Clinical Neurology News

TOPLINE:

Childhood trauma increases the risk of developing a primary headache disorder in adulthood, with more early adverse experiences raising the risk even more, a new study found.

METHODOLOGY:

• The meta-analysis included 28 observational studies with 154,739 persons in 19 countries that assessed the relationship between at least one adverse childhood experience (ACE) and primary headache (including migraine, tension-type headache, cluster headache, and chronic/severe headache) at age 21 years or older.
• From each study, researchers extracted outcome point estimates and corresponding 95% confidence intervals, number of events in each group, and covariates included in the model. They subcategorized ACEs according to those involving threat (for example, physical, emotional, or sexual abuse) and deprivation (for example, neglect, household substance misuse).
• For the primary analysis, the researchers calculated the odds ratios and hazard ratios of headache among persons with at least one ACE, compared with those with no ACEs.
• They also tested an underlying biological theory that threat and deprivation ACEs may manifest differently in neurodevelopment, with distinct impacts on primary headaches.
•  

TAKEAWAY:

• The most commonly reported ACEs were physical abuse (77%), sexual abuse (73%), and exposure to family violence (38%).
• Compared with having experienced no ACEs, experiencing at least one was associated with primary headaches (pooled OR, 1.48; 95% confidence interval, 1.36-1.61).
• As the number of ACEs increased, the strength of the association with primary headaches increased in a dose-response relationship (P for trend < .0001).
• Both threat and deprivation were independently associated with primary headaches; the pooled main effect was consistent for threat (OR, 1.46; 95% CI, 1.32-1.60) and for deprivation (OR, 1.35; 95% CI, 1.23-1.49), suggesting possible distinct pathways of early adversity.
•  

IN PRACTICE:

Clinicians who treat primary headaches in adults “should routinely screen for ACEs, educate patients on the connection between ACEs and health, and provide referrals for treatment strategies,” the investigators write. Strategies such as trauma-informed or attachment-based therapy may help rewire parts of the brain that have been dysregulated, they add.

SOURCE:

The study was led by Claudia Sikorski, department of health research methods, evidence, and impact, McMaster University, Hamilton, Ont. It was published online in Neurology.

LIMITATIONS:

The findings reflect a conservative estimate of the true impact of ACEs on primary headaches, because ACEs are commonly underreported. The analysis could not statistically disentangle younger adults with developing brains (age 21-26 years) from older adults. Not all included studies adjusted for age and sex, which are known risk factors for headaches. The study did not explore the relationship between ACEs and primary headache disorders in childhood and adolescence. Owing to the inherent nature of studies investigating ACEs, causation cannot be inferred.

DISCLOSURES:

The authors report no targeted funding and no relevant conflicts of interest.

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

TOPLINE:

Childhood trauma increases the risk of developing a primary headache disorder in adulthood, with more early adverse experiences raising the risk even more, a new study found.

METHODOLOGY:

• The meta-analysis included 28 observational studies with 154,739 persons in 19 countries that assessed the relationship between at least one adverse childhood experience (ACE) and primary headache (including migraine, tension-type headache, cluster headache, and chronic/severe headache) at age 21 years or older.
• From each study, researchers extracted outcome point estimates and corresponding 95% confidence intervals, number of events in each group, and covariates included in the model. They subcategorized ACEs according to those involving threat (for example, physical, emotional, or sexual abuse) and deprivation (for example, neglect, household substance misuse).
• For the primary analysis, the researchers calculated the odds ratios and hazard ratios of headache among persons with at least one ACE, compared with those with no ACEs.
• They also tested an underlying biological theory that threat and deprivation ACEs may manifest differently in neurodevelopment, with distinct impacts on primary headaches.
•  

TAKEAWAY:

• The most commonly reported ACEs were physical abuse (77%), sexual abuse (73%), and exposure to family violence (38%).
• Compared with having experienced no ACEs, experiencing at least one was associated with primary headaches (pooled OR, 1.48; 95% confidence interval, 1.36-1.61).
• As the number of ACEs increased, the strength of the association with primary headaches increased in a dose-response relationship (P for trend < .0001).
• Both threat and deprivation were independently associated with primary headaches; the pooled main effect was consistent for threat (OR, 1.46; 95% CI, 1.32-1.60) and for deprivation (OR, 1.35; 95% CI, 1.23-1.49), suggesting possible distinct pathways of early adversity.
•  

IN PRACTICE:

Clinicians who treat primary headaches in adults “should routinely screen for ACEs, educate patients on the connection between ACEs and health, and provide referrals for treatment strategies,” the investigators write. Strategies such as trauma-informed or attachment-based therapy may help rewire parts of the brain that have been dysregulated, they add.

SOURCE:

The study was led by Claudia Sikorski, department of health research methods, evidence, and impact, McMaster University, Hamilton, Ont. It was published online in Neurology.

LIMITATIONS:

The findings reflect a conservative estimate of the true impact of ACEs on primary headaches, because ACEs are commonly underreported. The analysis could not statistically disentangle younger adults with developing brains (age 21-26 years) from older adults. Not all included studies adjusted for age and sex, which are known risk factors for headaches. The study did not explore the relationship between ACEs and primary headache disorders in childhood and adolescence. Owing to the inherent nature of studies investigating ACEs, causation cannot be inferred.

DISCLOSURES:

The authors report no targeted funding and no relevant conflicts of interest.

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

TOPLINE:

Childhood trauma increases the risk of developing a primary headache disorder in adulthood, with more early adverse experiences raising the risk even more, a new study found.

METHODOLOGY:

• The meta-analysis included 28 observational studies with 154,739 persons in 19 countries that assessed the relationship between at least one adverse childhood experience (ACE) and primary headache (including migraine, tension-type headache, cluster headache, and chronic/severe headache) at age 21 years or older.
• From each study, researchers extracted outcome point estimates and corresponding 95% confidence intervals, number of events in each group, and covariates included in the model. They subcategorized ACEs according to those involving threat (for example, physical, emotional, or sexual abuse) and deprivation (for example, neglect, household substance misuse).
• For the primary analysis, the researchers calculated the odds ratios and hazard ratios of headache among persons with at least one ACE, compared with those with no ACEs.
• They also tested an underlying biological theory that threat and deprivation ACEs may manifest differently in neurodevelopment, with distinct impacts on primary headaches.
•  

TAKEAWAY:

• The most commonly reported ACEs were physical abuse (77%), sexual abuse (73%), and exposure to family violence (38%).
• Compared with having experienced no ACEs, experiencing at least one was associated with primary headaches (pooled OR, 1.48; 95% confidence interval, 1.36-1.61).
• As the number of ACEs increased, the strength of the association with primary headaches increased in a dose-response relationship (P for trend < .0001).
• Both threat and deprivation were independently associated with primary headaches; the pooled main effect was consistent for threat (OR, 1.46; 95% CI, 1.32-1.60) and for deprivation (OR, 1.35; 95% CI, 1.23-1.49), suggesting possible distinct pathways of early adversity.
•  

IN PRACTICE:

Clinicians who treat primary headaches in adults “should routinely screen for ACEs, educate patients on the connection between ACEs and health, and provide referrals for treatment strategies,” the investigators write. Strategies such as trauma-informed or attachment-based therapy may help rewire parts of the brain that have been dysregulated, they add.

SOURCE:

The study was led by Claudia Sikorski, department of health research methods, evidence, and impact, McMaster University, Hamilton, Ont. It was published online in Neurology.

LIMITATIONS:

The findings reflect a conservative estimate of the true impact of ACEs on primary headaches, because ACEs are commonly underreported. The analysis could not statistically disentangle younger adults with developing brains (age 21-26 years) from older adults. Not all included studies adjusted for age and sex, which are known risk factors for headaches. The study did not explore the relationship between ACEs and primary headache disorders in childhood and adolescence. Owing to the inherent nature of studies investigating ACEs, causation cannot be inferred.

DISCLOSURES:

The authors report no targeted funding and no relevant conflicts of interest.

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

The enteric nervous system (ENS), which is regarded as our second brain, is the part of the autonomic nervous system that controls the digestive tract. Housed along the entire length of the digestive tract, it is made up of more than 100 million neurons. It plays a central role in controlling the regulation of gastrointestinal motility, absorption of nutrients, and control of the intestinal barrier that protects the body from external pathogens.

Braak’s hypothesis suggests that the digestive tract could be the starting point for Parkinson’s disease. The fact that nearly all patients with Parkinson’s disease experience digestive problems and have neuropathological lesions in intrinsic and extrinsic innervation of the gastrointestinal tract suggests that Parkinson’s disease also has a gastrointestinal component.

Besides the ascending pathway formulated by Braak, a descending etiology in which gastrointestinal symptoms are present in early stages when neurological signposts have not yet been noticed is supported by evidence from trials. These gastrointestinal symptoms then represent a risk factor. Links have also been described between a history of gastrointestinal symptoms and Alzheimer’s disease and cerebrovascular diseases (CVD), thus justifying studies on a larger scale.
 

Large combined study

The authors have conducted a combined case-control and cohort study using TriNetX, a national network of medical records based in the United States. They identified 24,624 patients with idiopathic Parkinson’s disease in the case-control analysis and compared them with control subjects without neurological disease. They also identified subjects with Alzheimer’s disease and CVD, to study previous gastrointestinal signs. Secondly, 18 cohorts with each exposure (various gastrointestinal symptoms, appendectomy, vagotomy) were compared with their negative controls (NC) for the development of Parkinson’s disease, Alzheimer’s disease, or CVD in 5 years.

Gastroparesis, dysphagia, and irritable bowel syndrome (IBS) without diarrhea or constipation were shown to have specific associations with Parkinson’s disease (vs. NC, Alzheimer’s disease, and CVD) in both case-controls (odds ratios all P < .0001) and cohort analyses (relative risks all P < .05). While functional dyspepsia, IBS with diarrhea, diarrhea, and fecal incontinence were not specific to Parkinson’s disease, IBS with constipation and intestinal pseudo-obstruction showed specificity to Parkinson’s disease in the case-control (OR, 4.11) and cohort (RR, 1.84) analyses. Appendectomy reduced the risk of Parkinson’s disease in the cohort study (RR, 0.48). Neither inflammatory bowel disease nor vagotomy was associated with Parkinson’s disease.
 

A ‘second brain’

This broad study attempted to explore the gut-brain axis by looking for associations between neurological diagnoses and prior gastrointestinal symptoms and later development of Parkinson’s disease. After adjustment to account for multiple comparisons and acknowledgment of the initial risk in patients with Alzheimer’s disease and CVD, only dysphagia, gastroparesis, IBS without diarrhea, and isolated constipation were significantly and specifically associated with Parkinson’s disease.

Numerous literature reviews mention that ENS lesions are responsible for gastrointestinal disorders observed in patients with Parkinson’s disease. Tests on gastrointestinal autopsy and biopsy specimens have established that alpha synuclein clusters, which are morphologically similar to Lewy bodies in the CNS, are seen in the vagus nerve and in the ENS in most subjects with Parkinson’s disease. However, these studies have not shown any loss of neurons in the ENS in Parkinson’s disease, and the presence of alpha synuclein deposits in the ENS is not sufficient in itself to explain these gastrointestinal disorders.

It therefore remains to be determined whether vagal nerve damage alone can explain gastrointestinal disorders or whether dysfunction of enteric neurons without neuronal loss is occurring. So, damage to the ENS from alpha synuclein deposits would be early and would precede damage to the CNS, thus affording evidence in support of Braak’s hypothesis, which relies on autopsy data that does not allow for longitudinal monitoring in a single individual.

Appendectomy appeared to be protective, leading to additional speculation about its role in the pathophysiology of Parkinson’s disease. Additional mechanistic studies are therefore needed to establish causality and confirm the gut-brain axis or the role of dysbiosis and of intestinal permeability problems.

In conclusion, this large, first-of-its-kind multicenter study conducted on a national scale shows that early gastrointestinal symptoms (dysphagia, gastroparesis, constipation, and IBS without diarrhea) are associated with an increased risk of Parkinson’s disease, as is suggested by Braak’s hypothesis. Subject to future longitudinal mechanistic studies, early detection of these gastrointestinal disorders could aid in identifying patients at risk of Parkinson’s, and it could then be assumed that disease-modifying treatments could, at this early stage, halt progression of the disease linked to toxic clusters of alpha synuclein.

This article was translated from JIM, which is part of the Medscape professional network.

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

The enteric nervous system (ENS), which is regarded as our second brain, is the part of the autonomic nervous system that controls the digestive tract. Housed along the entire length of the digestive tract, it is made up of more than 100 million neurons. It plays a central role in controlling the regulation of gastrointestinal motility, absorption of nutrients, and control of the intestinal barrier that protects the body from external pathogens.

Braak’s hypothesis suggests that the digestive tract could be the starting point for Parkinson’s disease. The fact that nearly all patients with Parkinson’s disease experience digestive problems and have neuropathological lesions in intrinsic and extrinsic innervation of the gastrointestinal tract suggests that Parkinson’s disease also has a gastrointestinal component.

Besides the ascending pathway formulated by Braak, a descending etiology in which gastrointestinal symptoms are present in early stages when neurological signposts have not yet been noticed is supported by evidence from trials. These gastrointestinal symptoms then represent a risk factor. Links have also been described between a history of gastrointestinal symptoms and Alzheimer’s disease and cerebrovascular diseases (CVD), thus justifying studies on a larger scale.
 

Large combined study

The authors have conducted a combined case-control and cohort study using TriNetX, a national network of medical records based in the United States. They identified 24,624 patients with idiopathic Parkinson’s disease in the case-control analysis and compared them with control subjects without neurological disease. They also identified subjects with Alzheimer’s disease and CVD, to study previous gastrointestinal signs. Secondly, 18 cohorts with each exposure (various gastrointestinal symptoms, appendectomy, vagotomy) were compared with their negative controls (NC) for the development of Parkinson’s disease, Alzheimer’s disease, or CVD in 5 years.

Gastroparesis, dysphagia, and irritable bowel syndrome (IBS) without diarrhea or constipation were shown to have specific associations with Parkinson’s disease (vs. NC, Alzheimer’s disease, and CVD) in both case-controls (odds ratios all P < .0001) and cohort analyses (relative risks all P < .05). While functional dyspepsia, IBS with diarrhea, diarrhea, and fecal incontinence were not specific to Parkinson’s disease, IBS with constipation and intestinal pseudo-obstruction showed specificity to Parkinson’s disease in the case-control (OR, 4.11) and cohort (RR, 1.84) analyses. Appendectomy reduced the risk of Parkinson’s disease in the cohort study (RR, 0.48). Neither inflammatory bowel disease nor vagotomy was associated with Parkinson’s disease.
 

A ‘second brain’

This broad study attempted to explore the gut-brain axis by looking for associations between neurological diagnoses and prior gastrointestinal symptoms and later development of Parkinson’s disease. After adjustment to account for multiple comparisons and acknowledgment of the initial risk in patients with Alzheimer’s disease and CVD, only dysphagia, gastroparesis, IBS without diarrhea, and isolated constipation were significantly and specifically associated with Parkinson’s disease.

Numerous literature reviews mention that ENS lesions are responsible for gastrointestinal disorders observed in patients with Parkinson’s disease. Tests on gastrointestinal autopsy and biopsy specimens have established that alpha synuclein clusters, which are morphologically similar to Lewy bodies in the CNS, are seen in the vagus nerve and in the ENS in most subjects with Parkinson’s disease. However, these studies have not shown any loss of neurons in the ENS in Parkinson’s disease, and the presence of alpha synuclein deposits in the ENS is not sufficient in itself to explain these gastrointestinal disorders.

It therefore remains to be determined whether vagal nerve damage alone can explain gastrointestinal disorders or whether dysfunction of enteric neurons without neuronal loss is occurring. So, damage to the ENS from alpha synuclein deposits would be early and would precede damage to the CNS, thus affording evidence in support of Braak’s hypothesis, which relies on autopsy data that does not allow for longitudinal monitoring in a single individual.

Appendectomy appeared to be protective, leading to additional speculation about its role in the pathophysiology of Parkinson’s disease. Additional mechanistic studies are therefore needed to establish causality and confirm the gut-brain axis or the role of dysbiosis and of intestinal permeability problems.

In conclusion, this large, first-of-its-kind multicenter study conducted on a national scale shows that early gastrointestinal symptoms (dysphagia, gastroparesis, constipation, and IBS without diarrhea) are associated with an increased risk of Parkinson’s disease, as is suggested by Braak’s hypothesis. Subject to future longitudinal mechanistic studies, early detection of these gastrointestinal disorders could aid in identifying patients at risk of Parkinson’s, and it could then be assumed that disease-modifying treatments could, at this early stage, halt progression of the disease linked to toxic clusters of alpha synuclein.

This article was translated from JIM, which is part of the Medscape professional network.

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

The enteric nervous system (ENS), which is regarded as our second brain, is the part of the autonomic nervous system that controls the digestive tract. Housed along the entire length of the digestive tract, it is made up of more than 100 million neurons. It plays a central role in controlling the regulation of gastrointestinal motility, absorption of nutrients, and control of the intestinal barrier that protects the body from external pathogens.

Braak’s hypothesis suggests that the digestive tract could be the starting point for Parkinson’s disease. The fact that nearly all patients with Parkinson’s disease experience digestive problems and have neuropathological lesions in intrinsic and extrinsic innervation of the gastrointestinal tract suggests that Parkinson’s disease also has a gastrointestinal component.

Besides the ascending pathway formulated by Braak, a descending etiology in which gastrointestinal symptoms are present in early stages when neurological signposts have not yet been noticed is supported by evidence from trials. These gastrointestinal symptoms then represent a risk factor. Links have also been described between a history of gastrointestinal symptoms and Alzheimer’s disease and cerebrovascular diseases (CVD), thus justifying studies on a larger scale.
 

Large combined study

The authors have conducted a combined case-control and cohort study using TriNetX, a national network of medical records based in the United States. They identified 24,624 patients with idiopathic Parkinson’s disease in the case-control analysis and compared them with control subjects without neurological disease. They also identified subjects with Alzheimer’s disease and CVD, to study previous gastrointestinal signs. Secondly, 18 cohorts with each exposure (various gastrointestinal symptoms, appendectomy, vagotomy) were compared with their negative controls (NC) for the development of Parkinson’s disease, Alzheimer’s disease, or CVD in 5 years.

Gastroparesis, dysphagia, and irritable bowel syndrome (IBS) without diarrhea or constipation were shown to have specific associations with Parkinson’s disease (vs. NC, Alzheimer’s disease, and CVD) in both case-controls (odds ratios all P < .0001) and cohort analyses (relative risks all P < .05). While functional dyspepsia, IBS with diarrhea, diarrhea, and fecal incontinence were not specific to Parkinson’s disease, IBS with constipation and intestinal pseudo-obstruction showed specificity to Parkinson’s disease in the case-control (OR, 4.11) and cohort (RR, 1.84) analyses. Appendectomy reduced the risk of Parkinson’s disease in the cohort study (RR, 0.48). Neither inflammatory bowel disease nor vagotomy was associated with Parkinson’s disease.
 

A ‘second brain’

This broad study attempted to explore the gut-brain axis by looking for associations between neurological diagnoses and prior gastrointestinal symptoms and later development of Parkinson’s disease. After adjustment to account for multiple comparisons and acknowledgment of the initial risk in patients with Alzheimer’s disease and CVD, only dysphagia, gastroparesis, IBS without diarrhea, and isolated constipation were significantly and specifically associated with Parkinson’s disease.

Numerous literature reviews mention that ENS lesions are responsible for gastrointestinal disorders observed in patients with Parkinson’s disease. Tests on gastrointestinal autopsy and biopsy specimens have established that alpha synuclein clusters, which are morphologically similar to Lewy bodies in the CNS, are seen in the vagus nerve and in the ENS in most subjects with Parkinson’s disease. However, these studies have not shown any loss of neurons in the ENS in Parkinson’s disease, and the presence of alpha synuclein deposits in the ENS is not sufficient in itself to explain these gastrointestinal disorders.

It therefore remains to be determined whether vagal nerve damage alone can explain gastrointestinal disorders or whether dysfunction of enteric neurons without neuronal loss is occurring. So, damage to the ENS from alpha synuclein deposits would be early and would precede damage to the CNS, thus affording evidence in support of Braak’s hypothesis, which relies on autopsy data that does not allow for longitudinal monitoring in a single individual.

Appendectomy appeared to be protective, leading to additional speculation about its role in the pathophysiology of Parkinson’s disease. Additional mechanistic studies are therefore needed to establish causality and confirm the gut-brain axis or the role of dysbiosis and of intestinal permeability problems.

In conclusion, this large, first-of-its-kind multicenter study conducted on a national scale shows that early gastrointestinal symptoms (dysphagia, gastroparesis, constipation, and IBS without diarrhea) are associated with an increased risk of Parkinson’s disease, as is suggested by Braak’s hypothesis. Subject to future longitudinal mechanistic studies, early detection of these gastrointestinal disorders could aid in identifying patients at risk of Parkinson’s, and it could then be assumed that disease-modifying treatments could, at this early stage, halt progression of the disease linked to toxic clusters of alpha synuclein.

This article was translated from JIM, which is part of the Medscape professional network.

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

This transcript has been edited for clarity.

Dear colleagues, I’m Hans-Christoph Diener from the Faculty of Medicine at the University of Duisburg-Essen in Germany. I would like to give you an update on what was reported during the International Headache Congress in Seoul in September.
 

CGRP receptor agonists

Let me start with the treatment of acute migraine attacks. Until recently, we had analgesics, nonsteroidal anti-inflammatory drugs like ibuprofen, ergot alkaloids, and triptans. There are new developments, which are small molecules that are antagonists at the calcitonin gene-related peptide (CGRP) receptor. At the moment, we have three of them: rimegepant 75 mg, ubrogepant 50 mg or 100 mg, and zavegepant (a nasal spray) 10 mg.

These are all effective and superior to placebo. The 2-hour pain-free rate is somewhere between 25% and 30%. They have very few side effects; these include a little bit of nausea, somnolence, nasopharyngitis, and for zavegepant, the nasal spray, taste disturbance. In indirect comparisons, the so-called gepants are about as effective as ibuprofen and aspirin, and they seem to be less effective than sumatriptan 100 mg.

Unfortunately, until now, we have no direct comparison with triptans and we have no data demonstrating whether they are effective in people where triptans do not work. The major shortcoming is the cost in the United States. The cost per tablet or nasal spray is somewhere between $80 and $200. This means we definitely need more studies for these gepants.
 

Migraine prophylaxis

Let me move to the prophylaxis of migraine with drugs. Previously and still, we have all medications like beta-blockers, flunarizine, topiramate, valproic acid, amitriptyline, and candesartan, and for chronic migraine, onabotulinumtoxinA. We have now 5 years’ experience with the monoclonal antibodies against CGRP or the CGRP receptor like eptinezumab, erenumab, fremanezumab, and galcanezumab.

These are all equally effective. They reduce migraine-days between 3 and 7 per month. They are effective both in episodic and chronic migraine, and most importantly, they are effective in people with medication overuse headaches. The 50% responder rates are somewhere between 40% and 60%, and there are no significant differences between the four monoclonal antibodies.

The major advantage is a very good tolerability profile; very few patients terminate treatment because of adverse events. There has been, with one exception, no direct comparison of the monoclonal antibodies with traditional migraine preventive drugs or onabotulinumtoxinA. The only exception is a trial that compared topiramate and erenumab, showing that erenumab was definitely more effective and better tolerated.

At the moment, the recommendation is to use these monoclonal antibodies for 12 months in episodic migraine and 24 months in chronic migraine and then pause. It usually turns out that between 50% and 70% of these patients need to continue the treatment. If they are not working, there is a possibility to switch between the monoclonal antibodies, and the success rate after this is somewhere between 15% and 30%.

Gepants were also developed for the prevention of migraine. Here, we have rimegepant 75 mg every other day or atogepant 60 mg daily. They are effective, but in indirect comparisons, they are less effective than the monoclonal antibodies. At present, we have no comparative trials with monoclonal antibodies or the traditional migraine preventive drugs.

Potential patients are those who have needle phobia or patients who do not respond to monoclonal antibodies. Again, the biggest shortcoming is cost in the United States. The cost per year for migraine prevention or prophylaxis is between $12,000 and $20,000.

Finally, we also had very exciting news. There is a new therapeutic approach via PACAP. PACAP is pituitary adenylate cyclase-activating polypeptide, which has similar biological actions as CGRP but with additional actions. It could very well be that people who do not respond to a monoclonal antibody would respond to a monoclonal antibody against PACAP.

At the congress, the first randomized, placebo-controlled trial with a monoclonal antibody against PACAP was presented. This monoclonal antibody was effective in a population of people in whom prior preventive therapy had failed. A phase 3 study is planned, and most probably the PACAP monoclonal could work in people who do not respond to monoclonal antibodies against CGRP.

Dear colleagues, we have now many choices for the acute treatment of migraine and migraine prophylaxis. We have new kids on the block, and we have to learn more about how to use these drugs, their benefits, and their shortcomings.

He has disclosed the following relevant financial relationships:Received honoraria for participation in clinical trials, contribution to advisory boards or oral presentations from: Abbott; Addex Pharma; Alder; Allergan; Almirall; Amgen; Autonomic Technology; AstraZeneca; Bayer Vital; Berlin Chemie; Bristol-Myers Squibb; Boehringer Ingelheim; Chordate; CoAxia; Corimmun; Covidien; Coherex; CoLucid; Daiichi-Sankyo; D-Pharm; Electrocore; Fresenius; GlaxoSmithKline; Grunenthal; Janssen-Cilag; Labrys Biologics Lilly; La Roche; 3M Medica; MSD; Medtronic; Menarini; MindFrame; Minster; Neuroscore; Neurobiological Technologies; Novartis; Novo Nordisk; Johnson & Johnson; Knoll; Paion; Parke-Davis; Pierre Fabre; Pfizer; Schaper and Brummer; Sanofi-Aventis; Schering-Plough; Servier; Solvay; Syngis; St. Jude; Talecris; Thrombogenics; WebMD Global; Weber and Weber; Wyeth; and Yamanouchi.

Dr. Diener is professor, department of neurology, Stroke Center-Headache Center, University Duisburg-Essen (Germany).

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Dear colleagues, I’m Hans-Christoph Diener from the Faculty of Medicine at the University of Duisburg-Essen in Germany. I would like to give you an update on what was reported during the International Headache Congress in Seoul in September.
 

CGRP receptor agonists

Let me start with the treatment of acute migraine attacks. Until recently, we had analgesics, nonsteroidal anti-inflammatory drugs like ibuprofen, ergot alkaloids, and triptans. There are new developments, which are small molecules that are antagonists at the calcitonin gene-related peptide (CGRP) receptor. At the moment, we have three of them: rimegepant 75 mg, ubrogepant 50 mg or 100 mg, and zavegepant (a nasal spray) 10 mg.

These are all effective and superior to placebo. The 2-hour pain-free rate is somewhere between 25% and 30%. They have very few side effects; these include a little bit of nausea, somnolence, nasopharyngitis, and for zavegepant, the nasal spray, taste disturbance. In indirect comparisons, the so-called gepants are about as effective as ibuprofen and aspirin, and they seem to be less effective than sumatriptan 100 mg.

Unfortunately, until now, we have no direct comparison with triptans and we have no data demonstrating whether they are effective in people where triptans do not work. The major shortcoming is the cost in the United States. The cost per tablet or nasal spray is somewhere between $80 and $200. This means we definitely need more studies for these gepants.
 

Migraine prophylaxis

Let me move to the prophylaxis of migraine with drugs. Previously and still, we have all medications like beta-blockers, flunarizine, topiramate, valproic acid, amitriptyline, and candesartan, and for chronic migraine, onabotulinumtoxinA. We have now 5 years’ experience with the monoclonal antibodies against CGRP or the CGRP receptor like eptinezumab, erenumab, fremanezumab, and galcanezumab.

These are all equally effective. They reduce migraine-days between 3 and 7 per month. They are effective both in episodic and chronic migraine, and most importantly, they are effective in people with medication overuse headaches. The 50% responder rates are somewhere between 40% and 60%, and there are no significant differences between the four monoclonal antibodies.

The major advantage is a very good tolerability profile; very few patients terminate treatment because of adverse events. There has been, with one exception, no direct comparison of the monoclonal antibodies with traditional migraine preventive drugs or onabotulinumtoxinA. The only exception is a trial that compared topiramate and erenumab, showing that erenumab was definitely more effective and better tolerated.

At the moment, the recommendation is to use these monoclonal antibodies for 12 months in episodic migraine and 24 months in chronic migraine and then pause. It usually turns out that between 50% and 70% of these patients need to continue the treatment. If they are not working, there is a possibility to switch between the monoclonal antibodies, and the success rate after this is somewhere between 15% and 30%.

Gepants were also developed for the prevention of migraine. Here, we have rimegepant 75 mg every other day or atogepant 60 mg daily. They are effective, but in indirect comparisons, they are less effective than the monoclonal antibodies. At present, we have no comparative trials with monoclonal antibodies or the traditional migraine preventive drugs.

Potential patients are those who have needle phobia or patients who do not respond to monoclonal antibodies. Again, the biggest shortcoming is cost in the United States. The cost per year for migraine prevention or prophylaxis is between $12,000 and $20,000.

Finally, we also had very exciting news. There is a new therapeutic approach via PACAP. PACAP is pituitary adenylate cyclase-activating polypeptide, which has similar biological actions as CGRP but with additional actions. It could very well be that people who do not respond to a monoclonal antibody would respond to a monoclonal antibody against PACAP.

At the congress, the first randomized, placebo-controlled trial with a monoclonal antibody against PACAP was presented. This monoclonal antibody was effective in a population of people in whom prior preventive therapy had failed. A phase 3 study is planned, and most probably the PACAP monoclonal could work in people who do not respond to monoclonal antibodies against CGRP.

Dear colleagues, we have now many choices for the acute treatment of migraine and migraine prophylaxis. We have new kids on the block, and we have to learn more about how to use these drugs, their benefits, and their shortcomings.

He has disclosed the following relevant financial relationships:Received honoraria for participation in clinical trials, contribution to advisory boards or oral presentations from: Abbott; Addex Pharma; Alder; Allergan; Almirall; Amgen; Autonomic Technology; AstraZeneca; Bayer Vital; Berlin Chemie; Bristol-Myers Squibb; Boehringer Ingelheim; Chordate; CoAxia; Corimmun; Covidien; Coherex; CoLucid; Daiichi-Sankyo; D-Pharm; Electrocore; Fresenius; GlaxoSmithKline; Grunenthal; Janssen-Cilag; Labrys Biologics Lilly; La Roche; 3M Medica; MSD; Medtronic; Menarini; MindFrame; Minster; Neuroscore; Neurobiological Technologies; Novartis; Novo Nordisk; Johnson & Johnson; Knoll; Paion; Parke-Davis; Pierre Fabre; Pfizer; Schaper and Brummer; Sanofi-Aventis; Schering-Plough; Servier; Solvay; Syngis; St. Jude; Talecris; Thrombogenics; WebMD Global; Weber and Weber; Wyeth; and Yamanouchi.

Dr. Diener is professor, department of neurology, Stroke Center-Headache Center, University Duisburg-Essen (Germany).

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Dear colleagues, I’m Hans-Christoph Diener from the Faculty of Medicine at the University of Duisburg-Essen in Germany. I would like to give you an update on what was reported during the International Headache Congress in Seoul in September.
 

CGRP receptor agonists

Let me start with the treatment of acute migraine attacks. Until recently, we had analgesics, nonsteroidal anti-inflammatory drugs like ibuprofen, ergot alkaloids, and triptans. There are new developments, which are small molecules that are antagonists at the calcitonin gene-related peptide (CGRP) receptor. At the moment, we have three of them: rimegepant 75 mg, ubrogepant 50 mg or 100 mg, and zavegepant (a nasal spray) 10 mg.

These are all effective and superior to placebo. The 2-hour pain-free rate is somewhere between 25% and 30%. They have very few side effects; these include a little bit of nausea, somnolence, nasopharyngitis, and for zavegepant, the nasal spray, taste disturbance. In indirect comparisons, the so-called gepants are about as effective as ibuprofen and aspirin, and they seem to be less effective than sumatriptan 100 mg.

Unfortunately, until now, we have no direct comparison with triptans and we have no data demonstrating whether they are effective in people where triptans do not work. The major shortcoming is the cost in the United States. The cost per tablet or nasal spray is somewhere between $80 and $200. This means we definitely need more studies for these gepants.
 

Migraine prophylaxis

Let me move to the prophylaxis of migraine with drugs. Previously and still, we have all medications like beta-blockers, flunarizine, topiramate, valproic acid, amitriptyline, and candesartan, and for chronic migraine, onabotulinumtoxinA. We have now 5 years’ experience with the monoclonal antibodies against CGRP or the CGRP receptor like eptinezumab, erenumab, fremanezumab, and galcanezumab.

These are all equally effective. They reduce migraine-days between 3 and 7 per month. They are effective both in episodic and chronic migraine, and most importantly, they are effective in people with medication overuse headaches. The 50% responder rates are somewhere between 40% and 60%, and there are no significant differences between the four monoclonal antibodies.

The major advantage is a very good tolerability profile; very few patients terminate treatment because of adverse events. There has been, with one exception, no direct comparison of the monoclonal antibodies with traditional migraine preventive drugs or onabotulinumtoxinA. The only exception is a trial that compared topiramate and erenumab, showing that erenumab was definitely more effective and better tolerated.

At the moment, the recommendation is to use these monoclonal antibodies for 12 months in episodic migraine and 24 months in chronic migraine and then pause. It usually turns out that between 50% and 70% of these patients need to continue the treatment. If they are not working, there is a possibility to switch between the monoclonal antibodies, and the success rate after this is somewhere between 15% and 30%.

Gepants were also developed for the prevention of migraine. Here, we have rimegepant 75 mg every other day or atogepant 60 mg daily. They are effective, but in indirect comparisons, they are less effective than the monoclonal antibodies. At present, we have no comparative trials with monoclonal antibodies or the traditional migraine preventive drugs.

Potential patients are those who have needle phobia or patients who do not respond to monoclonal antibodies. Again, the biggest shortcoming is cost in the United States. The cost per year for migraine prevention or prophylaxis is between $12,000 and $20,000.

Finally, we also had very exciting news. There is a new therapeutic approach via PACAP. PACAP is pituitary adenylate cyclase-activating polypeptide, which has similar biological actions as CGRP but with additional actions. It could very well be that people who do not respond to a monoclonal antibody would respond to a monoclonal antibody against PACAP.

At the congress, the first randomized, placebo-controlled trial with a monoclonal antibody against PACAP was presented. This monoclonal antibody was effective in a population of people in whom prior preventive therapy had failed. A phase 3 study is planned, and most probably the PACAP monoclonal could work in people who do not respond to monoclonal antibodies against CGRP.

Dear colleagues, we have now many choices for the acute treatment of migraine and migraine prophylaxis. We have new kids on the block, and we have to learn more about how to use these drugs, their benefits, and their shortcomings.

He has disclosed the following relevant financial relationships:Received honoraria for participation in clinical trials, contribution to advisory boards or oral presentations from: Abbott; Addex Pharma; Alder; Allergan; Almirall; Amgen; Autonomic Technology; AstraZeneca; Bayer Vital; Berlin Chemie; Bristol-Myers Squibb; Boehringer Ingelheim; Chordate; CoAxia; Corimmun; Covidien; Coherex; CoLucid; Daiichi-Sankyo; D-Pharm; Electrocore; Fresenius; GlaxoSmithKline; Grunenthal; Janssen-Cilag; Labrys Biologics Lilly; La Roche; 3M Medica; MSD; Medtronic; Menarini; MindFrame; Minster; Neuroscore; Neurobiological Technologies; Novartis; Novo Nordisk; Johnson & Johnson; Knoll; Paion; Parke-Davis; Pierre Fabre; Pfizer; Schaper and Brummer; Sanofi-Aventis; Schering-Plough; Servier; Solvay; Syngis; St. Jude; Talecris; Thrombogenics; WebMD Global; Weber and Weber; Wyeth; and Yamanouchi.

Dr. Diener is professor, department of neurology, Stroke Center-Headache Center, University Duisburg-Essen (Germany).

A version of this article appeared on Medscape.com.

TOPLINE:

People with a history of depression or stress were significantly more likely to be diagnosed with mild cognitive impairment (MCI) or Alzheimer’s disease (AD) later in life compared with those without either condition, a new study found.

METHODOLOGY:

• Longitudinal cohort study of 1,362,548 people with records in the Region Stockholm administrative health care database with a diagnosis of stress-induced exhaustion disorder (SED), depression, or both between 2012 and 2013.
• Cohort followed for diagnosis of MCI or AD between 2014 and 2022.

TAKEAWAY:

• SED diagnosed in 0.3%, depression in 2.9% and both SED and depression in 0.1%
• Compared with people without SED or depression, AD risk was more than double in patients with SED (adjusted odds ratio [aOR], 2.45; 99% confidence interval [CI], 1.22-4.91) or depression (aOR, 2.32; 99% CI, 1.85-2.90) and four times higher in patients with both SED and depression (aOR, 4.00; 99% CI, 1.67-9.58)
• Risk for MCI was also higher in people with SED (aOR, 1.87; 99% CI,1.20-2.91), depression (aOR, 2.85; 99% CI, 2.53-3.22) or both SED and depression (aOR, 3.87; 99% CI, 2.39-6.27) vs patients with no history of SED or depression.
• Only patients with depression had a higher risk for another dementia type (aOR, 2.39; 99% CI, 1.92-2.96).

IN PRACTICE:

“Future studies should examine the possibility that symptoms of depression and/or chronic stress could be prodromal symptoms of dementia rather than risk factors,” study authors wrote.

SOURCE:

The study was conducted by Johanna Wallensten, doctoral student, department of clinical sciences, Danderyd Hospital, Stockholm, and colleagues and funded by the Karolinska Institute. It was published online in Alzheimer’s Research and Therapy.

LIMITATIONS:

Use of a health care registry could have led to over- or underestimation of depression, MCI and AD. The study probably captures most people with depression but not most people with depressive symptoms.

DISCLOSURES:

The authors reported no relevant conflicts.

A version of this article appeared on Medscape.com.

TOPLINE:

People with a history of depression or stress were significantly more likely to be diagnosed with mild cognitive impairment (MCI) or Alzheimer’s disease (AD) later in life compared with those without either condition, a new study found.

METHODOLOGY:

• Longitudinal cohort study of 1,362,548 people with records in the Region Stockholm administrative health care database with a diagnosis of stress-induced exhaustion disorder (SED), depression, or both between 2012 and 2013.
• Cohort followed for diagnosis of MCI or AD between 2014 and 2022.

TAKEAWAY:

• SED diagnosed in 0.3%, depression in 2.9% and both SED and depression in 0.1%
• Compared with people without SED or depression, AD risk was more than double in patients with SED (adjusted odds ratio [aOR], 2.45; 99% confidence interval [CI], 1.22-4.91) or depression (aOR, 2.32; 99% CI, 1.85-2.90) and four times higher in patients with both SED and depression (aOR, 4.00; 99% CI, 1.67-9.58)
• Risk for MCI was also higher in people with SED (aOR, 1.87; 99% CI,1.20-2.91), depression (aOR, 2.85; 99% CI, 2.53-3.22) or both SED and depression (aOR, 3.87; 99% CI, 2.39-6.27) vs patients with no history of SED or depression.
• Only patients with depression had a higher risk for another dementia type (aOR, 2.39; 99% CI, 1.92-2.96).

IN PRACTICE:

“Future studies should examine the possibility that symptoms of depression and/or chronic stress could be prodromal symptoms of dementia rather than risk factors,” study authors wrote.

SOURCE:

The study was conducted by Johanna Wallensten, doctoral student, department of clinical sciences, Danderyd Hospital, Stockholm, and colleagues and funded by the Karolinska Institute. It was published online in Alzheimer’s Research and Therapy.

LIMITATIONS:

Use of a health care registry could have led to over- or underestimation of depression, MCI and AD. The study probably captures most people with depression but not most people with depressive symptoms.

DISCLOSURES:

The authors reported no relevant conflicts.

A version of this article appeared on Medscape.com.

TOPLINE:

People with a history of depression or stress were significantly more likely to be diagnosed with mild cognitive impairment (MCI) or Alzheimer’s disease (AD) later in life compared with those without either condition, a new study found.

METHODOLOGY:

• Longitudinal cohort study of 1,362,548 people with records in the Region Stockholm administrative health care database with a diagnosis of stress-induced exhaustion disorder (SED), depression, or both between 2012 and 2013.
• Cohort followed for diagnosis of MCI or AD between 2014 and 2022.

TAKEAWAY:

• SED diagnosed in 0.3%, depression in 2.9% and both SED and depression in 0.1%
• Compared with people without SED or depression, AD risk was more than double in patients with SED (adjusted odds ratio [aOR], 2.45; 99% confidence interval [CI], 1.22-4.91) or depression (aOR, 2.32; 99% CI, 1.85-2.90) and four times higher in patients with both SED and depression (aOR, 4.00; 99% CI, 1.67-9.58)
• Risk for MCI was also higher in people with SED (aOR, 1.87; 99% CI,1.20-2.91), depression (aOR, 2.85; 99% CI, 2.53-3.22) or both SED and depression (aOR, 3.87; 99% CI, 2.39-6.27) vs patients with no history of SED or depression.
• Only patients with depression had a higher risk for another dementia type (aOR, 2.39; 99% CI, 1.92-2.96).

IN PRACTICE:

“Future studies should examine the possibility that symptoms of depression and/or chronic stress could be prodromal symptoms of dementia rather than risk factors,” study authors wrote.

SOURCE:

The study was conducted by Johanna Wallensten, doctoral student, department of clinical sciences, Danderyd Hospital, Stockholm, and colleagues and funded by the Karolinska Institute. It was published online in Alzheimer’s Research and Therapy.

LIMITATIONS:

Use of a health care registry could have led to over- or underestimation of depression, MCI and AD. The study probably captures most people with depression but not most people with depressive symptoms.

DISCLOSURES:

The authors reported no relevant conflicts.

A version of this article appeared on Medscape.com.

TOPLINE:

Loneliness is associated with a higher risk of developing Parkinson’s disease (PD) across demographic groups and independent of other risk factors, data from nearly 500,000 U.K. adults suggest.

METHODOLOGY:

• Loneliness is associated with illness and death, including higher risk of neurodegenerative diseases, but no study has examined whether the association between loneliness and detrimental outcomes extends to PD.
• The current analysis included 491,603 U.K. Biobank participants (mean age, 56; 54% women) without a diagnosis of PD at baseline.
• Loneliness was assessed by a single question at baseline and incident PD was ascertained via health records over 15 years.
• Researchers assessed whether the association between loneliness and PD was moderated by age, sex, or genetic risk and whether the association was accounted for by sociodemographic factors; behavioral, mental, physical, or social factors; or genetic risk.

TAKEAWAY:

• Roughly 19% of the cohort reported being lonely. Compared with those who were not lonely, those who did report being lonely were slightly younger and were more likely to be women. They also had fewer resources, more health risk behaviors (current smoker and physically inactive), and worse physical and mental health.
• Over 15+ years of follow-up, 2,822 participants developed PD (incidence rate: 47 per 100,000 person-years). Compared with those who did not develop PD, those who did were older and more likely to be male, former smokers, have higher BMI and PD polygenetic risk score, and to have diabetes, hypertension, myocardial infarction or stroke, anxiety, or depression.
• In the primary analysis, individuals who reported being lonely had a higher risk for PD (hazard ratio, 1.37) – an association that remained after accounting for demographic and socioeconomic status, social isolation, PD polygenetic risk score, smoking, physical activity, BMI, diabetes, hypertension, stroke, myocardial infarction, depression, and having ever seen a psychiatrist (fully adjusted HR, 1.25). 
• The association between loneliness and incident PD was not moderated by sex, age, or polygenetic risk score.
• Contrary to expectations for a prodromal syndrome, loneliness was not associated with incident PD in the first 5 years after baseline but was associated with PD risk in the subsequent 10 years of follow-up (HR, 1.32).

IN PRACTICE:

“Our findings complement other evidence that loneliness is a psychosocial determinant of health associated with increased risk of morbidity and mortality [and] supports recent calls for the protective and healing effects of personally meaningful social connection,” the authors write.

SOURCE:

The study, with first author Antonio Terracciano, PhD, of Florida State University College of Medicine, Tallahassee, was published online  in JAMA Neurology.

LIMITATIONS:

This observational study could not determine causality or whether reverse causality could explain the association. Loneliness was assessed by a single yes/no question. PD diagnosis relied on hospital admission and death records and may have missed early PD diagnoses.

DISCLOSURES:

Funding for the study was provided by the National Institutes of Health and National Institute on Aging. The authors report no relevant financial relationships.

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

TOPLINE:

Loneliness is associated with a higher risk of developing Parkinson’s disease (PD) across demographic groups and independent of other risk factors, data from nearly 500,000 U.K. adults suggest.

METHODOLOGY:

• Loneliness is associated with illness and death, including higher risk of neurodegenerative diseases, but no study has examined whether the association between loneliness and detrimental outcomes extends to PD.
• The current analysis included 491,603 U.K. Biobank participants (mean age, 56; 54% women) without a diagnosis of PD at baseline.
• Loneliness was assessed by a single question at baseline and incident PD was ascertained via health records over 15 years.
• Researchers assessed whether the association between loneliness and PD was moderated by age, sex, or genetic risk and whether the association was accounted for by sociodemographic factors; behavioral, mental, physical, or social factors; or genetic risk.

TAKEAWAY:

• Roughly 19% of the cohort reported being lonely. Compared with those who were not lonely, those who did report being lonely were slightly younger and were more likely to be women. They also had fewer resources, more health risk behaviors (current smoker and physically inactive), and worse physical and mental health.
• Over 15+ years of follow-up, 2,822 participants developed PD (incidence rate: 47 per 100,000 person-years). Compared with those who did not develop PD, those who did were older and more likely to be male, former smokers, have higher BMI and PD polygenetic risk score, and to have diabetes, hypertension, myocardial infarction or stroke, anxiety, or depression.
• In the primary analysis, individuals who reported being lonely had a higher risk for PD (hazard ratio, 1.37) – an association that remained after accounting for demographic and socioeconomic status, social isolation, PD polygenetic risk score, smoking, physical activity, BMI, diabetes, hypertension, stroke, myocardial infarction, depression, and having ever seen a psychiatrist (fully adjusted HR, 1.25). 
• The association between loneliness and incident PD was not moderated by sex, age, or polygenetic risk score.
• Contrary to expectations for a prodromal syndrome, loneliness was not associated with incident PD in the first 5 years after baseline but was associated with PD risk in the subsequent 10 years of follow-up (HR, 1.32).

IN PRACTICE:

“Our findings complement other evidence that loneliness is a psychosocial determinant of health associated with increased risk of morbidity and mortality [and] supports recent calls for the protective and healing effects of personally meaningful social connection,” the authors write.

SOURCE:

The study, with first author Antonio Terracciano, PhD, of Florida State University College of Medicine, Tallahassee, was published online  in JAMA Neurology.

LIMITATIONS:

This observational study could not determine causality or whether reverse causality could explain the association. Loneliness was assessed by a single yes/no question. PD diagnosis relied on hospital admission and death records and may have missed early PD diagnoses.

DISCLOSURES:

Funding for the study was provided by the National Institutes of Health and National Institute on Aging. The authors report no relevant financial relationships.

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

TOPLINE:

Loneliness is associated with a higher risk of developing Parkinson’s disease (PD) across demographic groups and independent of other risk factors, data from nearly 500,000 U.K. adults suggest.

METHODOLOGY:

• Loneliness is associated with illness and death, including higher risk of neurodegenerative diseases, but no study has examined whether the association between loneliness and detrimental outcomes extends to PD.
• The current analysis included 491,603 U.K. Biobank participants (mean age, 56; 54% women) without a diagnosis of PD at baseline.
• Loneliness was assessed by a single question at baseline and incident PD was ascertained via health records over 15 years.
• Researchers assessed whether the association between loneliness and PD was moderated by age, sex, or genetic risk and whether the association was accounted for by sociodemographic factors; behavioral, mental, physical, or social factors; or genetic risk.

TAKEAWAY:

• Roughly 19% of the cohort reported being lonely. Compared with those who were not lonely, those who did report being lonely were slightly younger and were more likely to be women. They also had fewer resources, more health risk behaviors (current smoker and physically inactive), and worse physical and mental health.
• Over 15+ years of follow-up, 2,822 participants developed PD (incidence rate: 47 per 100,000 person-years). Compared with those who did not develop PD, those who did were older and more likely to be male, former smokers, have higher BMI and PD polygenetic risk score, and to have diabetes, hypertension, myocardial infarction or stroke, anxiety, or depression.
• In the primary analysis, individuals who reported being lonely had a higher risk for PD (hazard ratio, 1.37) – an association that remained after accounting for demographic and socioeconomic status, social isolation, PD polygenetic risk score, smoking, physical activity, BMI, diabetes, hypertension, stroke, myocardial infarction, depression, and having ever seen a psychiatrist (fully adjusted HR, 1.25). 
• The association between loneliness and incident PD was not moderated by sex, age, or polygenetic risk score.
• Contrary to expectations for a prodromal syndrome, loneliness was not associated with incident PD in the first 5 years after baseline but was associated with PD risk in the subsequent 10 years of follow-up (HR, 1.32).

IN PRACTICE:

“Our findings complement other evidence that loneliness is a psychosocial determinant of health associated with increased risk of morbidity and mortality [and] supports recent calls for the protective and healing effects of personally meaningful social connection,” the authors write.

SOURCE:

The study, with first author Antonio Terracciano, PhD, of Florida State University College of Medicine, Tallahassee, was published online  in JAMA Neurology.

LIMITATIONS:

This observational study could not determine causality or whether reverse causality could explain the association. Loneliness was assessed by a single yes/no question. PD diagnosis relied on hospital admission and death records and may have missed early PD diagnoses.

DISCLOSURES:

Funding for the study was provided by the National Institutes of Health and National Institute on Aging. The authors report no relevant financial relationships.

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

Moderna says its upcoming COVID-19 vaccine should work against the BA.2.86 variant that has caused worry about a possible surge in cases.

“The company said its shot generated an 8.7-fold increase in neutralizing antibodies in humans against BA.2.86, which is being tracked by the World Health Organization and the U.S. Centers for Disease Control and Prevention,” Reuters reported.

“We think this is news people will want to hear as they prepare to go out and get their fall boosters,” Jacqueline Miller, Moderna head of infectious diseases, told the news agency.

The CDC said that the BA.2.86 variant might be more likely to infect people who have already had COVID or previous vaccinations. BA.2.86 is an Omicron variant. It has undergone more mutations than XBB.1.5, which has dominated most of this year and was the intended target of the updated shots.

BA.2.86 does not have a strong presence in the United States yet. However, officials are concerned about its high number of mutations, NBC News reported.

The FDA is expected to approve the new Moderna shot by early October.

Pfizer told NBC that its updated booster also generated a strong antibody response against Omicron variants, including BA.2.86.

COVID-19 cases and hospitalizations have been increasing in the U.S. because of the rise of several variants. 

Experts told Reuters that BA.2.86 probably won’t cause a wave of severe disease and death because immunity has been built up around the world through previous infections and mass vaccinations.

A version of this article appeared on WebMD.com.

Moderna says its upcoming COVID-19 vaccine should work against the BA.2.86 variant that has caused worry about a possible surge in cases.

“The company said its shot generated an 8.7-fold increase in neutralizing antibodies in humans against BA.2.86, which is being tracked by the World Health Organization and the U.S. Centers for Disease Control and Prevention,” Reuters reported.

“We think this is news people will want to hear as they prepare to go out and get their fall boosters,” Jacqueline Miller, Moderna head of infectious diseases, told the news agency.

The CDC said that the BA.2.86 variant might be more likely to infect people who have already had COVID or previous vaccinations. BA.2.86 is an Omicron variant. It has undergone more mutations than XBB.1.5, which has dominated most of this year and was the intended target of the updated shots.

BA.2.86 does not have a strong presence in the United States yet. However, officials are concerned about its high number of mutations, NBC News reported.

The FDA is expected to approve the new Moderna shot by early October.

Pfizer told NBC that its updated booster also generated a strong antibody response against Omicron variants, including BA.2.86.

COVID-19 cases and hospitalizations have been increasing in the U.S. because of the rise of several variants. 

Experts told Reuters that BA.2.86 probably won’t cause a wave of severe disease and death because immunity has been built up around the world through previous infections and mass vaccinations.

A version of this article appeared on WebMD.com.

Moderna says its upcoming COVID-19 vaccine should work against the BA.2.86 variant that has caused worry about a possible surge in cases.

“The company said its shot generated an 8.7-fold increase in neutralizing antibodies in humans against BA.2.86, which is being tracked by the World Health Organization and the U.S. Centers for Disease Control and Prevention,” Reuters reported.

“We think this is news people will want to hear as they prepare to go out and get their fall boosters,” Jacqueline Miller, Moderna head of infectious diseases, told the news agency.

The CDC said that the BA.2.86 variant might be more likely to infect people who have already had COVID or previous vaccinations. BA.2.86 is an Omicron variant. It has undergone more mutations than XBB.1.5, which has dominated most of this year and was the intended target of the updated shots.

BA.2.86 does not have a strong presence in the United States yet. However, officials are concerned about its high number of mutations, NBC News reported.

The FDA is expected to approve the new Moderna shot by early October.

Pfizer told NBC that its updated booster also generated a strong antibody response against Omicron variants, including BA.2.86.

COVID-19 cases and hospitalizations have been increasing in the U.S. because of the rise of several variants. 

Experts told Reuters that BA.2.86 probably won’t cause a wave of severe disease and death because immunity has been built up around the world through previous infections and mass vaccinations.

A version of this article appeared on WebMD.com.

Intense throbbing, sensitivity to light and sound, nausea: These were the symptoms Nathan Solomon experienced during his first-ever migraine about a month after receiving a diagnosis of long COVID.

“I’ve also noticed visual disturbances, like flickering lights or blurred vision, which I later learned are called auras,” the 30-year-old medical billing specialist in Seattle told this news organization.

Mr. Solomon isn’t alone. It’s estimated that 1 out of 8 people with COVID develop long COVID. Of those persons, 44% also experience headaches. Research has found that many of those headaches are migraines – and many patients who are afflicted say they had never had a migraine before. These migraines tend to persist for at least 5 or 6 months, according to data from the American Headache Society.

What’s more, other patients may suddenly have more frequent or intense versions of headaches they’ve not noticed before.

The mechanism as to how long COVID could manifest migraines is not yet fully understood, but many doctors believe that inflammation caused by the virus plays a key role.

“To understand why some patients have migraine in long COVID, we have to go back to understand the role of inflammation in COVID-19 itself,” says Emad Estemalik, MD, clinical assistant professor of neurology at Cleveland Clinic Lerner College of Medicine and section head of headache medicine at Cleveland Clinic.

In COVID-19, inflammation occurs because of a cytokine storm. Cytokines, which are proteins essential for a strong immune system, can be overproduced in a patient with COVID, which causes too much inflammation in any organ in the body, including the brain. This can result in new daily headache for some patients.

A new study from Italian researchers found that many patients who develop migraines for the first time while ill with long COVID are middle-aged women (traditionally a late point in life for a first migraine) who have a family history of migraine. Potential causes could have to do with the immune system remaining persistently activated from inflammation during long COVID, as well as the activation of the trigeminovascular system in the brain, which contains neurons that can trigger a migraine.

What treatments can work for migraines related to long COVID?

Long COVID usually causes a constellation of other symptoms at the same time as migraine.

“It’s so important for patients to take an interdisciplinary approach,” Dr. Estemalik stresses. “Patients should make sure their doctors are addressing all of their symptoms.”

When it comes to specifically targeting migraines, standard treatments can be effective.

“In terms of treating migraine in long COVID patients, we don’t do anything different or special,” says Matthew E. Fink, MD, chair of neurology at Weill Cornell Medical College and chief of the Division of Stroke and Critical Care Neurology at New York–Presbyterian Hospital/Weill Cornell Medical Center. “We treat these patients with standard migraine medications.”

Mr. Solomon is following this course of action.

“My doctor prescribed triptans, which have been somewhat effective in reducing the severity and duration of the migraines,” he says. A daily supplement of magnesium and a daily dose of aspirin can also work for some patients, according to Dr. Fink.

Lifestyle modification is also a great idea.

“Patients should keep regular sleep hours, getting up and going to bed at the same time every day,” Dr. Fink continues. “Daily exercise is also recommended.”

Mr. Solomon suggests tracking migraine triggers and patterns in a journal.

“Try to identify lifestyle changes that help, like managing stress and staying hydrated,” Mr. Solomon advises. “Seeking support from health care professionals and support groups can make a significant difference.”

The best news of all: for patients that are diligent in following these strategies, they’ve been proven to work.

“We doctors are very optimistic when it comes to good outcomes for patients with long COVID and migraine,” Dr. Fink says. “I reassure my patients by telling them, ‘You will get better long-term.’ ”

A version of this article appeared on Medscape.com.

Intense throbbing, sensitivity to light and sound, nausea: These were the symptoms Nathan Solomon experienced during his first-ever migraine about a month after receiving a diagnosis of long COVID.

“I’ve also noticed visual disturbances, like flickering lights or blurred vision, which I later learned are called auras,” the 30-year-old medical billing specialist in Seattle told this news organization.

Mr. Solomon isn’t alone. It’s estimated that 1 out of 8 people with COVID develop long COVID. Of those persons, 44% also experience headaches. Research has found that many of those headaches are migraines – and many patients who are afflicted say they had never had a migraine before. These migraines tend to persist for at least 5 or 6 months, according to data from the American Headache Society.

What’s more, other patients may suddenly have more frequent or intense versions of headaches they’ve not noticed before.

The mechanism as to how long COVID could manifest migraines is not yet fully understood, but many doctors believe that inflammation caused by the virus plays a key role.

“To understand why some patients have migraine in long COVID, we have to go back to understand the role of inflammation in COVID-19 itself,” says Emad Estemalik, MD, clinical assistant professor of neurology at Cleveland Clinic Lerner College of Medicine and section head of headache medicine at Cleveland Clinic.

In COVID-19, inflammation occurs because of a cytokine storm. Cytokines, which are proteins essential for a strong immune system, can be overproduced in a patient with COVID, which causes too much inflammation in any organ in the body, including the brain. This can result in new daily headache for some patients.

A new study from Italian researchers found that many patients who develop migraines for the first time while ill with long COVID are middle-aged women (traditionally a late point in life for a first migraine) who have a family history of migraine. Potential causes could have to do with the immune system remaining persistently activated from inflammation during long COVID, as well as the activation of the trigeminovascular system in the brain, which contains neurons that can trigger a migraine.

What treatments can work for migraines related to long COVID?

Long COVID usually causes a constellation of other symptoms at the same time as migraine.

“It’s so important for patients to take an interdisciplinary approach,” Dr. Estemalik stresses. “Patients should make sure their doctors are addressing all of their symptoms.”

When it comes to specifically targeting migraines, standard treatments can be effective.

“In terms of treating migraine in long COVID patients, we don’t do anything different or special,” says Matthew E. Fink, MD, chair of neurology at Weill Cornell Medical College and chief of the Division of Stroke and Critical Care Neurology at New York–Presbyterian Hospital/Weill Cornell Medical Center. “We treat these patients with standard migraine medications.”

Mr. Solomon is following this course of action.

“My doctor prescribed triptans, which have been somewhat effective in reducing the severity and duration of the migraines,” he says. A daily supplement of magnesium and a daily dose of aspirin can also work for some patients, according to Dr. Fink.

Lifestyle modification is also a great idea.

“Patients should keep regular sleep hours, getting up and going to bed at the same time every day,” Dr. Fink continues. “Daily exercise is also recommended.”

Mr. Solomon suggests tracking migraine triggers and patterns in a journal.

“Try to identify lifestyle changes that help, like managing stress and staying hydrated,” Mr. Solomon advises. “Seeking support from health care professionals and support groups can make a significant difference.”

The best news of all: for patients that are diligent in following these strategies, they’ve been proven to work.

“We doctors are very optimistic when it comes to good outcomes for patients with long COVID and migraine,” Dr. Fink says. “I reassure my patients by telling them, ‘You will get better long-term.’ ”

A version of this article appeared on Medscape.com.

Intense throbbing, sensitivity to light and sound, nausea: These were the symptoms Nathan Solomon experienced during his first-ever migraine about a month after receiving a diagnosis of long COVID.

“I’ve also noticed visual disturbances, like flickering lights or blurred vision, which I later learned are called auras,” the 30-year-old medical billing specialist in Seattle told this news organization.

Mr. Solomon isn’t alone. It’s estimated that 1 out of 8 people with COVID develop long COVID. Of those persons, 44% also experience headaches. Research has found that many of those headaches are migraines – and many patients who are afflicted say they had never had a migraine before. These migraines tend to persist for at least 5 or 6 months, according to data from the American Headache Society.

What’s more, other patients may suddenly have more frequent or intense versions of headaches they’ve not noticed before.

The mechanism as to how long COVID could manifest migraines is not yet fully understood, but many doctors believe that inflammation caused by the virus plays a key role.

“To understand why some patients have migraine in long COVID, we have to go back to understand the role of inflammation in COVID-19 itself,” says Emad Estemalik, MD, clinical assistant professor of neurology at Cleveland Clinic Lerner College of Medicine and section head of headache medicine at Cleveland Clinic.

In COVID-19, inflammation occurs because of a cytokine storm. Cytokines, which are proteins essential for a strong immune system, can be overproduced in a patient with COVID, which causes too much inflammation in any organ in the body, including the brain. This can result in new daily headache for some patients.

A new study from Italian researchers found that many patients who develop migraines for the first time while ill with long COVID are middle-aged women (traditionally a late point in life for a first migraine) who have a family history of migraine. Potential causes could have to do with the immune system remaining persistently activated from inflammation during long COVID, as well as the activation of the trigeminovascular system in the brain, which contains neurons that can trigger a migraine.

What treatments can work for migraines related to long COVID?

Long COVID usually causes a constellation of other symptoms at the same time as migraine.

“It’s so important for patients to take an interdisciplinary approach,” Dr. Estemalik stresses. “Patients should make sure their doctors are addressing all of their symptoms.”

When it comes to specifically targeting migraines, standard treatments can be effective.

“In terms of treating migraine in long COVID patients, we don’t do anything different or special,” says Matthew E. Fink, MD, chair of neurology at Weill Cornell Medical College and chief of the Division of Stroke and Critical Care Neurology at New York–Presbyterian Hospital/Weill Cornell Medical Center. “We treat these patients with standard migraine medications.”

Mr. Solomon is following this course of action.

“My doctor prescribed triptans, which have been somewhat effective in reducing the severity and duration of the migraines,” he says. A daily supplement of magnesium and a daily dose of aspirin can also work for some patients, according to Dr. Fink.

Lifestyle modification is also a great idea.

“Patients should keep regular sleep hours, getting up and going to bed at the same time every day,” Dr. Fink continues. “Daily exercise is also recommended.”

Mr. Solomon suggests tracking migraine triggers and patterns in a journal.

“Try to identify lifestyle changes that help, like managing stress and staying hydrated,” Mr. Solomon advises. “Seeking support from health care professionals and support groups can make a significant difference.”

The best news of all: for patients that are diligent in following these strategies, they’ve been proven to work.

“We doctors are very optimistic when it comes to good outcomes for patients with long COVID and migraine,” Dr. Fink says. “I reassure my patients by telling them, ‘You will get better long-term.’ ”

A version of this article appeared on Medscape.com.

U.S. regulators this year will begin to demand reports from cosmetics manufacturers about the ingredients used in their products. They are also preparing to assess potential risks of so-called forever chemicals in these products.

The Food and Drug Administration last year gained new authority over cosmetics when Congress passed the Modernization of Cosmetics Regulation Act of 2022 (MoCRA) by adding this bill to a December budget package.

Yulia Lisitsa/iStock/Getty Images Plus

“On average, consumers in the U.S. use six to 12 cosmetics products daily. But, until recently the FDA didn’t have the authority to require manufacturers to submit cosmetic product listings, including a list of ingredients used in these products, or register the facilities where they were produced,” Namandjé Bumpus, PhD, FDA’s chief scientist, said in a press release.

In the statement, the FDA announced the release of a draft guidance document that is intended to help companies comply with the transparency requirements slated to kick in this December. The agency is accepting comments on this draft guidance through Sept. 7.

“Later this year, registration and listing of cosmetic product facilities and products will become a requirement, making information about cosmetic products, including the ingredients used in products and the facilities where they are produced, readily available to the agency,” Dr. Bumpus said.

The products, according to the FDA statement, include makeup, nail polishes, shaving creams, other grooming products, perfumes, face and body cleansers, hair products, moisturizers, and other skin care items.

MoCRA “represents a sea change in how FDA regulates the cosmetics industry,” attorneys Frederick R. Ball, Alyson Walker Lotman, and Kelly A. Bonner, wrote in an article for the Food and Drug Law Institute published in spring 2023.

The FDA has called the MoCRA law “the most significant expansion” of its authority to regulate cosmetics since the Federal Food, Drug, and Cosmetic Act was passed in 1938.

The agency is in the process of expanding its staff to carry out newly authorized duties, including the tracking of adverse events. The FDA budget request for fiscal 2024, which begins Oct. 1, seeks $5 million for work needed to implement MoCRA.

PFAS, or ‘forever chemicals’

Some of the requested FDA funding is intended to prepare the agency to assess the use of per-and polyfluoroalkyl substances (PFAS) in cosmetics.

MoCRA sets a 3-year deadline for the FDA to issue an assessment of the use and potential risks of PFAS in cosmetics products. PFAS are sometimes added as ingredients in some cosmetic products, including lotions, cleansers, nail polish, shaving cream, foundation, lipstick, eyeliner, eyeshadow, and mascara, according to the FDA. Sometimes the presence of PFAS in cosmetics is unintentional and is the result of impurities in raw materials or is due to the breakdown of ingredients, the FDA said.

The FDA’s website says that so far, the available research doesn’t allow for “definitive conclusions about the potential health risks of PFAS in cosmetics.”

The Centers for Disease Control and Prevention has stated that research has suggested potential links between high levels of certain PFAS, in general, with increased cholesterol levels, changes in liver enzyme levels, increased risk of hypertension or preeclampsia in pregnant women, and increased risk of kidney or testicular cancer.

PFAS compounds often are used to resist grease, oil, water, and heat in industrial settings. They are used in thousands of products, from nonstick cookware to firefighting foams and protective gear, because they can reduce friction, according to a National Academies of Sciences, Engineering, and Medicine report on PFAS that was issued last year.

PFAS are known as “forever chemicals” because they contain a carbon-fluorine bond, which does not break naturally. Even when PFAS are transformed in the body, they can assume other forms of PFAS that preserve the troublesome carbon-fluorine bond. With PFAS, the human body is confronted with a substance it doesn’t have the tools to process.

This is in contrast to proteins and carbohydrates, which are in a sense prepackaged for relatively easy disassembly in the human body. Many of these compounds have weak links that enzymes and stomach acid can take apart, such as sulfur-to-sulfur (disulfide) bonds. That’s why protein-based biotech drugs are injected instead of administered as pills. The ultimate goal of this digestion is for the body to gain energy from these compounds.

But with PFAS, the body faces the challenge of carbon-fluorine bonds that are very hard to break down, and there is no payoff for these efforts, Graham F. Peaslee, PhD, professor of physics at the University of Notre Dame (Indiana), told this news organization.

“Nothing will naturally eat it because when you break the bond, it’s like eating celery,” he said. “You use more calories to eat the celery than you gain back from it.”
 

Interest from a U.S. senator

Dr. Peaslee was one of the authors of a 2021 article about PFAS in cosmetics that appeared in the journal Environmental Science and Technology Letters.

In the article, Dr. Peaslee and colleagues reported on their screening of 231 cosmetic products purchased in the United States and Canada using particle-induced gamma-ray emission spectroscopy. They found cases of undisclosed PFAS in cosmetic products. Foundations, mascaras, and lip products were noted as being especially problematic.

Sen. Susan Collins (R-ME) cited Dr. Peaslee’s article in a 2021 floor speech as she argued for having the FDA ban the intentional addition of PFAS to cosmetics.

“The findings of this study are particularly alarming, as many of these products are subject to direct human exposure,” Sen. Collins said. “For example, lipstick is often inadvertently ingested, and mascara is sometimes absorbed through tear ducts.”

In addition, workers at cosmetics plants may be exposed to PFAS and discarded cosmetics that have these compounds, which could potentially contaminate drinking water, Sen. Collins said. In 2021, she introduced legislation seeking a ban on PFAS that are intentionally added to cosmetics. That legislation did not advance through the Senate.

But the Senate Appropriations Committee, on which Sen. Collins is the ranking Republican, wants the FDA to keep a ban on PFAS in mind.

The Senate Agriculture Appropriations subcommittee, which oversees the FDA’s budget, raised the issue of PFAS and cosmetics in a June report. The FDA should develop a plan outlining research needed to inform “regulatory decision making, including potential development of a proposed rule to ban intentionally added PFAS substances in cosmetics,” the subcommittee said.
 

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

U.S. regulators this year will begin to demand reports from cosmetics manufacturers about the ingredients used in their products. They are also preparing to assess potential risks of so-called forever chemicals in these products.

The Food and Drug Administration last year gained new authority over cosmetics when Congress passed the Modernization of Cosmetics Regulation Act of 2022 (MoCRA) by adding this bill to a December budget package.

Yulia Lisitsa/iStock/Getty Images Plus

“On average, consumers in the U.S. use six to 12 cosmetics products daily. But, until recently the FDA didn’t have the authority to require manufacturers to submit cosmetic product listings, including a list of ingredients used in these products, or register the facilities where they were produced,” Namandjé Bumpus, PhD, FDA’s chief scientist, said in a press release.

In the statement, the FDA announced the release of a draft guidance document that is intended to help companies comply with the transparency requirements slated to kick in this December. The agency is accepting comments on this draft guidance through Sept. 7.

“Later this year, registration and listing of cosmetic product facilities and products will become a requirement, making information about cosmetic products, including the ingredients used in products and the facilities where they are produced, readily available to the agency,” Dr. Bumpus said.

The products, according to the FDA statement, include makeup, nail polishes, shaving creams, other grooming products, perfumes, face and body cleansers, hair products, moisturizers, and other skin care items.

MoCRA “represents a sea change in how FDA regulates the cosmetics industry,” attorneys Frederick R. Ball, Alyson Walker Lotman, and Kelly A. Bonner, wrote in an article for the Food and Drug Law Institute published in spring 2023.

The FDA has called the MoCRA law “the most significant expansion” of its authority to regulate cosmetics since the Federal Food, Drug, and Cosmetic Act was passed in 1938.

The agency is in the process of expanding its staff to carry out newly authorized duties, including the tracking of adverse events. The FDA budget request for fiscal 2024, which begins Oct. 1, seeks $5 million for work needed to implement MoCRA.

PFAS, or ‘forever chemicals’

Some of the requested FDA funding is intended to prepare the agency to assess the use of per-and polyfluoroalkyl substances (PFAS) in cosmetics.

MoCRA sets a 3-year deadline for the FDA to issue an assessment of the use and potential risks of PFAS in cosmetics products. PFAS are sometimes added as ingredients in some cosmetic products, including lotions, cleansers, nail polish, shaving cream, foundation, lipstick, eyeliner, eyeshadow, and mascara, according to the FDA. Sometimes the presence of PFAS in cosmetics is unintentional and is the result of impurities in raw materials or is due to the breakdown of ingredients, the FDA said.

The FDA’s website says that so far, the available research doesn’t allow for “definitive conclusions about the potential health risks of PFAS in cosmetics.”

The Centers for Disease Control and Prevention has stated that research has suggested potential links between high levels of certain PFAS, in general, with increased cholesterol levels, changes in liver enzyme levels, increased risk of hypertension or preeclampsia in pregnant women, and increased risk of kidney or testicular cancer.

PFAS compounds often are used to resist grease, oil, water, and heat in industrial settings. They are used in thousands of products, from nonstick cookware to firefighting foams and protective gear, because they can reduce friction, according to a National Academies of Sciences, Engineering, and Medicine report on PFAS that was issued last year.

PFAS are known as “forever chemicals” because they contain a carbon-fluorine bond, which does not break naturally. Even when PFAS are transformed in the body, they can assume other forms of PFAS that preserve the troublesome carbon-fluorine bond. With PFAS, the human body is confronted with a substance it doesn’t have the tools to process.

This is in contrast to proteins and carbohydrates, which are in a sense prepackaged for relatively easy disassembly in the human body. Many of these compounds have weak links that enzymes and stomach acid can take apart, such as sulfur-to-sulfur (disulfide) bonds. That’s why protein-based biotech drugs are injected instead of administered as pills. The ultimate goal of this digestion is for the body to gain energy from these compounds.

But with PFAS, the body faces the challenge of carbon-fluorine bonds that are very hard to break down, and there is no payoff for these efforts, Graham F. Peaslee, PhD, professor of physics at the University of Notre Dame (Indiana), told this news organization.

“Nothing will naturally eat it because when you break the bond, it’s like eating celery,” he said. “You use more calories to eat the celery than you gain back from it.”
 

Interest from a U.S. senator

Dr. Peaslee was one of the authors of a 2021 article about PFAS in cosmetics that appeared in the journal Environmental Science and Technology Letters.

In the article, Dr. Peaslee and colleagues reported on their screening of 231 cosmetic products purchased in the United States and Canada using particle-induced gamma-ray emission spectroscopy. They found cases of undisclosed PFAS in cosmetic products. Foundations, mascaras, and lip products were noted as being especially problematic.

Sen. Susan Collins (R-ME) cited Dr. Peaslee’s article in a 2021 floor speech as she argued for having the FDA ban the intentional addition of PFAS to cosmetics.

“The findings of this study are particularly alarming, as many of these products are subject to direct human exposure,” Sen. Collins said. “For example, lipstick is often inadvertently ingested, and mascara is sometimes absorbed through tear ducts.”

In addition, workers at cosmetics plants may be exposed to PFAS and discarded cosmetics that have these compounds, which could potentially contaminate drinking water, Sen. Collins said. In 2021, she introduced legislation seeking a ban on PFAS that are intentionally added to cosmetics. That legislation did not advance through the Senate.

But the Senate Appropriations Committee, on which Sen. Collins is the ranking Republican, wants the FDA to keep a ban on PFAS in mind.

The Senate Agriculture Appropriations subcommittee, which oversees the FDA’s budget, raised the issue of PFAS and cosmetics in a June report. The FDA should develop a plan outlining research needed to inform “regulatory decision making, including potential development of a proposed rule to ban intentionally added PFAS substances in cosmetics,” the subcommittee said.
 

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

U.S. regulators this year will begin to demand reports from cosmetics manufacturers about the ingredients used in their products. They are also preparing to assess potential risks of so-called forever chemicals in these products.

The Food and Drug Administration last year gained new authority over cosmetics when Congress passed the Modernization of Cosmetics Regulation Act of 2022 (MoCRA) by adding this bill to a December budget package.

Yulia Lisitsa/iStock/Getty Images Plus

“On average, consumers in the U.S. use six to 12 cosmetics products daily. But, until recently the FDA didn’t have the authority to require manufacturers to submit cosmetic product listings, including a list of ingredients used in these products, or register the facilities where they were produced,” Namandjé Bumpus, PhD, FDA’s chief scientist, said in a press release.

In the statement, the FDA announced the release of a draft guidance document that is intended to help companies comply with the transparency requirements slated to kick in this December. The agency is accepting comments on this draft guidance through Sept. 7.

“Later this year, registration and listing of cosmetic product facilities and products will become a requirement, making information about cosmetic products, including the ingredients used in products and the facilities where they are produced, readily available to the agency,” Dr. Bumpus said.

The products, according to the FDA statement, include makeup, nail polishes, shaving creams, other grooming products, perfumes, face and body cleansers, hair products, moisturizers, and other skin care items.

MoCRA “represents a sea change in how FDA regulates the cosmetics industry,” attorneys Frederick R. Ball, Alyson Walker Lotman, and Kelly A. Bonner, wrote in an article for the Food and Drug Law Institute published in spring 2023.

The FDA has called the MoCRA law “the most significant expansion” of its authority to regulate cosmetics since the Federal Food, Drug, and Cosmetic Act was passed in 1938.

The agency is in the process of expanding its staff to carry out newly authorized duties, including the tracking of adverse events. The FDA budget request for fiscal 2024, which begins Oct. 1, seeks $5 million for work needed to implement MoCRA.

PFAS, or ‘forever chemicals’

Some of the requested FDA funding is intended to prepare the agency to assess the use of per-and polyfluoroalkyl substances (PFAS) in cosmetics.

MoCRA sets a 3-year deadline for the FDA to issue an assessment of the use and potential risks of PFAS in cosmetics products. PFAS are sometimes added as ingredients in some cosmetic products, including lotions, cleansers, nail polish, shaving cream, foundation, lipstick, eyeliner, eyeshadow, and mascara, according to the FDA. Sometimes the presence of PFAS in cosmetics is unintentional and is the result of impurities in raw materials or is due to the breakdown of ingredients, the FDA said.

The FDA’s website says that so far, the available research doesn’t allow for “definitive conclusions about the potential health risks of PFAS in cosmetics.”

The Centers for Disease Control and Prevention has stated that research has suggested potential links between high levels of certain PFAS, in general, with increased cholesterol levels, changes in liver enzyme levels, increased risk of hypertension or preeclampsia in pregnant women, and increased risk of kidney or testicular cancer.

PFAS compounds often are used to resist grease, oil, water, and heat in industrial settings. They are used in thousands of products, from nonstick cookware to firefighting foams and protective gear, because they can reduce friction, according to a National Academies of Sciences, Engineering, and Medicine report on PFAS that was issued last year.

PFAS are known as “forever chemicals” because they contain a carbon-fluorine bond, which does not break naturally. Even when PFAS are transformed in the body, they can assume other forms of PFAS that preserve the troublesome carbon-fluorine bond. With PFAS, the human body is confronted with a substance it doesn’t have the tools to process.

This is in contrast to proteins and carbohydrates, which are in a sense prepackaged for relatively easy disassembly in the human body. Many of these compounds have weak links that enzymes and stomach acid can take apart, such as sulfur-to-sulfur (disulfide) bonds. That’s why protein-based biotech drugs are injected instead of administered as pills. The ultimate goal of this digestion is for the body to gain energy from these compounds.

But with PFAS, the body faces the challenge of carbon-fluorine bonds that are very hard to break down, and there is no payoff for these efforts, Graham F. Peaslee, PhD, professor of physics at the University of Notre Dame (Indiana), told this news organization.

“Nothing will naturally eat it because when you break the bond, it’s like eating celery,” he said. “You use more calories to eat the celery than you gain back from it.”
 

Interest from a U.S. senator

Dr. Peaslee was one of the authors of a 2021 article about PFAS in cosmetics that appeared in the journal Environmental Science and Technology Letters.

In the article, Dr. Peaslee and colleagues reported on their screening of 231 cosmetic products purchased in the United States and Canada using particle-induced gamma-ray emission spectroscopy. They found cases of undisclosed PFAS in cosmetic products. Foundations, mascaras, and lip products were noted as being especially problematic.

Sen. Susan Collins (R-ME) cited Dr. Peaslee’s article in a 2021 floor speech as she argued for having the FDA ban the intentional addition of PFAS to cosmetics.

“The findings of this study are particularly alarming, as many of these products are subject to direct human exposure,” Sen. Collins said. “For example, lipstick is often inadvertently ingested, and mascara is sometimes absorbed through tear ducts.”

In addition, workers at cosmetics plants may be exposed to PFAS and discarded cosmetics that have these compounds, which could potentially contaminate drinking water, Sen. Collins said. In 2021, she introduced legislation seeking a ban on PFAS that are intentionally added to cosmetics. That legislation did not advance through the Senate.

But the Senate Appropriations Committee, on which Sen. Collins is the ranking Republican, wants the FDA to keep a ban on PFAS in mind.

The Senate Agriculture Appropriations subcommittee, which oversees the FDA’s budget, raised the issue of PFAS and cosmetics in a June report. The FDA should develop a plan outlining research needed to inform “regulatory decision making, including potential development of a proposed rule to ban intentionally added PFAS substances in cosmetics,” the subcommittee said.
 

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

“We were all of us cogs in a great machine which sometimes rolled forward, nobody knew where, sometimes backwards, nobody knew why.” – Ernst Toller

A nice feature of the Apple watch is the stopwatch. With it, I can discreetly click the timer and watch seconds tick away. Tap. There’s one lap. Tap. Two. Tap. That was a quick visit, 6 minutes and 42 seconds. Tap. Under 2 minutes to close the chart. Let’s see if I can beat it. Tap. Tap. What if I moved my Mayo stand over to this side of the room? How about a sign, “All patients must have clothes off if you want a skin exam.” You think ob.gyns. are quick from skin to baby in a stat C-section? You should see how fast I can go from alcohol wipe to Drysol on a biopsy. Seconds. Tick, tick, tap.

Every day I look for ways to go faster. This is not so I can be out the door by 3. Rather, it’s simply to make it through the day without having to log on after we put the kids to bed at night.

Speaking of bedtimes, another nice feature of the Apple watch is the timer. With it, I can set a timer and a lovely chimey alarm will go off. This comes in handy with 3-year-olds. “Sloan, in two minutes we are going to brush your teeth.” Ding. “Sloan, you have one minute to get your pajamas on.” Ding. “Sloanie, I’ll give you 3 more minutes to put the kitties away, then get into bed.” Ding, ding, ding ...

As you can see, using the stopwatch to time a bedtime routine would be demoralizing. If you’ve tried to put a toddler to bed in summer you know. They explore every option to avoid sleeping: one more book (that would make 3), “accidentally” putting their pajamas on backwards, offering to brush their teeth a second time. And once the light is off, “Papa, I have to potty.” No, bedtime routines cannot be standardized. They resist being made efficient.

In contrast, we think of seeing patients as a standardizable process; work to be optimized. This idea that work should be as efficient as possible came from the father of business management, Frederick Taylor. Taylor, a mechanical engineer, observed inefficiencies on the factory floor. His work was seminal in the development of the second industrial revolution. Before then no one had applied scientific rigor to productivity. His book, “The Principles of Scientific Management,” written in 1909, is considered the most influential management book of the 20th century. He was the first to use stopwatches to perform time studies, noting how long each task took with the belief that there was one best way. The worker was an extension of the machine, tuned by management such that he was as efficient as possible.

PublicDomain/commons.wikimedia.org/wiki/File:Ford_assembly_line_-_1913.jpg

A more insidious downside on the drive to efficiency lies in the nature of what we do. We aren’t factory workers punching out widgets, we’re physicians caring for people and people cannot be standardized. In this way, seeing patients is more like putting a toddler to bed than like assembling an iPhone. There will always be by-the-ways, basal cells hiding behind the ear, traffic jams, and bags of products that they want to review. Not sure how to use your fluorouracil? Let’s go over it again. Need to talk more about why you have granuloma annulare? Let me explain. Despite Taylor’s vision, some work simply cannot be optimized. And shouldn’t.

“Where’s my 11:30 patient who checked in half an hour ago?!” I asked my medical assistant. “Oh, she had to go to the bathroom.” Tap.
 

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at dermnews@mdedge.com.

“We were all of us cogs in a great machine which sometimes rolled forward, nobody knew where, sometimes backwards, nobody knew why.” – Ernst Toller

A nice feature of the Apple watch is the stopwatch. With it, I can discreetly click the timer and watch seconds tick away. Tap. There’s one lap. Tap. Two. Tap. That was a quick visit, 6 minutes and 42 seconds. Tap. Under 2 minutes to close the chart. Let’s see if I can beat it. Tap. Tap. What if I moved my Mayo stand over to this side of the room? How about a sign, “All patients must have clothes off if you want a skin exam.” You think ob.gyns. are quick from skin to baby in a stat C-section? You should see how fast I can go from alcohol wipe to Drysol on a biopsy. Seconds. Tick, tick, tap.

Every day I look for ways to go faster. This is not so I can be out the door by 3. Rather, it’s simply to make it through the day without having to log on after we put the kids to bed at night.

Speaking of bedtimes, another nice feature of the Apple watch is the timer. With it, I can set a timer and a lovely chimey alarm will go off. This comes in handy with 3-year-olds. “Sloan, in two minutes we are going to brush your teeth.” Ding. “Sloan, you have one minute to get your pajamas on.” Ding. “Sloanie, I’ll give you 3 more minutes to put the kitties away, then get into bed.” Ding, ding, ding ...

As you can see, using the stopwatch to time a bedtime routine would be demoralizing. If you’ve tried to put a toddler to bed in summer you know. They explore every option to avoid sleeping: one more book (that would make 3), “accidentally” putting their pajamas on backwards, offering to brush their teeth a second time. And once the light is off, “Papa, I have to potty.” No, bedtime routines cannot be standardized. They resist being made efficient.

In contrast, we think of seeing patients as a standardizable process; work to be optimized. This idea that work should be as efficient as possible came from the father of business management, Frederick Taylor. Taylor, a mechanical engineer, observed inefficiencies on the factory floor. His work was seminal in the development of the second industrial revolution. Before then no one had applied scientific rigor to productivity. His book, “The Principles of Scientific Management,” written in 1909, is considered the most influential management book of the 20th century. He was the first to use stopwatches to perform time studies, noting how long each task took with the belief that there was one best way. The worker was an extension of the machine, tuned by management such that he was as efficient as possible.

PublicDomain/commons.wikimedia.org/wiki/File:Ford_assembly_line_-_1913.jpg

A more insidious downside on the drive to efficiency lies in the nature of what we do. We aren’t factory workers punching out widgets, we’re physicians caring for people and people cannot be standardized. In this way, seeing patients is more like putting a toddler to bed than like assembling an iPhone. There will always be by-the-ways, basal cells hiding behind the ear, traffic jams, and bags of products that they want to review. Not sure how to use your fluorouracil? Let’s go over it again. Need to talk more about why you have granuloma annulare? Let me explain. Despite Taylor’s vision, some work simply cannot be optimized. And shouldn’t.

“Where’s my 11:30 patient who checked in half an hour ago?!” I asked my medical assistant. “Oh, she had to go to the bathroom.” Tap.
 

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at dermnews@mdedge.com.

“We were all of us cogs in a great machine which sometimes rolled forward, nobody knew where, sometimes backwards, nobody knew why.” – Ernst Toller

A nice feature of the Apple watch is the stopwatch. With it, I can discreetly click the timer and watch seconds tick away. Tap. There’s one lap. Tap. Two. Tap. That was a quick visit, 6 minutes and 42 seconds. Tap. Under 2 minutes to close the chart. Let’s see if I can beat it. Tap. Tap. What if I moved my Mayo stand over to this side of the room? How about a sign, “All patients must have clothes off if you want a skin exam.” You think ob.gyns. are quick from skin to baby in a stat C-section? You should see how fast I can go from alcohol wipe to Drysol on a biopsy. Seconds. Tick, tick, tap.

Every day I look for ways to go faster. This is not so I can be out the door by 3. Rather, it’s simply to make it through the day without having to log on after we put the kids to bed at night.

Speaking of bedtimes, another nice feature of the Apple watch is the timer. With it, I can set a timer and a lovely chimey alarm will go off. This comes in handy with 3-year-olds. “Sloan, in two minutes we are going to brush your teeth.” Ding. “Sloan, you have one minute to get your pajamas on.” Ding. “Sloanie, I’ll give you 3 more minutes to put the kitties away, then get into bed.” Ding, ding, ding ...

As you can see, using the stopwatch to time a bedtime routine would be demoralizing. If you’ve tried to put a toddler to bed in summer you know. They explore every option to avoid sleeping: one more book (that would make 3), “accidentally” putting their pajamas on backwards, offering to brush their teeth a second time. And once the light is off, “Papa, I have to potty.” No, bedtime routines cannot be standardized. They resist being made efficient.

In contrast, we think of seeing patients as a standardizable process; work to be optimized. This idea that work should be as efficient as possible came from the father of business management, Frederick Taylor. Taylor, a mechanical engineer, observed inefficiencies on the factory floor. His work was seminal in the development of the second industrial revolution. Before then no one had applied scientific rigor to productivity. His book, “The Principles of Scientific Management,” written in 1909, is considered the most influential management book of the 20th century. He was the first to use stopwatches to perform time studies, noting how long each task took with the belief that there was one best way. The worker was an extension of the machine, tuned by management such that he was as efficient as possible.

PublicDomain/commons.wikimedia.org/wiki/File:Ford_assembly_line_-_1913.jpg

A more insidious downside on the drive to efficiency lies in the nature of what we do. We aren’t factory workers punching out widgets, we’re physicians caring for people and people cannot be standardized. In this way, seeing patients is more like putting a toddler to bed than like assembling an iPhone. There will always be by-the-ways, basal cells hiding behind the ear, traffic jams, and bags of products that they want to review. Not sure how to use your fluorouracil? Let’s go over it again. Need to talk more about why you have granuloma annulare? Let me explain. Despite Taylor’s vision, some work simply cannot be optimized. And shouldn’t.

“Where’s my 11:30 patient who checked in half an hour ago?!” I asked my medical assistant. “Oh, she had to go to the bathroom.” Tap.
 

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at dermnews@mdedge.com.

Physicians tend to be compulsive multitaskers. We switch from one task to another all the time – even in front of patients. We think we are more efficient and productive, and that we are accomplishing more in less time. In fact, there is no credible evidence that this is true, and a mountain of evidence showing exactly the opposite.

According to this study and others, multitasking results in an average of 2 hours per day of lost productivity. It decreases the quality of work performed and increases cortisol levels, which impedes cognitive functioning, leading to a further decrease in productivity in a vicious cycle, making you increasingly ineffective and destroying your motivation and mood.

On the surface, the reasons for this are not intuitively obvious. After all, simple and routine tasks are easy to perform simultaneously; we can all walk and chew gum at the same time or eat a snack while watching TV. The problems arise when we try to multitask more complex tasks that require thought and decision-making.

It turns out that the pressures of our modern world have evolved faster than our brains. We are still hard-wired for monotasking. When we think we are completing two tasks simultaneously, we are actually performing individual actions in rapid succession. Each time you switch tasks, your brain must turn off the cognitive rules of the previous task and turn on new rules for the next one. When you switch back, the process repeats in reverse. Each of those mental gear shifts takes time and costs us productivity. According to one psychologist, even brief mental blocks created by shifting between tasks can cost as much as 40% of someone’s productive time. We are also far more likely to make mistakes while we are doing it.

Furthermore, you are stifling your creativity and innovation because you don’t focus on one task long enough to come up with original insights. Multitasking also slows down your general cognitive functions, in the same way that keeping many windows are open on your computer slows down the entire system. A study from my alma mater, the University of California, San Francisco, concluded that multitasking negativity affects memory in both younger and older adults (although the effects were greater in older adults) .

So, what to do? The fact remains that, all too often, there really are too many tasks and not enough hours in the day. How can you get through them without falling into the multitasking trap?

The first rule is to prioritize. In his book “The Seven Habits of Highly Effective People,” Stephen Covey makes an important distinction between tasks that are important and those that are merely urgent. Tasks that are important and urgent tend to make time for themselves, because they must be taken care of immediately.

Jobs that are important but not urgent are the ones we tend to try to multitask. Because there is no immediate deadline, we think we can do two or more of them simultaneously, or we fall into the other major productivity trap: procrastination. Neither of those strategies tends to end well. Identify those important but not urgent tasks and force yourself to go through them one by one.

Urgent but unimportant tasks are the productivity thieves. They demand your attention but are not worthy of it. Most tasks in this category can be delegated. I have written about physicians’ workaholic and perfectionist tendencies that drive our conviction that no one else can do anything as well as we can. Does that unimportant task, even if urgent, really demand your time, skills, education, and medical license? Is there someone in your office, or possibly an outside contractor, who could do it just as well, and maybe faster?

In fact, that is the question you should ask every time a project triggers your urge to multitask: “Who could be doing this job – or at least a major part of it – instead of me?”

If your multitasking urges are deeply ingrained – particularly those that involve phones, laptops, and the cloud – you might consider employing electronic aids. SelfControl, for example, is a free, open-sourced app that lets you block your own access to distracting websites, your email servers, social media, or anything else on the Internet. You list the sites you wish to block and set a period of time to block them. Until the set time expires, you will be unable to access those sites, even if you restart your computer or delete the application.

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

Physicians tend to be compulsive multitaskers. We switch from one task to another all the time – even in front of patients. We think we are more efficient and productive, and that we are accomplishing more in less time. In fact, there is no credible evidence that this is true, and a mountain of evidence showing exactly the opposite.

According to this study and others, multitasking results in an average of 2 hours per day of lost productivity. It decreases the quality of work performed and increases cortisol levels, which impedes cognitive functioning, leading to a further decrease in productivity in a vicious cycle, making you increasingly ineffective and destroying your motivation and mood.

On the surface, the reasons for this are not intuitively obvious. After all, simple and routine tasks are easy to perform simultaneously; we can all walk and chew gum at the same time or eat a snack while watching TV. The problems arise when we try to multitask more complex tasks that require thought and decision-making.

It turns out that the pressures of our modern world have evolved faster than our brains. We are still hard-wired for monotasking. When we think we are completing two tasks simultaneously, we are actually performing individual actions in rapid succession. Each time you switch tasks, your brain must turn off the cognitive rules of the previous task and turn on new rules for the next one. When you switch back, the process repeats in reverse. Each of those mental gear shifts takes time and costs us productivity. According to one psychologist, even brief mental blocks created by shifting between tasks can cost as much as 40% of someone’s productive time. We are also far more likely to make mistakes while we are doing it.

Furthermore, you are stifling your creativity and innovation because you don’t focus on one task long enough to come up with original insights. Multitasking also slows down your general cognitive functions, in the same way that keeping many windows are open on your computer slows down the entire system. A study from my alma mater, the University of California, San Francisco, concluded that multitasking negativity affects memory in both younger and older adults (although the effects were greater in older adults) .

So, what to do? The fact remains that, all too often, there really are too many tasks and not enough hours in the day. How can you get through them without falling into the multitasking trap?

The first rule is to prioritize. In his book “The Seven Habits of Highly Effective People,” Stephen Covey makes an important distinction between tasks that are important and those that are merely urgent. Tasks that are important and urgent tend to make time for themselves, because they must be taken care of immediately.

Jobs that are important but not urgent are the ones we tend to try to multitask. Because there is no immediate deadline, we think we can do two or more of them simultaneously, or we fall into the other major productivity trap: procrastination. Neither of those strategies tends to end well. Identify those important but not urgent tasks and force yourself to go through them one by one.

Urgent but unimportant tasks are the productivity thieves. They demand your attention but are not worthy of it. Most tasks in this category can be delegated. I have written about physicians’ workaholic and perfectionist tendencies that drive our conviction that no one else can do anything as well as we can. Does that unimportant task, even if urgent, really demand your time, skills, education, and medical license? Is there someone in your office, or possibly an outside contractor, who could do it just as well, and maybe faster?

In fact, that is the question you should ask every time a project triggers your urge to multitask: “Who could be doing this job – or at least a major part of it – instead of me?”

If your multitasking urges are deeply ingrained – particularly those that involve phones, laptops, and the cloud – you might consider employing electronic aids. SelfControl, for example, is a free, open-sourced app that lets you block your own access to distracting websites, your email servers, social media, or anything else on the Internet. You list the sites you wish to block and set a period of time to block them. Until the set time expires, you will be unable to access those sites, even if you restart your computer or delete the application.

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

Physicians tend to be compulsive multitaskers. We switch from one task to another all the time – even in front of patients. We think we are more efficient and productive, and that we are accomplishing more in less time. In fact, there is no credible evidence that this is true, and a mountain of evidence showing exactly the opposite.

According to this study and others, multitasking results in an average of 2 hours per day of lost productivity. It decreases the quality of work performed and increases cortisol levels, which impedes cognitive functioning, leading to a further decrease in productivity in a vicious cycle, making you increasingly ineffective and destroying your motivation and mood.

On the surface, the reasons for this are not intuitively obvious. After all, simple and routine tasks are easy to perform simultaneously; we can all walk and chew gum at the same time or eat a snack while watching TV. The problems arise when we try to multitask more complex tasks that require thought and decision-making.

It turns out that the pressures of our modern world have evolved faster than our brains. We are still hard-wired for monotasking. When we think we are completing two tasks simultaneously, we are actually performing individual actions in rapid succession. Each time you switch tasks, your brain must turn off the cognitive rules of the previous task and turn on new rules for the next one. When you switch back, the process repeats in reverse. Each of those mental gear shifts takes time and costs us productivity. According to one psychologist, even brief mental blocks created by shifting between tasks can cost as much as 40% of someone’s productive time. We are also far more likely to make mistakes while we are doing it.

Furthermore, you are stifling your creativity and innovation because you don’t focus on one task long enough to come up with original insights. Multitasking also slows down your general cognitive functions, in the same way that keeping many windows are open on your computer slows down the entire system. A study from my alma mater, the University of California, San Francisco, concluded that multitasking negativity affects memory in both younger and older adults (although the effects were greater in older adults) .

So, what to do? The fact remains that, all too often, there really are too many tasks and not enough hours in the day. How can you get through them without falling into the multitasking trap?

The first rule is to prioritize. In his book “The Seven Habits of Highly Effective People,” Stephen Covey makes an important distinction between tasks that are important and those that are merely urgent. Tasks that are important and urgent tend to make time for themselves, because they must be taken care of immediately.

Jobs that are important but not urgent are the ones we tend to try to multitask. Because there is no immediate deadline, we think we can do two or more of them simultaneously, or we fall into the other major productivity trap: procrastination. Neither of those strategies tends to end well. Identify those important but not urgent tasks and force yourself to go through them one by one.

Urgent but unimportant tasks are the productivity thieves. They demand your attention but are not worthy of it. Most tasks in this category can be delegated. I have written about physicians’ workaholic and perfectionist tendencies that drive our conviction that no one else can do anything as well as we can. Does that unimportant task, even if urgent, really demand your time, skills, education, and medical license? Is there someone in your office, or possibly an outside contractor, who could do it just as well, and maybe faster?

In fact, that is the question you should ask every time a project triggers your urge to multitask: “Who could be doing this job – or at least a major part of it – instead of me?”

If your multitasking urges are deeply ingrained – particularly those that involve phones, laptops, and the cloud – you might consider employing electronic aids. SelfControl, for example, is a free, open-sourced app that lets you block your own access to distracting websites, your email servers, social media, or anything else on the Internet. You list the sites you wish to block and set a period of time to block them. Until the set time expires, you will be unable to access those sites, even if you restart your computer or delete the application.

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