hallucinogens for alcohol use disorder. In a study published in , people with alcohol use disorder who were given the hallucinogen psilocybin along with therapy spent fewer days drinking heavily over the following 32 weeks than people who received a different medication. Don’t try to do this yourself, though. “It’s not just taking a hallucinogen and having a trip,” Dr. Swift said. “It’s a therapy-guided session, so it’s a combination of using the hallucinogenic substance with a skilled therapist, and sometimes two skilled therapists, helping to guide the experience.”
• Epigenetic editing. Alcohol exposure can affect the activity of a gene in the amygdala, a brain region involved in emotional processing.  found that, by editing that gene in rats through an intravenous line of genetic material, they reduced the rodents’ drinking and anxiety. 
• Oxytocin. The so-called love hormone could help reset the dopamine system to make alcohol less appealing. “There are oxytocin receptors on dopamine neurons, and oxytocin makes your dopamine system more effective,” Dr. Swift said. In a  from the Medical University of South Carolina, Charleston, mice injected with oxytocin didn’t drink during a stressful situation that could have otherwise led to relapse.
• Ghrelin. This stomach hormone could help curb drinking. In a study published in , mice that received drugs that increased ghrelin reduced their alcohol intake.

A version of this article first appeared on WebMD.com.

A type of gene therapy that reboots the brain’s reward system could curb drinking in those with severe alcohol use disorder. 

Researchers from Oregon Health & Science University, Portland implanted the therapy directly into the brains of rhesus monkeys that had been conditioned to drink 8-10 alcoholic drinks a day. A harmless virus that carried a specific gene was placed in the region of the brain that regulates dopamine, which provides feelings of reward and pleasure. 

“We wanted to see if we could normalize the dopamine in these motivational areas – if, indeed, motivation to overdrink or drink heavily would be mitigated,” said study author Kathleen Grant, PhD, a professor and chief of the division of neuroscience at the university’s Oregon National Primate Research Center.

The need for new alcohol use disorder treatments may be more dire than ever. Alcohol-related deaths in the United States increased dramatically between 2007 and 2020, especially in women, according to research published in the journal  JAMA Network Open. The next year, they spiked again, to 108,791 alcohol-related deaths in 2021 alone, according to the National Institutes of Health. That’s slightly more than the number of drug overdoses recorded in 2021.

For the 29.5 million Americans with alcohol use disorder, also known as alcohol abuse or dependence, the road to recovery can be challenging. One reason is that the reward systems in their brains are working against them. 

At the first taste of alcohol, the body releases dopamine. But if a person drinks too much for too long, the brain reduces dopamine production and even more alcohol is needed to feel good again.

The gene researchers placed in the monkeys’ brains is called glial-derived neurotrophic factor. It is a growth factor, stimulating cells to multiply. It may help improve function of brain cells that synthesize dopamine, effectively resetting the whole system and reducing the urge to drink. 

The study was surprisingly successful. Compared with primates that received a placebo, those that received the growth factor gene decreased their drinking by about 90%. They basically quit drinking, while the primates that got the placebo resumed their habit. 

A similar procedure is already used in patients with Parkinson’s disease. But more animal studies, and human clinical trials, would be needed before this therapy could be used in humans with alcohol use disorder. This invasive treatment involves brain surgery, which has risks, so it would likely be reserved for those with the most severe, dangerous drinking habits.

“I think it’d be appropriate for individuals where other treatment modalities just weren’t effective, and they’re worried for their lives,” Dr. Grant said.
 

Alcohol use disorder treatments

Today, treatment for alcohol use disorder ranges from a brief conversation with a health care provider, in mild cases, to psychiatric treatment or medication in moderate or severe cases.

There are four Food and Drug Administration–approved treatments for alcohol use disorder and a few more medications that health care providers can prescribe off label.

“They’re not widely used,” said Henry Kranzler, MD, a professor of psychiatry and director of the Center for Studies of Addiction at the University of Pennsylvania, Philadelphia. “They’re shockingly underutilized.”

One reason: Just 4.6% of people with alcohol use disorder seek treatment each year, according to NIH data. 

“Some of the issues include the ubiquity of alcohol, and its acceptance in American culture – and the fact that that makes it difficult for people to acknowledge that they have a problem with alcohol,” said Dr. Kranzler.

But another problem is that many health care professionals don’t recognize and treat alcohol use disorder in patients who do seek care. Those seeking treatment for alcohol use disorder can find a qualified provider at the American Academy of Addiction Psychiatry or American Society of Addiction Medicine directories.
 

The future of treatment

Ongoing research could lead to more treatments, and make them more available and more appealing.

Unlike many other drugs that work on a single receptor in the body – like opioids that target opioid receptors, or nicotine, which targets choline receptors – alcohol affects many different receptors, said Robert Swift, MD, PhD, a professor of psychiatry and human behavior at Brown University, Providence, R.I. It also penetrates cells at high doses.

“There are so many different effects of alcohol, which makes it very hard to treat,” he said. “But on the other hand, it gives us an advantage, and there are probably different points that we can attack.”

Other exciting developments are underway, although more research, including clinical trials in humans, is needed before they arrive.

Some of the most promising:

• Hallucinogens. In the 1950s, before they became illegal, these drugs helped people drink less. Even Bill Wilson, cofounder of Alcoholics Anonymous, used hallucinogenic treatment in his recovery; it helped him envision overcoming a challenge. Today, there is renewed interest in hallucinogens for alcohol use disorder. In a study published in , people with alcohol use disorder who were given the hallucinogen psilocybin along with therapy spent fewer days drinking heavily over the following 32 weeks than people who received a different medication. Don’t try to do this yourself, though. “It’s not just taking a hallucinogen and having a trip,” Dr. Swift said. “It’s a therapy-guided session, so it’s a combination of using the hallucinogenic substance with a skilled therapist, and sometimes two skilled therapists, helping to guide the experience.”
• Epigenetic editing. Alcohol exposure can affect the activity of a gene in the amygdala, a brain region involved in emotional processing.  found that, by editing that gene in rats through an intravenous line of genetic material, they reduced the rodents’ drinking and anxiety. 
• Oxytocin. The so-called love hormone could help reset the dopamine system to make alcohol less appealing. “There are oxytocin receptors on dopamine neurons, and oxytocin makes your dopamine system more effective,” Dr. Swift said. In a  from the Medical University of South Carolina, Charleston, mice injected with oxytocin didn’t drink during a stressful situation that could have otherwise led to relapse.
• Ghrelin. This stomach hormone could help curb drinking. In a study published in , mice that received drugs that increased ghrelin reduced their alcohol intake.

A version of this article first appeared on WebMD.com.

A type of gene therapy that reboots the brain’s reward system could curb drinking in those with severe alcohol use disorder. 

Researchers from Oregon Health & Science University, Portland implanted the therapy directly into the brains of rhesus monkeys that had been conditioned to drink 8-10 alcoholic drinks a day. A harmless virus that carried a specific gene was placed in the region of the brain that regulates dopamine, which provides feelings of reward and pleasure. 

“We wanted to see if we could normalize the dopamine in these motivational areas – if, indeed, motivation to overdrink or drink heavily would be mitigated,” said study author Kathleen Grant, PhD, a professor and chief of the division of neuroscience at the university’s Oregon National Primate Research Center.

The need for new alcohol use disorder treatments may be more dire than ever. Alcohol-related deaths in the United States increased dramatically between 2007 and 2020, especially in women, according to research published in the journal  JAMA Network Open. The next year, they spiked again, to 108,791 alcohol-related deaths in 2021 alone, according to the National Institutes of Health. That’s slightly more than the number of drug overdoses recorded in 2021.

For the 29.5 million Americans with alcohol use disorder, also known as alcohol abuse or dependence, the road to recovery can be challenging. One reason is that the reward systems in their brains are working against them. 

At the first taste of alcohol, the body releases dopamine. But if a person drinks too much for too long, the brain reduces dopamine production and even more alcohol is needed to feel good again.

The gene researchers placed in the monkeys’ brains is called glial-derived neurotrophic factor. It is a growth factor, stimulating cells to multiply. It may help improve function of brain cells that synthesize dopamine, effectively resetting the whole system and reducing the urge to drink. 

The study was surprisingly successful. Compared with primates that received a placebo, those that received the growth factor gene decreased their drinking by about 90%. They basically quit drinking, while the primates that got the placebo resumed their habit. 

A similar procedure is already used in patients with Parkinson’s disease. But more animal studies, and human clinical trials, would be needed before this therapy could be used in humans with alcohol use disorder. This invasive treatment involves brain surgery, which has risks, so it would likely be reserved for those with the most severe, dangerous drinking habits.

“I think it’d be appropriate for individuals where other treatment modalities just weren’t effective, and they’re worried for their lives,” Dr. Grant said.
 

Alcohol use disorder treatments

Today, treatment for alcohol use disorder ranges from a brief conversation with a health care provider, in mild cases, to psychiatric treatment or medication in moderate or severe cases.

There are four Food and Drug Administration–approved treatments for alcohol use disorder and a few more medications that health care providers can prescribe off label.

“They’re not widely used,” said Henry Kranzler, MD, a professor of psychiatry and director of the Center for Studies of Addiction at the University of Pennsylvania, Philadelphia. “They’re shockingly underutilized.”

One reason: Just 4.6% of people with alcohol use disorder seek treatment each year, according to NIH data. 

“Some of the issues include the ubiquity of alcohol, and its acceptance in American culture – and the fact that that makes it difficult for people to acknowledge that they have a problem with alcohol,” said Dr. Kranzler.

But another problem is that many health care professionals don’t recognize and treat alcohol use disorder in patients who do seek care. Those seeking treatment for alcohol use disorder can find a qualified provider at the American Academy of Addiction Psychiatry or American Society of Addiction Medicine directories.
 

The future of treatment

Ongoing research could lead to more treatments, and make them more available and more appealing.

Unlike many other drugs that work on a single receptor in the body – like opioids that target opioid receptors, or nicotine, which targets choline receptors – alcohol affects many different receptors, said Robert Swift, MD, PhD, a professor of psychiatry and human behavior at Brown University, Providence, R.I. It also penetrates cells at high doses.

“There are so many different effects of alcohol, which makes it very hard to treat,” he said. “But on the other hand, it gives us an advantage, and there are probably different points that we can attack.”

Other exciting developments are underway, although more research, including clinical trials in humans, is needed before they arrive.

Some of the most promising:

• Hallucinogens. In the 1950s, before they became illegal, these drugs helped people drink less. Even Bill Wilson, cofounder of Alcoholics Anonymous, used hallucinogenic treatment in his recovery; it helped him envision overcoming a challenge. Today, there is renewed interest in hallucinogens for alcohol use disorder. In a study published in , people with alcohol use disorder who were given the hallucinogen psilocybin along with therapy spent fewer days drinking heavily over the following 32 weeks than people who received a different medication. Don’t try to do this yourself, though. “It’s not just taking a hallucinogen and having a trip,” Dr. Swift said. “It’s a therapy-guided session, so it’s a combination of using the hallucinogenic substance with a skilled therapist, and sometimes two skilled therapists, helping to guide the experience.”
• Epigenetic editing. Alcohol exposure can affect the activity of a gene in the amygdala, a brain region involved in emotional processing.  found that, by editing that gene in rats through an intravenous line of genetic material, they reduced the rodents’ drinking and anxiety. 
• Oxytocin. The so-called love hormone could help reset the dopamine system to make alcohol less appealing. “There are oxytocin receptors on dopamine neurons, and oxytocin makes your dopamine system more effective,” Dr. Swift said. In a  from the Medical University of South Carolina, Charleston, mice injected with oxytocin didn’t drink during a stressful situation that could have otherwise led to relapse.
• Ghrelin. This stomach hormone could help curb drinking. In a study published in , mice that received drugs that increased ghrelin reduced their alcohol intake.

A version of this article first appeared on WebMD.com.

The Diagnosis: Neonatal Lupus Erythematosus

A review of the medical records of the patient’s mother from her first pregnancy revealed positive anti-Ro/SSA (Sjögren syndrome A) (>8.0 U [reference range <1.0 U]) and anti-La/SSB (Sjögren syndrome B) antibodies (>8.0 U [reference range <1.0 U]), which were reconfirmed during her pregnancy with our patient (the second child). The patient’s older brother was diagnosed with neonatal lupus erythematosus (NLE) 2 years prior at 1 month of age; therefore, the mother took hydroxychloroquine during the pregnancy with the second child to help prevent heart block if the child was diagnosed with NLE. Given the family history, positive antibodies in the mother, and clinical presentation, our patient was diagnosed with NLE. He was referred to a pediatric cardiologist and pediatrician to continue the workup of systemic manifestations of NLE and to rule out the presence of congenital heart block. The rash resolved 6 months after the initial presentation, and he did not develop any systemic manifestations of NLE.

Neonatal lupus erythematosus is a rare acquired autoimmune disorder caused by the placental transfer of anti-Ro/SSA and anti-La/SSB antibodies and less commonly anti-U1 ribonucleoprotein antinuclear autoantibodies.^1,2 Approximately 1% to 2% of mothers with these positive antibodies will have infants affected with NLE.² The annual prevalence of NLE in the United States is approximately 1 in 20,000 live births. Mothers of children with NLE most commonly have clinical Sjögren syndrome; however, anti-Ro/SSA and anti-LA/SSB antibodies may be present in 0.1% to 1.5% of healthy women, and 25% to 60% of women with autoimmune disease may be asymptomatic.¹ As demonstrated in our case, when there is a family history of NLE in an infant from an earlier pregnancy, the risk for NLE increases to 17% to 20% in subsequent pregnancies^1,3 and up to 25% in subsequent pregnancies if the initial child was diagnosed with a congenital heart block in the setting of NLE.¹

Neonatal lupus erythematosus classically presents as annular erythematous macules and plaques with central scaling, telangictasia, atrophy, and pigmentary changes. It may start on the scalp and face and spread caudally.^1,2 Patients may develop these lesions after UV exposure, and 80% of infants may not have dermatologic findings at birth. Importantly, 40% to 60% of mothers may be asymptomatic at the time of presentation of their child’s NLE.¹ The diagnosis can be confirmed via antibody testing in the mother and/or infant. If performed, a punch biopsy shows interface dermatitis, vacuolar degeneration, and possible periadnexal lymphocytic infiltrates on histopathology.^1,2

Management of cutaneous NLE includes sun protection (eg, application of sunscreen) and topical corticosteroids. Most dermatologic manifestations of NLE are transient, resolving after clearance of maternal IgG antibodies in 6 to 9 months; however, some telangiectasia, dyspigmentation, and atrophic scarring may persist.^1-3

Neonatal lupus erythematosus also may have hepatobiliary, cardiac, hematologic, and less commonly neurologic manifestations. Hepatobiliary manifestations usually present as hepatomegaly or asymptomatic elevated transaminases or γ-glutamyl transferase.^1,3 Approximately 10% to 20% of infants with NLE may present with transient anemia and thrombocytopenia.¹ Cardiac manifestations are permanent and may require pacemaker implantation.^1,3 The incidence of a congenital heart block in infants with NLE is 15% to 30%.³ Cardiac NLE most commonly injures the conductive tissue, leading to a congenital atrioventricular block. The development of a congenital heart block develops in the 18th to 24th week of gestation. Manifestations of a more advanced condition can include dilation of the ascending aorta and dilated cardiomyopathy.¹ As such, patients need to be followed by a pediatric cardiologist for monitoring and treatment of any cardiac manifestations.

The overall prognosis of infants affected with NLE varies. Cardiac involvement is associated with a poor prognosis, while isolated cutaneous involvement requires little treatment and portends a favorable prognosis. It is critical for dermatologists to recognize NLE to refer patients to appropriate specialists to investigate and further monitor possible extracutaneous manifestations. With an understanding of the increased risk for a congenital heart block and NLE in subsequent pregnancies, mothers with positive anti-Ro/La antibodies should receive timely counseling and screening. In expectant mothers with suspected autoimmune disease, testing for antinuclear antibodies and SSA and SSB antibodies can be considered, as administration of hydroxychloroquine or prenatal systemic corticosteroids has proven to be effective in preventing a congenital heart block.¹ Our patient was followed by pediatric cardiology and was not found to have a congenital heart block.

The differential diagnosis includes other causes of annular erythema in infants, as NLE can mimic several conditions. Tinea corporis may present as scaly annular plaques with central clearing; however, it rarely is encountered fulminantly in neonates.⁴ Erythema multiforme is a mucocutaneous hypersensitivy reaction distinguished by targetoid morphology.⁵ It is an exceedingly rare diagnosis in neonates; the average pediatric age of onset is 5.6 years.⁶ Erythema multiforme often is associated with an infection, most commonly herpes simplex virus,⁵ and mucosal involvement is common.⁶ Urticaria multiforme (also known as acute annular urticaria) is a benign disease that appears between 2 months to 3 years of age with blanchable urticarial plaques that likely are triggered by viral or bacterial infections, antibiotics, or vaccines.⁶ Specific lesions usually will resolve within 24 hours. Annular erythema of infancy is a benign and asymptomatic gyrate erythema that presents as annular plaques with palpable borders that spread centrifugally in patients younger than 1 year. Notably, lesions should periodically fade and may reappear cyclically for months to years. Evaluation for underlying disease usually is negative.⁶

The Diagnosis: Neonatal Lupus Erythematosus

A review of the medical records of the patient’s mother from her first pregnancy revealed positive anti-Ro/SSA (Sjögren syndrome A) (>8.0 U [reference range <1.0 U]) and anti-La/SSB (Sjögren syndrome B) antibodies (>8.0 U [reference range <1.0 U]), which were reconfirmed during her pregnancy with our patient (the second child). The patient’s older brother was diagnosed with neonatal lupus erythematosus (NLE) 2 years prior at 1 month of age; therefore, the mother took hydroxychloroquine during the pregnancy with the second child to help prevent heart block if the child was diagnosed with NLE. Given the family history, positive antibodies in the mother, and clinical presentation, our patient was diagnosed with NLE. He was referred to a pediatric cardiologist and pediatrician to continue the workup of systemic manifestations of NLE and to rule out the presence of congenital heart block. The rash resolved 6 months after the initial presentation, and he did not develop any systemic manifestations of NLE.

Neonatal lupus erythematosus is a rare acquired autoimmune disorder caused by the placental transfer of anti-Ro/SSA and anti-La/SSB antibodies and less commonly anti-U1 ribonucleoprotein antinuclear autoantibodies.^1,2 Approximately 1% to 2% of mothers with these positive antibodies will have infants affected with NLE.² The annual prevalence of NLE in the United States is approximately 1 in 20,000 live births. Mothers of children with NLE most commonly have clinical Sjögren syndrome; however, anti-Ro/SSA and anti-LA/SSB antibodies may be present in 0.1% to 1.5% of healthy women, and 25% to 60% of women with autoimmune disease may be asymptomatic.¹ As demonstrated in our case, when there is a family history of NLE in an infant from an earlier pregnancy, the risk for NLE increases to 17% to 20% in subsequent pregnancies^1,3 and up to 25% in subsequent pregnancies if the initial child was diagnosed with a congenital heart block in the setting of NLE.¹

Neonatal lupus erythematosus classically presents as annular erythematous macules and plaques with central scaling, telangictasia, atrophy, and pigmentary changes. It may start on the scalp and face and spread caudally.^1,2 Patients may develop these lesions after UV exposure, and 80% of infants may not have dermatologic findings at birth. Importantly, 40% to 60% of mothers may be asymptomatic at the time of presentation of their child’s NLE.¹ The diagnosis can be confirmed via antibody testing in the mother and/or infant. If performed, a punch biopsy shows interface dermatitis, vacuolar degeneration, and possible periadnexal lymphocytic infiltrates on histopathology.^1,2

Management of cutaneous NLE includes sun protection (eg, application of sunscreen) and topical corticosteroids. Most dermatologic manifestations of NLE are transient, resolving after clearance of maternal IgG antibodies in 6 to 9 months; however, some telangiectasia, dyspigmentation, and atrophic scarring may persist.^1-3

Neonatal lupus erythematosus also may have hepatobiliary, cardiac, hematologic, and less commonly neurologic manifestations. Hepatobiliary manifestations usually present as hepatomegaly or asymptomatic elevated transaminases or γ-glutamyl transferase.^1,3 Approximately 10% to 20% of infants with NLE may present with transient anemia and thrombocytopenia.¹ Cardiac manifestations are permanent and may require pacemaker implantation.^1,3 The incidence of a congenital heart block in infants with NLE is 15% to 30%.³ Cardiac NLE most commonly injures the conductive tissue, leading to a congenital atrioventricular block. The development of a congenital heart block develops in the 18th to 24th week of gestation. Manifestations of a more advanced condition can include dilation of the ascending aorta and dilated cardiomyopathy.¹ As such, patients need to be followed by a pediatric cardiologist for monitoring and treatment of any cardiac manifestations.

The overall prognosis of infants affected with NLE varies. Cardiac involvement is associated with a poor prognosis, while isolated cutaneous involvement requires little treatment and portends a favorable prognosis. It is critical for dermatologists to recognize NLE to refer patients to appropriate specialists to investigate and further monitor possible extracutaneous manifestations. With an understanding of the increased risk for a congenital heart block and NLE in subsequent pregnancies, mothers with positive anti-Ro/La antibodies should receive timely counseling and screening. In expectant mothers with suspected autoimmune disease, testing for antinuclear antibodies and SSA and SSB antibodies can be considered, as administration of hydroxychloroquine or prenatal systemic corticosteroids has proven to be effective in preventing a congenital heart block.¹ Our patient was followed by pediatric cardiology and was not found to have a congenital heart block.

The differential diagnosis includes other causes of annular erythema in infants, as NLE can mimic several conditions. Tinea corporis may present as scaly annular plaques with central clearing; however, it rarely is encountered fulminantly in neonates.⁴ Erythema multiforme is a mucocutaneous hypersensitivy reaction distinguished by targetoid morphology.⁵ It is an exceedingly rare diagnosis in neonates; the average pediatric age of onset is 5.6 years.⁶ Erythema multiforme often is associated with an infection, most commonly herpes simplex virus,⁵ and mucosal involvement is common.⁶ Urticaria multiforme (also known as acute annular urticaria) is a benign disease that appears between 2 months to 3 years of age with blanchable urticarial plaques that likely are triggered by viral or bacterial infections, antibiotics, or vaccines.⁶ Specific lesions usually will resolve within 24 hours. Annular erythema of infancy is a benign and asymptomatic gyrate erythema that presents as annular plaques with palpable borders that spread centrifugally in patients younger than 1 year. Notably, lesions should periodically fade and may reappear cyclically for months to years. Evaluation for underlying disease usually is negative.⁶

The Diagnosis: Neonatal Lupus Erythematosus

A review of the medical records of the patient’s mother from her first pregnancy revealed positive anti-Ro/SSA (Sjögren syndrome A) (>8.0 U [reference range <1.0 U]) and anti-La/SSB (Sjögren syndrome B) antibodies (>8.0 U [reference range <1.0 U]), which were reconfirmed during her pregnancy with our patient (the second child). The patient’s older brother was diagnosed with neonatal lupus erythematosus (NLE) 2 years prior at 1 month of age; therefore, the mother took hydroxychloroquine during the pregnancy with the second child to help prevent heart block if the child was diagnosed with NLE. Given the family history, positive antibodies in the mother, and clinical presentation, our patient was diagnosed with NLE. He was referred to a pediatric cardiologist and pediatrician to continue the workup of systemic manifestations of NLE and to rule out the presence of congenital heart block. The rash resolved 6 months after the initial presentation, and he did not develop any systemic manifestations of NLE.

Neonatal lupus erythematosus is a rare acquired autoimmune disorder caused by the placental transfer of anti-Ro/SSA and anti-La/SSB antibodies and less commonly anti-U1 ribonucleoprotein antinuclear autoantibodies.^1,2 Approximately 1% to 2% of mothers with these positive antibodies will have infants affected with NLE.² The annual prevalence of NLE in the United States is approximately 1 in 20,000 live births. Mothers of children with NLE most commonly have clinical Sjögren syndrome; however, anti-Ro/SSA and anti-LA/SSB antibodies may be present in 0.1% to 1.5% of healthy women, and 25% to 60% of women with autoimmune disease may be asymptomatic.¹ As demonstrated in our case, when there is a family history of NLE in an infant from an earlier pregnancy, the risk for NLE increases to 17% to 20% in subsequent pregnancies^1,3 and up to 25% in subsequent pregnancies if the initial child was diagnosed with a congenital heart block in the setting of NLE.¹

Neonatal lupus erythematosus classically presents as annular erythematous macules and plaques with central scaling, telangictasia, atrophy, and pigmentary changes. It may start on the scalp and face and spread caudally.^1,2 Patients may develop these lesions after UV exposure, and 80% of infants may not have dermatologic findings at birth. Importantly, 40% to 60% of mothers may be asymptomatic at the time of presentation of their child’s NLE.¹ The diagnosis can be confirmed via antibody testing in the mother and/or infant. If performed, a punch biopsy shows interface dermatitis, vacuolar degeneration, and possible periadnexal lymphocytic infiltrates on histopathology.^1,2

Management of cutaneous NLE includes sun protection (eg, application of sunscreen) and topical corticosteroids. Most dermatologic manifestations of NLE are transient, resolving after clearance of maternal IgG antibodies in 6 to 9 months; however, some telangiectasia, dyspigmentation, and atrophic scarring may persist.^1-3

Neonatal lupus erythematosus also may have hepatobiliary, cardiac, hematologic, and less commonly neurologic manifestations. Hepatobiliary manifestations usually present as hepatomegaly or asymptomatic elevated transaminases or γ-glutamyl transferase.^1,3 Approximately 10% to 20% of infants with NLE may present with transient anemia and thrombocytopenia.¹ Cardiac manifestations are permanent and may require pacemaker implantation.^1,3 The incidence of a congenital heart block in infants with NLE is 15% to 30%.³ Cardiac NLE most commonly injures the conductive tissue, leading to a congenital atrioventricular block. The development of a congenital heart block develops in the 18th to 24th week of gestation. Manifestations of a more advanced condition can include dilation of the ascending aorta and dilated cardiomyopathy.¹ As such, patients need to be followed by a pediatric cardiologist for monitoring and treatment of any cardiac manifestations.

The overall prognosis of infants affected with NLE varies. Cardiac involvement is associated with a poor prognosis, while isolated cutaneous involvement requires little treatment and portends a favorable prognosis. It is critical for dermatologists to recognize NLE to refer patients to appropriate specialists to investigate and further monitor possible extracutaneous manifestations. With an understanding of the increased risk for a congenital heart block and NLE in subsequent pregnancies, mothers with positive anti-Ro/La antibodies should receive timely counseling and screening. In expectant mothers with suspected autoimmune disease, testing for antinuclear antibodies and SSA and SSB antibodies can be considered, as administration of hydroxychloroquine or prenatal systemic corticosteroids has proven to be effective in preventing a congenital heart block.¹ Our patient was followed by pediatric cardiology and was not found to have a congenital heart block.

The differential diagnosis includes other causes of annular erythema in infants, as NLE can mimic several conditions. Tinea corporis may present as scaly annular plaques with central clearing; however, it rarely is encountered fulminantly in neonates.⁴ Erythema multiforme is a mucocutaneous hypersensitivy reaction distinguished by targetoid morphology.⁵ It is an exceedingly rare diagnosis in neonates; the average pediatric age of onset is 5.6 years.⁶ Erythema multiforme often is associated with an infection, most commonly herpes simplex virus,⁵ and mucosal involvement is common.⁶ Urticaria multiforme (also known as acute annular urticaria) is a benign disease that appears between 2 months to 3 years of age with blanchable urticarial plaques that likely are triggered by viral or bacterial infections, antibiotics, or vaccines.⁶ Specific lesions usually will resolve within 24 hours. Annular erythema of infancy is a benign and asymptomatic gyrate erythema that presents as annular plaques with palpable borders that spread centrifugally in patients younger than 1 year. Notably, lesions should periodically fade and may reappear cyclically for months to years. Evaluation for underlying disease usually is negative.⁶

Several features of sleep disturbance, including nightmares, sleep onset latency, and sleep quality, were associated with a significantly increased risk of suicidal ideation (SI), based on data from 102 individuals.

Suicide remains the second leading cause of death in young adults, but factors that may predict increased suicide risk have not been characterized, wrote Rebecca C. Cox, PhD, of the University of Colorado Boulder, and colleagues.

“Sleep disturbance is a promising modifiable risk factor for acute changes in suicide risk,” they noted. “Previous research has found multiple aspects of sleep disturbance are linked to elevated SI, including insomnia symptoms, both short and long sleep duration, nocturnal wakefulness, and nightmares.”

However, data on the impact of nightly sleep disturbance on suicide risk are limited, the researchers said. They hypothesized that use of ecological momentary assessment (EMA) to assess daily variability in sleep might offer more insight into the relationship between various components of sleep disturbance and changes in suicide risk.

In a study published in Psychiatry Research , the investigators recruited 102 young adults aged 18-35 years who had a history of suicidal behavior; 74.5% were female, 64.7% were White. Participants completed seven semi-random surveys per day for between wake and sleep schedules over 21 days. Each survey asked participants to report on whether they had experienced suicidal ideation (SI) since the last survey. The researchers examined within-person and between-person sleep variables including bedtime, sleep onset latency, sleep onset, number of awakenings, wake after sleep onset, sleep duration, sleep timing, sleep quality, and nightmares.

Overall, nightmares had a significant, positive effect on passive SI at both within- and between-person levels, but no significant effect on active SI. Sleep latency showed a significant, positive effect on passive and active SI at the between-person level, meaning that “participants who took longer to fall asleep on average were more likely to experience passive and active SI during the sampling period,” the researchers noted.

In addition, days following nights of more time awake between sleep onset and offset were days with increased likelihood of passive and active SI. Similarly, days following nights of worse sleep quality than normally reported for an individual were days with increased likelihood of passive and active SI. Sleep timing and duration had no significant effects on SI at the within- or between-person level.

“Notably, tests of reverse models found no relation between daily passive or active SI and any component of the subsequent night’s sleep, suggesting a unidirectional relation between sleep disturbance and subsequent SI,” the researchers wrote in their discussion. If future research replicates the study findings, the results could support the inclusion of sleep difficulties on standard risk assessments as a way to identify risk for SI and initiate prevention approaches, they said.

The findings were limited by several factors including the potential for unmeasured variables impacting the associations between sleep and SI, the researchers noted. Other limitations included the lack of data on more severe levels of SI such as planning and intent, and on suicidal behaviors such as preparatory behaviors, aborted attempts, and actual attempts. The findings also may not generalize to other age groups such as children, adolescents, or older adults, they said.

More research is needed to determine which sleep disturbance components are acute risk factors for which suicide-related outcomes, the researchers said. However, the study is the first to provide evidence for daily sleep disturbances as a near-term predictor of SI in young adults, they concluded.

The study was supported in part by the National Institutes of Health. The researchers had no financial conflicts to disclose.

Several features of sleep disturbance, including nightmares, sleep onset latency, and sleep quality, were associated with a significantly increased risk of suicidal ideation (SI), based on data from 102 individuals.

Suicide remains the second leading cause of death in young adults, but factors that may predict increased suicide risk have not been characterized, wrote Rebecca C. Cox, PhD, of the University of Colorado Boulder, and colleagues.

“Sleep disturbance is a promising modifiable risk factor for acute changes in suicide risk,” they noted. “Previous research has found multiple aspects of sleep disturbance are linked to elevated SI, including insomnia symptoms, both short and long sleep duration, nocturnal wakefulness, and nightmares.”

However, data on the impact of nightly sleep disturbance on suicide risk are limited, the researchers said. They hypothesized that use of ecological momentary assessment (EMA) to assess daily variability in sleep might offer more insight into the relationship between various components of sleep disturbance and changes in suicide risk.

In a study published in Psychiatry Research , the investigators recruited 102 young adults aged 18-35 years who had a history of suicidal behavior; 74.5% were female, 64.7% were White. Participants completed seven semi-random surveys per day for between wake and sleep schedules over 21 days. Each survey asked participants to report on whether they had experienced suicidal ideation (SI) since the last survey. The researchers examined within-person and between-person sleep variables including bedtime, sleep onset latency, sleep onset, number of awakenings, wake after sleep onset, sleep duration, sleep timing, sleep quality, and nightmares.

Overall, nightmares had a significant, positive effect on passive SI at both within- and between-person levels, but no significant effect on active SI. Sleep latency showed a significant, positive effect on passive and active SI at the between-person level, meaning that “participants who took longer to fall asleep on average were more likely to experience passive and active SI during the sampling period,” the researchers noted.

In addition, days following nights of more time awake between sleep onset and offset were days with increased likelihood of passive and active SI. Similarly, days following nights of worse sleep quality than normally reported for an individual were days with increased likelihood of passive and active SI. Sleep timing and duration had no significant effects on SI at the within- or between-person level.

“Notably, tests of reverse models found no relation between daily passive or active SI and any component of the subsequent night’s sleep, suggesting a unidirectional relation between sleep disturbance and subsequent SI,” the researchers wrote in their discussion. If future research replicates the study findings, the results could support the inclusion of sleep difficulties on standard risk assessments as a way to identify risk for SI and initiate prevention approaches, they said.

The findings were limited by several factors including the potential for unmeasured variables impacting the associations between sleep and SI, the researchers noted. Other limitations included the lack of data on more severe levels of SI such as planning and intent, and on suicidal behaviors such as preparatory behaviors, aborted attempts, and actual attempts. The findings also may not generalize to other age groups such as children, adolescents, or older adults, they said.

More research is needed to determine which sleep disturbance components are acute risk factors for which suicide-related outcomes, the researchers said. However, the study is the first to provide evidence for daily sleep disturbances as a near-term predictor of SI in young adults, they concluded.

The study was supported in part by the National Institutes of Health. The researchers had no financial conflicts to disclose.

Several features of sleep disturbance, including nightmares, sleep onset latency, and sleep quality, were associated with a significantly increased risk of suicidal ideation (SI), based on data from 102 individuals.

Suicide remains the second leading cause of death in young adults, but factors that may predict increased suicide risk have not been characterized, wrote Rebecca C. Cox, PhD, of the University of Colorado Boulder, and colleagues.

“Sleep disturbance is a promising modifiable risk factor for acute changes in suicide risk,” they noted. “Previous research has found multiple aspects of sleep disturbance are linked to elevated SI, including insomnia symptoms, both short and long sleep duration, nocturnal wakefulness, and nightmares.”

However, data on the impact of nightly sleep disturbance on suicide risk are limited, the researchers said. They hypothesized that use of ecological momentary assessment (EMA) to assess daily variability in sleep might offer more insight into the relationship between various components of sleep disturbance and changes in suicide risk.

In a study published in Psychiatry Research , the investigators recruited 102 young adults aged 18-35 years who had a history of suicidal behavior; 74.5% were female, 64.7% were White. Participants completed seven semi-random surveys per day for between wake and sleep schedules over 21 days. Each survey asked participants to report on whether they had experienced suicidal ideation (SI) since the last survey. The researchers examined within-person and between-person sleep variables including bedtime, sleep onset latency, sleep onset, number of awakenings, wake after sleep onset, sleep duration, sleep timing, sleep quality, and nightmares.

Overall, nightmares had a significant, positive effect on passive SI at both within- and between-person levels, but no significant effect on active SI. Sleep latency showed a significant, positive effect on passive and active SI at the between-person level, meaning that “participants who took longer to fall asleep on average were more likely to experience passive and active SI during the sampling period,” the researchers noted.

In addition, days following nights of more time awake between sleep onset and offset were days with increased likelihood of passive and active SI. Similarly, days following nights of worse sleep quality than normally reported for an individual were days with increased likelihood of passive and active SI. Sleep timing and duration had no significant effects on SI at the within- or between-person level.

“Notably, tests of reverse models found no relation between daily passive or active SI and any component of the subsequent night’s sleep, suggesting a unidirectional relation between sleep disturbance and subsequent SI,” the researchers wrote in their discussion. If future research replicates the study findings, the results could support the inclusion of sleep difficulties on standard risk assessments as a way to identify risk for SI and initiate prevention approaches, they said.

The findings were limited by several factors including the potential for unmeasured variables impacting the associations between sleep and SI, the researchers noted. Other limitations included the lack of data on more severe levels of SI such as planning and intent, and on suicidal behaviors such as preparatory behaviors, aborted attempts, and actual attempts. The findings also may not generalize to other age groups such as children, adolescents, or older adults, they said.

More research is needed to determine which sleep disturbance components are acute risk factors for which suicide-related outcomes, the researchers said. However, the study is the first to provide evidence for daily sleep disturbances as a near-term predictor of SI in young adults, they concluded.

The study was supported in part by the National Institutes of Health. The researchers had no financial conflicts to disclose.

Back in 1997, a young Stanford (Calif.) University student named Christopher Flowers made his debut in the medical literature with a Nature Medicine report that called out the pharmaceutical industry for overlooking the crucial role of clinical investigators in drug development.

“My research uncovered a series of physicians who served as ‘clinical champions’ and dramatically sped the process of drug development,” Dr. Flowers recalled in an interview. “This early career research inspired me to become the type of clinical champion that I uncovered.”

MD Anderson Cancer Center

Over his career, hematologist-oncologist Dr. Flowers has developed lifesaving therapies for lymphoma, which has transformed into a highly treatable and even curable disease. He’s listed as a coauthor of hundreds of peer-reviewed cancer studies, reports, and medical society guidelines. And he’s revealed stark disparities in blood cancer care: His research shows that non-White patients suffer from worse outcomes, regardless of factors like income and insurance coverage.

The University of Texas MD Anderson Cancer Center, Houston, recently named physician-scientist Dr. Flowers as division head of cancer medicine, a position he’s held on an interim basis. As of Sept. 1, he will permanently oversee 300 faculty and more than 2,000 staff members.
 

A running start in Seattle

For Dr. Flowers, track and field is a sport that runs in the family. His grandfather was a top runner in both high school and college, and both Dr. Flowers and his brother ran competitively in Seattle, where they grew up. But Dr. Flowers chose a career in oncology, earning a medical degree at Stanford and master’s degrees at both Stanford and the University of Washington, Seattle.

The late Kenneth Melmon, MD, a groundbreaking pharmacologist, was a major influence. “He was one of the first people that I met when I began as an undergraduate at Stanford. We grew to be long-standing friends, and he demonstrated what outstanding mentorship looks like. In our research collaboration, we investigated the work of Dr. Gertrude Elion and Dr. George Hitchings involving the translation of pharmacological data from cellular and animal models to clinically useful drugs including 6-mercaptopurine, allopurinol, azathioprine, acyclovir, and zidovudine.”

The late Oliver Press, MD, a blood cancer specialist, inspired Dr. Flower’s interest in lymphoma. “I began work with him during an internship at the University of Washington. Ollie was a great inspiration and a key leader in the development of innovative therapies for lymphoma. He embodied the role of a clinical champion translating work in radioimmunotherapy to new therapeutics for patients with lymphomas. Working with him ultimately led me to pursue a career in hematology and oncology with a focus on the care for patients with lymphomas.”
 

Career blooms as lymphoma care advances

Dr. Flowers went on to Emory University, Atlanta, where he served as scientific director of the Research Informatics Shared Resource and a faculty member in the department of biomedical informatics. “I applied my training in informatics and my clinical expertise to support active grants from the Burroughs Wellcome Fund for Innovation in Regulatory Science and from the National Cancer Institute to develop informatics tools for pathology image analysis and prognostic modeling.”

For 13 years, he also served the Winship Cancer Institute as director of the Emory Healthcare lymphoma program (where his patients included Kansas City Chiefs football star Eric Berry), and for 4 years as scientific director of research informatics. Meanwhile, Dr. Flowers helped develop national practice guidelines for the American Society of Clinical Oncology, the American Cancer Society, and the American College of Radiology. He also chaired the ASCO guideline on management of febrile neutropenia.

In 2019, MD Anderson hired Dr. Flowers as chair of the department of lymphoma/myeloma. A year later, he was appointed division head ad interim for cancer medicine.

“Chris is a unique leader who expertly combines mentorship, sponsorship, and bidirectional open, honest communication,” said Sairah Ahmed, MD, associate professor of lymphoma at MD Anderson. “He doesn’t just empower his team to reach their goals. He also inspires those around him to turn vision into reality.”

As Dr. Flowers noted, many patients with lymphoma are now able to recover and live normal lives. He himself played a direct role himself in boosting lifespans.

“I have been fortunate to play a role in the development of several treatments that have led to advances in first-line therapy for patients with aggressive lymphomas. I partnered with others at MD Anderson, including Dr. Sattva Neelapu and Dr. Jason Westin, who have developed novel therapies like chimeric antigen receptor T-cell therapy for patients with relapse lymphomas,” he said. “Leaders in the field at MD Anderson like Dr. Michael Wang have developed new oral treatments for patients with rare lymphoma subtypes like mantle cell lymphoma. Other colleagues such as Dr. Nathan Fowler and Dr. Loretta Nastoupil have focused on the care for patients with indolent lymphomas and developed less-toxic therapies that are now in common use.”
 

Exposing the disparities in blood cancer care

Dr. Flowers, who’s African American, has also been a leader in health disparity research. In 2016, for example, he was coauthor of a study into non-Hodgkin’s lymphoma that revealed that Blacks in the United States have dramatically lower survival rates than Whites. The 10-year survival rate for Black women with chronic lymphocytic leukemia was just 47%, for example, compared with 66% for White females. “Although incidence rates of lymphoid neoplasms are generally higher among Whites, Black men tend to have poorer survival,” Dr. Flowers and colleagues wrote.

In a 2021 report for the ASCO Educational Book, Dr. Flowers and hematologist-oncologist Demetria Smith-Graziani, MD, now with Emory University, explored disparities across blood cancers and barriers to minority enrollment in clinical trials. “Some approaches that clinicians can apply to address these disparities include increasing systems-level awareness, improving access to care, and reducing biases in clinical setting,” the authors wrote.

Luis Malpica Castillo, MD, assistant professor of lymphoma at MD Anderson Cancer Center, lauded the work of Dr. Flowers in expanding opportunities for minority patients with the disease.

“During the past years, Dr. Flowers’ work has not only had a positive impact on the Texan community, but minority populations living with cancer in the United States and abroad,” he said. “Currently, we are implementing cancer care networks aimed to increase diversity in clinical trials by enrolling a larger number of Hispanic and African American patients, who otherwise may not have benefited from novel therapies. The ultimate goal is to provide high-quality care to all patients living with cancer.”

In addition to his research work, Dr. Flowers is an advocate for diversity within the hematology community. He’s a founding member and former chair of the American Society of Hematology’s Committee on Diversity, Equity and Inclusion (formerly the Committee on Promoting Diversity), and he helped develop the society’s Minority Recruitment Initiative.

What’s next for Dr. Flowers? For one, he plans to continue working as a mentor; he received the ASH Mentor Award in honor of his service in 2022. “I am strongly committed to increasing the number of tenure-track investigators trained in clinical and translational cancer research and to promote their career development.”

And he looks forward to helping develop MD Anderson’s recently announced $2.5 billion hospital in Austin. “This will extend the exceptional care that we provide as the No. 1 cancer center in the United States,” he said. “It will also create new opportunities for research and collaboration with experts at UT Austin.”

When he’s not in clinic, Dr. Flowers embraces his lifelong love of speeding through life on his own two feet. He’s even inspired his children to share his passion. “I run most days of the week,” he said. “Running provides a great opportunity to think and process new research ideas, work through leadership challenges, and sometimes just to relax and let go of the day.”

Back in 1997, a young Stanford (Calif.) University student named Christopher Flowers made his debut in the medical literature with a Nature Medicine report that called out the pharmaceutical industry for overlooking the crucial role of clinical investigators in drug development.

“My research uncovered a series of physicians who served as ‘clinical champions’ and dramatically sped the process of drug development,” Dr. Flowers recalled in an interview. “This early career research inspired me to become the type of clinical champion that I uncovered.”

MD Anderson Cancer Center

Over his career, hematologist-oncologist Dr. Flowers has developed lifesaving therapies for lymphoma, which has transformed into a highly treatable and even curable disease. He’s listed as a coauthor of hundreds of peer-reviewed cancer studies, reports, and medical society guidelines. And he’s revealed stark disparities in blood cancer care: His research shows that non-White patients suffer from worse outcomes, regardless of factors like income and insurance coverage.

The University of Texas MD Anderson Cancer Center, Houston, recently named physician-scientist Dr. Flowers as division head of cancer medicine, a position he’s held on an interim basis. As of Sept. 1, he will permanently oversee 300 faculty and more than 2,000 staff members.
 

A running start in Seattle

For Dr. Flowers, track and field is a sport that runs in the family. His grandfather was a top runner in both high school and college, and both Dr. Flowers and his brother ran competitively in Seattle, where they grew up. But Dr. Flowers chose a career in oncology, earning a medical degree at Stanford and master’s degrees at both Stanford and the University of Washington, Seattle.

The late Kenneth Melmon, MD, a groundbreaking pharmacologist, was a major influence. “He was one of the first people that I met when I began as an undergraduate at Stanford. We grew to be long-standing friends, and he demonstrated what outstanding mentorship looks like. In our research collaboration, we investigated the work of Dr. Gertrude Elion and Dr. George Hitchings involving the translation of pharmacological data from cellular and animal models to clinically useful drugs including 6-mercaptopurine, allopurinol, azathioprine, acyclovir, and zidovudine.”

The late Oliver Press, MD, a blood cancer specialist, inspired Dr. Flower’s interest in lymphoma. “I began work with him during an internship at the University of Washington. Ollie was a great inspiration and a key leader in the development of innovative therapies for lymphoma. He embodied the role of a clinical champion translating work in radioimmunotherapy to new therapeutics for patients with lymphomas. Working with him ultimately led me to pursue a career in hematology and oncology with a focus on the care for patients with lymphomas.”
 

Career blooms as lymphoma care advances

Dr. Flowers went on to Emory University, Atlanta, where he served as scientific director of the Research Informatics Shared Resource and a faculty member in the department of biomedical informatics. “I applied my training in informatics and my clinical expertise to support active grants from the Burroughs Wellcome Fund for Innovation in Regulatory Science and from the National Cancer Institute to develop informatics tools for pathology image analysis and prognostic modeling.”

For 13 years, he also served the Winship Cancer Institute as director of the Emory Healthcare lymphoma program (where his patients included Kansas City Chiefs football star Eric Berry), and for 4 years as scientific director of research informatics. Meanwhile, Dr. Flowers helped develop national practice guidelines for the American Society of Clinical Oncology, the American Cancer Society, and the American College of Radiology. He also chaired the ASCO guideline on management of febrile neutropenia.

In 2019, MD Anderson hired Dr. Flowers as chair of the department of lymphoma/myeloma. A year later, he was appointed division head ad interim for cancer medicine.

“Chris is a unique leader who expertly combines mentorship, sponsorship, and bidirectional open, honest communication,” said Sairah Ahmed, MD, associate professor of lymphoma at MD Anderson. “He doesn’t just empower his team to reach their goals. He also inspires those around him to turn vision into reality.”

As Dr. Flowers noted, many patients with lymphoma are now able to recover and live normal lives. He himself played a direct role himself in boosting lifespans.

“I have been fortunate to play a role in the development of several treatments that have led to advances in first-line therapy for patients with aggressive lymphomas. I partnered with others at MD Anderson, including Dr. Sattva Neelapu and Dr. Jason Westin, who have developed novel therapies like chimeric antigen receptor T-cell therapy for patients with relapse lymphomas,” he said. “Leaders in the field at MD Anderson like Dr. Michael Wang have developed new oral treatments for patients with rare lymphoma subtypes like mantle cell lymphoma. Other colleagues such as Dr. Nathan Fowler and Dr. Loretta Nastoupil have focused on the care for patients with indolent lymphomas and developed less-toxic therapies that are now in common use.”
 

Exposing the disparities in blood cancer care

Dr. Flowers, who’s African American, has also been a leader in health disparity research. In 2016, for example, he was coauthor of a study into non-Hodgkin’s lymphoma that revealed that Blacks in the United States have dramatically lower survival rates than Whites. The 10-year survival rate for Black women with chronic lymphocytic leukemia was just 47%, for example, compared with 66% for White females. “Although incidence rates of lymphoid neoplasms are generally higher among Whites, Black men tend to have poorer survival,” Dr. Flowers and colleagues wrote.

In a 2021 report for the ASCO Educational Book, Dr. Flowers and hematologist-oncologist Demetria Smith-Graziani, MD, now with Emory University, explored disparities across blood cancers and barriers to minority enrollment in clinical trials. “Some approaches that clinicians can apply to address these disparities include increasing systems-level awareness, improving access to care, and reducing biases in clinical setting,” the authors wrote.

Luis Malpica Castillo, MD, assistant professor of lymphoma at MD Anderson Cancer Center, lauded the work of Dr. Flowers in expanding opportunities for minority patients with the disease.

“During the past years, Dr. Flowers’ work has not only had a positive impact on the Texan community, but minority populations living with cancer in the United States and abroad,” he said. “Currently, we are implementing cancer care networks aimed to increase diversity in clinical trials by enrolling a larger number of Hispanic and African American patients, who otherwise may not have benefited from novel therapies. The ultimate goal is to provide high-quality care to all patients living with cancer.”

In addition to his research work, Dr. Flowers is an advocate for diversity within the hematology community. He’s a founding member and former chair of the American Society of Hematology’s Committee on Diversity, Equity and Inclusion (formerly the Committee on Promoting Diversity), and he helped develop the society’s Minority Recruitment Initiative.

What’s next for Dr. Flowers? For one, he plans to continue working as a mentor; he received the ASH Mentor Award in honor of his service in 2022. “I am strongly committed to increasing the number of tenure-track investigators trained in clinical and translational cancer research and to promote their career development.”

And he looks forward to helping develop MD Anderson’s recently announced $2.5 billion hospital in Austin. “This will extend the exceptional care that we provide as the No. 1 cancer center in the United States,” he said. “It will also create new opportunities for research and collaboration with experts at UT Austin.”

When he’s not in clinic, Dr. Flowers embraces his lifelong love of speeding through life on his own two feet. He’s even inspired his children to share his passion. “I run most days of the week,” he said. “Running provides a great opportunity to think and process new research ideas, work through leadership challenges, and sometimes just to relax and let go of the day.”

Back in 1997, a young Stanford (Calif.) University student named Christopher Flowers made his debut in the medical literature with a Nature Medicine report that called out the pharmaceutical industry for overlooking the crucial role of clinical investigators in drug development.

“My research uncovered a series of physicians who served as ‘clinical champions’ and dramatically sped the process of drug development,” Dr. Flowers recalled in an interview. “This early career research inspired me to become the type of clinical champion that I uncovered.”

MD Anderson Cancer Center

Over his career, hematologist-oncologist Dr. Flowers has developed lifesaving therapies for lymphoma, which has transformed into a highly treatable and even curable disease. He’s listed as a coauthor of hundreds of peer-reviewed cancer studies, reports, and medical society guidelines. And he’s revealed stark disparities in blood cancer care: His research shows that non-White patients suffer from worse outcomes, regardless of factors like income and insurance coverage.

The University of Texas MD Anderson Cancer Center, Houston, recently named physician-scientist Dr. Flowers as division head of cancer medicine, a position he’s held on an interim basis. As of Sept. 1, he will permanently oversee 300 faculty and more than 2,000 staff members.
 

A running start in Seattle

For Dr. Flowers, track and field is a sport that runs in the family. His grandfather was a top runner in both high school and college, and both Dr. Flowers and his brother ran competitively in Seattle, where they grew up. But Dr. Flowers chose a career in oncology, earning a medical degree at Stanford and master’s degrees at both Stanford and the University of Washington, Seattle.

The late Kenneth Melmon, MD, a groundbreaking pharmacologist, was a major influence. “He was one of the first people that I met when I began as an undergraduate at Stanford. We grew to be long-standing friends, and he demonstrated what outstanding mentorship looks like. In our research collaboration, we investigated the work of Dr. Gertrude Elion and Dr. George Hitchings involving the translation of pharmacological data from cellular and animal models to clinically useful drugs including 6-mercaptopurine, allopurinol, azathioprine, acyclovir, and zidovudine.”

The late Oliver Press, MD, a blood cancer specialist, inspired Dr. Flower’s interest in lymphoma. “I began work with him during an internship at the University of Washington. Ollie was a great inspiration and a key leader in the development of innovative therapies for lymphoma. He embodied the role of a clinical champion translating work in radioimmunotherapy to new therapeutics for patients with lymphomas. Working with him ultimately led me to pursue a career in hematology and oncology with a focus on the care for patients with lymphomas.”
 

Career blooms as lymphoma care advances

Dr. Flowers went on to Emory University, Atlanta, where he served as scientific director of the Research Informatics Shared Resource and a faculty member in the department of biomedical informatics. “I applied my training in informatics and my clinical expertise to support active grants from the Burroughs Wellcome Fund for Innovation in Regulatory Science and from the National Cancer Institute to develop informatics tools for pathology image analysis and prognostic modeling.”

For 13 years, he also served the Winship Cancer Institute as director of the Emory Healthcare lymphoma program (where his patients included Kansas City Chiefs football star Eric Berry), and for 4 years as scientific director of research informatics. Meanwhile, Dr. Flowers helped develop national practice guidelines for the American Society of Clinical Oncology, the American Cancer Society, and the American College of Radiology. He also chaired the ASCO guideline on management of febrile neutropenia.

In 2019, MD Anderson hired Dr. Flowers as chair of the department of lymphoma/myeloma. A year later, he was appointed division head ad interim for cancer medicine.

“Chris is a unique leader who expertly combines mentorship, sponsorship, and bidirectional open, honest communication,” said Sairah Ahmed, MD, associate professor of lymphoma at MD Anderson. “He doesn’t just empower his team to reach their goals. He also inspires those around him to turn vision into reality.”

As Dr. Flowers noted, many patients with lymphoma are now able to recover and live normal lives. He himself played a direct role himself in boosting lifespans.

“I have been fortunate to play a role in the development of several treatments that have led to advances in first-line therapy for patients with aggressive lymphomas. I partnered with others at MD Anderson, including Dr. Sattva Neelapu and Dr. Jason Westin, who have developed novel therapies like chimeric antigen receptor T-cell therapy for patients with relapse lymphomas,” he said. “Leaders in the field at MD Anderson like Dr. Michael Wang have developed new oral treatments for patients with rare lymphoma subtypes like mantle cell lymphoma. Other colleagues such as Dr. Nathan Fowler and Dr. Loretta Nastoupil have focused on the care for patients with indolent lymphomas and developed less-toxic therapies that are now in common use.”
 

Exposing the disparities in blood cancer care

Dr. Flowers, who’s African American, has also been a leader in health disparity research. In 2016, for example, he was coauthor of a study into non-Hodgkin’s lymphoma that revealed that Blacks in the United States have dramatically lower survival rates than Whites. The 10-year survival rate for Black women with chronic lymphocytic leukemia was just 47%, for example, compared with 66% for White females. “Although incidence rates of lymphoid neoplasms are generally higher among Whites, Black men tend to have poorer survival,” Dr. Flowers and colleagues wrote.

In a 2021 report for the ASCO Educational Book, Dr. Flowers and hematologist-oncologist Demetria Smith-Graziani, MD, now with Emory University, explored disparities across blood cancers and barriers to minority enrollment in clinical trials. “Some approaches that clinicians can apply to address these disparities include increasing systems-level awareness, improving access to care, and reducing biases in clinical setting,” the authors wrote.

Luis Malpica Castillo, MD, assistant professor of lymphoma at MD Anderson Cancer Center, lauded the work of Dr. Flowers in expanding opportunities for minority patients with the disease.

“During the past years, Dr. Flowers’ work has not only had a positive impact on the Texan community, but minority populations living with cancer in the United States and abroad,” he said. “Currently, we are implementing cancer care networks aimed to increase diversity in clinical trials by enrolling a larger number of Hispanic and African American patients, who otherwise may not have benefited from novel therapies. The ultimate goal is to provide high-quality care to all patients living with cancer.”

In addition to his research work, Dr. Flowers is an advocate for diversity within the hematology community. He’s a founding member and former chair of the American Society of Hematology’s Committee on Diversity, Equity and Inclusion (formerly the Committee on Promoting Diversity), and he helped develop the society’s Minority Recruitment Initiative.

What’s next for Dr. Flowers? For one, he plans to continue working as a mentor; he received the ASH Mentor Award in honor of his service in 2022. “I am strongly committed to increasing the number of tenure-track investigators trained in clinical and translational cancer research and to promote their career development.”

And he looks forward to helping develop MD Anderson’s recently announced $2.5 billion hospital in Austin. “This will extend the exceptional care that we provide as the No. 1 cancer center in the United States,” he said. “It will also create new opportunities for research and collaboration with experts at UT Austin.”

When he’s not in clinic, Dr. Flowers embraces his lifelong love of speeding through life on his own two feet. He’s even inspired his children to share his passion. “I run most days of the week,” he said. “Running provides a great opportunity to think and process new research ideas, work through leadership challenges, and sometimes just to relax and let go of the day.”