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Cell Phone Use Linked to Higher Heart Disease Risk
“We found that a poor sleep pattern, psychological distress, and neuroticism significantly mediated the positive association between weekly mobile phone usage time and the risk for incident CVD, with a mediating proportion of 5.11%, 11.50%, and 2.25%, respectively,” said principal investigator Xianhui Qin, MD, professor of nephrology at Southern Medical University, Guangzhou, China.
Poor sleep patterns and poor mental health could disrupt circadian rhythms and endocrine and metabolic functions, as well as increase inflammation, he explained.
In addition, chronic exposure to radiofrequency electromagnetic fields (RF-EMF) emitted from cell phones could lead to oxidative stress and an inflammatory response. Combined with smoking and diabetes, this exposure “may have a synergistic effect in increasing CVD risk,” Dr. Qin suggested.
The study was published online in the Canadian Journal of Cardiology.
Risk Underestimated?
The researchers aimed to examine the association of regular cell phone use with incident CVD and explore the mediating effects of sleep and mental health using linked hospital and mortality records.
Their analysis included 444,027 participants (mean age, 56 years; 44% men) without a history of CVD from the UK Biobank. A total of 378,161 participants were regular cell phone users.
Regular cell phone use was defined as at least one call per week. Weekly use was self-reported as the average time of calls per week during the previous 3 months.
The primary outcome was incident CVD. Secondary outcomes were each component of CVD (ie, coronary heart disease, stroke, atrial fibrillation, and heart failure) and increased carotid intima media thickness (CIMT).
Compared with nonregular cell phone users, regular users were younger, had higher proportions of current smokers and urban residents, and had lower proportions of history of hypertension and diabetes. They also had higher income, Townsend deprivation index, and body mass index, and lower education levels.
During a median follow-up of 12.3 years, 56,181 participants developed incident CVD. Compared with nonregular cell phone users, regular users had a significantly higher risk for incident CVD (hazard ratio, 1.04) and increased CIMT (odds ratio, 1.11).
Among regular cell phone users, the duration of cell phone use and hands-free device/speakerphone use during calls was not significantly associated with incident CVD. Yet a significant and positive dose-response relationship was seen between weekly cell phone usage time and the risk for CVD. The positive association was stronger in current vs noncurrent smokers and people with vs without diabetes.
To different extents, sleep patterns (5.11%), psychologic distress (11.5%), and neuroticism (2.25%) mediated the relationship between weekly cell phone usage time and the risk for incident CVD.
“Our study suggests that despite the advantages of mobile phone use, we should also pay attention to the potential harm of mobile phone use to cardiovascular health,” Dr. Qin said. “Future studies to assess the risk-benefit balance will help promote mobile phone use patterns that are conducive to cardiovascular health.”
Meanwhile, he added, “We encourage measures to reduce time spent on mobile phones to promote the primary prevention of CVD. On the other hand, improving sleep and mental health status may help reduce the higher risk of CVD associated with mobile phone use.”
There are several limitations to the study in addition to its observational nature, which cannot show cause and effect. The questionnaires on cell phone use were restricted to phone calls; other use patterns of cell phones (eg, messaging, watching videos, and browsing the web) were not considered. Although the researchers adjusted for many potential confounders, unmeasured confounding bias (eg, the type of cell phone used and other sources of RF-EMF) cannot be eliminated.
Weak Link?
In a comment, Nicholas Grubic, MSc, a PhD student in epidemiology at the University of Toronto, Ontario, Canada, and coauthor of a related editorial, said, “I found it interesting that there was a connection observed between mobile phone use and CVD. However, it is crucial to understand that this link appeared to be much weaker compared with other well-known cardiovascular risk factors, such as smoking, diabetes, and high blood pressure. For now, mobile phone use should not be a major concern for most people.”
Nevertheless, clinicians should encourage patients to practice healthy habits around their screen time, he advised. “This could include limiting mobile phone use before bedtime and taking regular breaks to engage in activities that promote heart health, such as exercising or spending time outdoors.
“For the time being, we probably won’t see mobile phone use included in standard assessments for cardiovascular risk or as a focal point of cardiovascular health promotion initiatives,” he added. Instead, clinicians should “focus on established risk factors that have a stronger impact on patients’ cardiovascular health.”
Nieca Goldberg, MD, a clinical associate professor of medicine at NYU Grossman School of Medicine in New York City and American Heart Association volunteer expert, had a similar message. “You don’t have to go back to using a landline,” she said. “Instead, patients should be more mindful of how much phone use is taking away from their physical activity, keeping them from sleeping, and causing them stress.” Clinicians should also remember to counsel smokers on smoking cessation.
“It would be important for future studies to look at time spent on the phone and the type of activities patients are doing on their phones, such as social media, calls, texts, movies, or streaming TV shows,” she said. “It would be important to see how phone use is leading to a sedentary lifestyle” and what that means for a larger, more diverse population.
The study was supported by the National Key R&D Program, the National Natural Science Foundation of China, and the Outstanding Youth Development Scheme of Nanfang Hospital, Southern Medical University. Dr. Qin, Dr. Grubic, and Dr. Goldberg reported having no relevant financial relationships.
A version of this article first appeared on Medscape.com.
“We found that a poor sleep pattern, psychological distress, and neuroticism significantly mediated the positive association between weekly mobile phone usage time and the risk for incident CVD, with a mediating proportion of 5.11%, 11.50%, and 2.25%, respectively,” said principal investigator Xianhui Qin, MD, professor of nephrology at Southern Medical University, Guangzhou, China.
Poor sleep patterns and poor mental health could disrupt circadian rhythms and endocrine and metabolic functions, as well as increase inflammation, he explained.
In addition, chronic exposure to radiofrequency electromagnetic fields (RF-EMF) emitted from cell phones could lead to oxidative stress and an inflammatory response. Combined with smoking and diabetes, this exposure “may have a synergistic effect in increasing CVD risk,” Dr. Qin suggested.
The study was published online in the Canadian Journal of Cardiology.
Risk Underestimated?
The researchers aimed to examine the association of regular cell phone use with incident CVD and explore the mediating effects of sleep and mental health using linked hospital and mortality records.
Their analysis included 444,027 participants (mean age, 56 years; 44% men) without a history of CVD from the UK Biobank. A total of 378,161 participants were regular cell phone users.
Regular cell phone use was defined as at least one call per week. Weekly use was self-reported as the average time of calls per week during the previous 3 months.
The primary outcome was incident CVD. Secondary outcomes were each component of CVD (ie, coronary heart disease, stroke, atrial fibrillation, and heart failure) and increased carotid intima media thickness (CIMT).
Compared with nonregular cell phone users, regular users were younger, had higher proportions of current smokers and urban residents, and had lower proportions of history of hypertension and diabetes. They also had higher income, Townsend deprivation index, and body mass index, and lower education levels.
During a median follow-up of 12.3 years, 56,181 participants developed incident CVD. Compared with nonregular cell phone users, regular users had a significantly higher risk for incident CVD (hazard ratio, 1.04) and increased CIMT (odds ratio, 1.11).
Among regular cell phone users, the duration of cell phone use and hands-free device/speakerphone use during calls was not significantly associated with incident CVD. Yet a significant and positive dose-response relationship was seen between weekly cell phone usage time and the risk for CVD. The positive association was stronger in current vs noncurrent smokers and people with vs without diabetes.
To different extents, sleep patterns (5.11%), psychologic distress (11.5%), and neuroticism (2.25%) mediated the relationship between weekly cell phone usage time and the risk for incident CVD.
“Our study suggests that despite the advantages of mobile phone use, we should also pay attention to the potential harm of mobile phone use to cardiovascular health,” Dr. Qin said. “Future studies to assess the risk-benefit balance will help promote mobile phone use patterns that are conducive to cardiovascular health.”
Meanwhile, he added, “We encourage measures to reduce time spent on mobile phones to promote the primary prevention of CVD. On the other hand, improving sleep and mental health status may help reduce the higher risk of CVD associated with mobile phone use.”
There are several limitations to the study in addition to its observational nature, which cannot show cause and effect. The questionnaires on cell phone use were restricted to phone calls; other use patterns of cell phones (eg, messaging, watching videos, and browsing the web) were not considered. Although the researchers adjusted for many potential confounders, unmeasured confounding bias (eg, the type of cell phone used and other sources of RF-EMF) cannot be eliminated.
Weak Link?
In a comment, Nicholas Grubic, MSc, a PhD student in epidemiology at the University of Toronto, Ontario, Canada, and coauthor of a related editorial, said, “I found it interesting that there was a connection observed between mobile phone use and CVD. However, it is crucial to understand that this link appeared to be much weaker compared with other well-known cardiovascular risk factors, such as smoking, diabetes, and high blood pressure. For now, mobile phone use should not be a major concern for most people.”
Nevertheless, clinicians should encourage patients to practice healthy habits around their screen time, he advised. “This could include limiting mobile phone use before bedtime and taking regular breaks to engage in activities that promote heart health, such as exercising or spending time outdoors.
“For the time being, we probably won’t see mobile phone use included in standard assessments for cardiovascular risk or as a focal point of cardiovascular health promotion initiatives,” he added. Instead, clinicians should “focus on established risk factors that have a stronger impact on patients’ cardiovascular health.”
Nieca Goldberg, MD, a clinical associate professor of medicine at NYU Grossman School of Medicine in New York City and American Heart Association volunteer expert, had a similar message. “You don’t have to go back to using a landline,” she said. “Instead, patients should be more mindful of how much phone use is taking away from their physical activity, keeping them from sleeping, and causing them stress.” Clinicians should also remember to counsel smokers on smoking cessation.
“It would be important for future studies to look at time spent on the phone and the type of activities patients are doing on their phones, such as social media, calls, texts, movies, or streaming TV shows,” she said. “It would be important to see how phone use is leading to a sedentary lifestyle” and what that means for a larger, more diverse population.
The study was supported by the National Key R&D Program, the National Natural Science Foundation of China, and the Outstanding Youth Development Scheme of Nanfang Hospital, Southern Medical University. Dr. Qin, Dr. Grubic, and Dr. Goldberg reported having no relevant financial relationships.
A version of this article first appeared on Medscape.com.
“We found that a poor sleep pattern, psychological distress, and neuroticism significantly mediated the positive association between weekly mobile phone usage time and the risk for incident CVD, with a mediating proportion of 5.11%, 11.50%, and 2.25%, respectively,” said principal investigator Xianhui Qin, MD, professor of nephrology at Southern Medical University, Guangzhou, China.
Poor sleep patterns and poor mental health could disrupt circadian rhythms and endocrine and metabolic functions, as well as increase inflammation, he explained.
In addition, chronic exposure to radiofrequency electromagnetic fields (RF-EMF) emitted from cell phones could lead to oxidative stress and an inflammatory response. Combined with smoking and diabetes, this exposure “may have a synergistic effect in increasing CVD risk,” Dr. Qin suggested.
The study was published online in the Canadian Journal of Cardiology.
Risk Underestimated?
The researchers aimed to examine the association of regular cell phone use with incident CVD and explore the mediating effects of sleep and mental health using linked hospital and mortality records.
Their analysis included 444,027 participants (mean age, 56 years; 44% men) without a history of CVD from the UK Biobank. A total of 378,161 participants were regular cell phone users.
Regular cell phone use was defined as at least one call per week. Weekly use was self-reported as the average time of calls per week during the previous 3 months.
The primary outcome was incident CVD. Secondary outcomes were each component of CVD (ie, coronary heart disease, stroke, atrial fibrillation, and heart failure) and increased carotid intima media thickness (CIMT).
Compared with nonregular cell phone users, regular users were younger, had higher proportions of current smokers and urban residents, and had lower proportions of history of hypertension and diabetes. They also had higher income, Townsend deprivation index, and body mass index, and lower education levels.
During a median follow-up of 12.3 years, 56,181 participants developed incident CVD. Compared with nonregular cell phone users, regular users had a significantly higher risk for incident CVD (hazard ratio, 1.04) and increased CIMT (odds ratio, 1.11).
Among regular cell phone users, the duration of cell phone use and hands-free device/speakerphone use during calls was not significantly associated with incident CVD. Yet a significant and positive dose-response relationship was seen between weekly cell phone usage time and the risk for CVD. The positive association was stronger in current vs noncurrent smokers and people with vs without diabetes.
To different extents, sleep patterns (5.11%), psychologic distress (11.5%), and neuroticism (2.25%) mediated the relationship between weekly cell phone usage time and the risk for incident CVD.
“Our study suggests that despite the advantages of mobile phone use, we should also pay attention to the potential harm of mobile phone use to cardiovascular health,” Dr. Qin said. “Future studies to assess the risk-benefit balance will help promote mobile phone use patterns that are conducive to cardiovascular health.”
Meanwhile, he added, “We encourage measures to reduce time spent on mobile phones to promote the primary prevention of CVD. On the other hand, improving sleep and mental health status may help reduce the higher risk of CVD associated with mobile phone use.”
There are several limitations to the study in addition to its observational nature, which cannot show cause and effect. The questionnaires on cell phone use were restricted to phone calls; other use patterns of cell phones (eg, messaging, watching videos, and browsing the web) were not considered. Although the researchers adjusted for many potential confounders, unmeasured confounding bias (eg, the type of cell phone used and other sources of RF-EMF) cannot be eliminated.
Weak Link?
In a comment, Nicholas Grubic, MSc, a PhD student in epidemiology at the University of Toronto, Ontario, Canada, and coauthor of a related editorial, said, “I found it interesting that there was a connection observed between mobile phone use and CVD. However, it is crucial to understand that this link appeared to be much weaker compared with other well-known cardiovascular risk factors, such as smoking, diabetes, and high blood pressure. For now, mobile phone use should not be a major concern for most people.”
Nevertheless, clinicians should encourage patients to practice healthy habits around their screen time, he advised. “This could include limiting mobile phone use before bedtime and taking regular breaks to engage in activities that promote heart health, such as exercising or spending time outdoors.
“For the time being, we probably won’t see mobile phone use included in standard assessments for cardiovascular risk or as a focal point of cardiovascular health promotion initiatives,” he added. Instead, clinicians should “focus on established risk factors that have a stronger impact on patients’ cardiovascular health.”
Nieca Goldberg, MD, a clinical associate professor of medicine at NYU Grossman School of Medicine in New York City and American Heart Association volunteer expert, had a similar message. “You don’t have to go back to using a landline,” she said. “Instead, patients should be more mindful of how much phone use is taking away from their physical activity, keeping them from sleeping, and causing them stress.” Clinicians should also remember to counsel smokers on smoking cessation.
“It would be important for future studies to look at time spent on the phone and the type of activities patients are doing on their phones, such as social media, calls, texts, movies, or streaming TV shows,” she said. “It would be important to see how phone use is leading to a sedentary lifestyle” and what that means for a larger, more diverse population.
The study was supported by the National Key R&D Program, the National Natural Science Foundation of China, and the Outstanding Youth Development Scheme of Nanfang Hospital, Southern Medical University. Dr. Qin, Dr. Grubic, and Dr. Goldberg reported having no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE CANADIAN JOURNAL OF CARDIOLOGY
First-Time Fathers Experience Period of High Psychological Risk
Anxiety and stress during fatherhood receive less research attention than do anxiety and stress during motherhood.
Longitudinal data tracking the evolution of men’s mental health following the birth of the first child are even rarer, especially in the French population. Only two studies of the subject have been conducted. They were dedicated solely to paternal depression and limited to the first 4 months post partum. Better understanding of the risk in the population can not only help identify public health issues, but also aid in defining targeted preventive approaches.
French researchers in epidemiology and public health sought to expand our knowledge of the mental health trajectories of new fathers using 9 years of data from the CONSTANCES cohort. Within this cohort, participants filled out self-administered questionnaires annually. They declared their parental status and the presence of mental illnesses. They also completed questionnaires to assess mental health, such as the Center for Epidemiologic Studies Depression Scale for depression and the General Health Questionnaire for depressive, anxious, and somatic disorders. Thresholds for each score were established to characterize the severity of symptoms. In addition, the researchers analyzed all factors (eg, sociodemographic, psychosocial, lifestyle, professional, family, or cultural) that potentially are associated with poor mental health and were available within the questionnaires.
The study included 6299 men who had their first child and for whom at least one mental health measure was collected during the follow-up period. These men had an average age of 38 years at inclusion, 88% lived with a partner, and 85% were employed. Overall, 7.9% of this male cohort self-reported a mental illness during the study, with 5.6% of illnesses occurring before the child’s birth and 9.7% after. Anxiety affected 6.5% of the cohort, and it was more pronounced after the birth than before (7.8% after vs 4.9% before).
The rate of clinically significant symptoms averaged 23.2% during the study period, increasing from 18.3% to 25.2% after the birth. The discrepancy between the self-declared diagnosis by new fathers and the symptom-related score highlights underreporting or insufficient awareness among men.
After conducting a latent class analysis, the researchers identified three homogeneous subgroups of men who had comparable mental health trajectories over time. The first group (90.3% of the cohort) maintained a constant and low risk for mental illnesses. The second (4.1%) presented a high and generally constant risk over time. Finally, 5.6% of the cohort had a temporarily high risk in the 2-4 years surrounding the birth.
The risk factors associated with being at a transiently high risk for mental illness were, in order of descending significance, not having a job, having had at least one negative experience during childhood, forgoing healthcare for financial reasons, and being aged 35-39 years (adjusted odds ratio [AOR] between 3.01 and 1.61). The risk factors associated with a high and constant mental illness risk were, in order of descending significance, being aged 60 years or older, not having a job, not living with a partner, being aged 40-44 years, and having other children in the following years (AOR between 3.79 and 1.85).
The authors noted that the risk factors for mental health challenges associated with fatherhood do not imply causality, the meaning of which would also need further study. They contended that French fathers, who on average are entitled to 2 weeks of paid paternity leave, may struggle to manage their time, professional responsibilities, and parenting duties. Consequently, they may experience dissatisfaction and difficulty seeking support, assistance, or a mental health diagnosis, especially in the face of a mental health risk to which they are less attuned than women.
This story was translated from Univadis France, which is part of the Medscape Professional Network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Anxiety and stress during fatherhood receive less research attention than do anxiety and stress during motherhood.
Longitudinal data tracking the evolution of men’s mental health following the birth of the first child are even rarer, especially in the French population. Only two studies of the subject have been conducted. They were dedicated solely to paternal depression and limited to the first 4 months post partum. Better understanding of the risk in the population can not only help identify public health issues, but also aid in defining targeted preventive approaches.
French researchers in epidemiology and public health sought to expand our knowledge of the mental health trajectories of new fathers using 9 years of data from the CONSTANCES cohort. Within this cohort, participants filled out self-administered questionnaires annually. They declared their parental status and the presence of mental illnesses. They also completed questionnaires to assess mental health, such as the Center for Epidemiologic Studies Depression Scale for depression and the General Health Questionnaire for depressive, anxious, and somatic disorders. Thresholds for each score were established to characterize the severity of symptoms. In addition, the researchers analyzed all factors (eg, sociodemographic, psychosocial, lifestyle, professional, family, or cultural) that potentially are associated with poor mental health and were available within the questionnaires.
The study included 6299 men who had their first child and for whom at least one mental health measure was collected during the follow-up period. These men had an average age of 38 years at inclusion, 88% lived with a partner, and 85% were employed. Overall, 7.9% of this male cohort self-reported a mental illness during the study, with 5.6% of illnesses occurring before the child’s birth and 9.7% after. Anxiety affected 6.5% of the cohort, and it was more pronounced after the birth than before (7.8% after vs 4.9% before).
The rate of clinically significant symptoms averaged 23.2% during the study period, increasing from 18.3% to 25.2% after the birth. The discrepancy between the self-declared diagnosis by new fathers and the symptom-related score highlights underreporting or insufficient awareness among men.
After conducting a latent class analysis, the researchers identified three homogeneous subgroups of men who had comparable mental health trajectories over time. The first group (90.3% of the cohort) maintained a constant and low risk for mental illnesses. The second (4.1%) presented a high and generally constant risk over time. Finally, 5.6% of the cohort had a temporarily high risk in the 2-4 years surrounding the birth.
The risk factors associated with being at a transiently high risk for mental illness were, in order of descending significance, not having a job, having had at least one negative experience during childhood, forgoing healthcare for financial reasons, and being aged 35-39 years (adjusted odds ratio [AOR] between 3.01 and 1.61). The risk factors associated with a high and constant mental illness risk were, in order of descending significance, being aged 60 years or older, not having a job, not living with a partner, being aged 40-44 years, and having other children in the following years (AOR between 3.79 and 1.85).
The authors noted that the risk factors for mental health challenges associated with fatherhood do not imply causality, the meaning of which would also need further study. They contended that French fathers, who on average are entitled to 2 weeks of paid paternity leave, may struggle to manage their time, professional responsibilities, and parenting duties. Consequently, they may experience dissatisfaction and difficulty seeking support, assistance, or a mental health diagnosis, especially in the face of a mental health risk to which they are less attuned than women.
This story was translated from Univadis France, which is part of the Medscape Professional Network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Anxiety and stress during fatherhood receive less research attention than do anxiety and stress during motherhood.
Longitudinal data tracking the evolution of men’s mental health following the birth of the first child are even rarer, especially in the French population. Only two studies of the subject have been conducted. They were dedicated solely to paternal depression and limited to the first 4 months post partum. Better understanding of the risk in the population can not only help identify public health issues, but also aid in defining targeted preventive approaches.
French researchers in epidemiology and public health sought to expand our knowledge of the mental health trajectories of new fathers using 9 years of data from the CONSTANCES cohort. Within this cohort, participants filled out self-administered questionnaires annually. They declared their parental status and the presence of mental illnesses. They also completed questionnaires to assess mental health, such as the Center for Epidemiologic Studies Depression Scale for depression and the General Health Questionnaire for depressive, anxious, and somatic disorders. Thresholds for each score were established to characterize the severity of symptoms. In addition, the researchers analyzed all factors (eg, sociodemographic, psychosocial, lifestyle, professional, family, or cultural) that potentially are associated with poor mental health and were available within the questionnaires.
The study included 6299 men who had their first child and for whom at least one mental health measure was collected during the follow-up period. These men had an average age of 38 years at inclusion, 88% lived with a partner, and 85% were employed. Overall, 7.9% of this male cohort self-reported a mental illness during the study, with 5.6% of illnesses occurring before the child’s birth and 9.7% after. Anxiety affected 6.5% of the cohort, and it was more pronounced after the birth than before (7.8% after vs 4.9% before).
The rate of clinically significant symptoms averaged 23.2% during the study period, increasing from 18.3% to 25.2% after the birth. The discrepancy between the self-declared diagnosis by new fathers and the symptom-related score highlights underreporting or insufficient awareness among men.
After conducting a latent class analysis, the researchers identified three homogeneous subgroups of men who had comparable mental health trajectories over time. The first group (90.3% of the cohort) maintained a constant and low risk for mental illnesses. The second (4.1%) presented a high and generally constant risk over time. Finally, 5.6% of the cohort had a temporarily high risk in the 2-4 years surrounding the birth.
The risk factors associated with being at a transiently high risk for mental illness were, in order of descending significance, not having a job, having had at least one negative experience during childhood, forgoing healthcare for financial reasons, and being aged 35-39 years (adjusted odds ratio [AOR] between 3.01 and 1.61). The risk factors associated with a high and constant mental illness risk were, in order of descending significance, being aged 60 years or older, not having a job, not living with a partner, being aged 40-44 years, and having other children in the following years (AOR between 3.79 and 1.85).
The authors noted that the risk factors for mental health challenges associated with fatherhood do not imply causality, the meaning of which would also need further study. They contended that French fathers, who on average are entitled to 2 weeks of paid paternity leave, may struggle to manage their time, professional responsibilities, and parenting duties. Consequently, they may experience dissatisfaction and difficulty seeking support, assistance, or a mental health diagnosis, especially in the face of a mental health risk to which they are less attuned than women.
This story was translated from Univadis France, which is part of the Medscape Professional Network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Evidence Growing for Inflammation’s Role in Elevating Risk for Psychiatric Illness
New research provides more evidence that inflammation may contribute to the development of psychiatric disorders and suggests that measuring certain inflammatory biomarkers may aid in the early identification of individuals at high risk.
Using large-scale datasets, researchers found that elevated levels of certain inflammatory biomarkers, particularly leukocytes, haptoglobin, and C-reactive protein (CRP), and lower levels of anti-inflammatory immunoglobulin G (IgG) were associated with an increased risk for psychiatric disorders.
Individuals with psychiatric disorders had persistently higher levels of leukocytes and haptoglobin, as well as persistently lower levels of IgG, than controls during the 30 years before diagnosis, which suggest “long-term processes and may aid in the identification of individuals at high risk,” the researchers wrote.
In addition, a higher level of leukocytes was consistently associated with increased odds of depression across different methods of Mendelian randomization (MR) analysis, “indicating a possible causal relationship between leukocytes and depression,” they said.
The study, with first author Yu Zeng, MSc, with the Mental Health Center and West China Biomedical Big Data Center, West China Hospital, Sichuan University, Chengdu, China, was published online on August 21 in JAMA Psychiatry.
Inflammatory Phenotype
Individuals with psychiatric disorders have been found to have elevated levels of inflammatory biomarkers, but prospective evidence is limited regarding the association between inflammatory biomarkers and subsequent psychiatric disorders risk.
To investigate further, the researchers employed a “triangulation” approach consisting of an exploration dataset of 585,279 adults in the Swedish AMORIS cohort with no prior psychiatric diagnoses and a measurement of at least one inflammatory biomarker, a validation dataset of 485,620 UK Biobank participants, and genetic and MR analyses using genome-wide association study summary statistics.
In the AMORIS cohort, individuals with a higher than median level of leukocytes (hazard ratio [HR], 1.11), haptoglobin (HR, 1.13), or CRP (HR, 1.02) had an elevated risk for any psychiatric disorder. In contrast, there was an inverse association for IgG level (HR, 0.92).
“The estimates were comparable for depression, anxiety, and stress-related disorders, specifically, and these results were largely validated in the UK Biobank,” the authors reported.
In trajectory analyses, compared with controls, individuals with psychiatric disorders had higher leukocyte and haptoglobin levels and lower IgG up to three decades before being diagnosed.
The MR analysis suggested a possible causal relationship between leukocytes and depression.
The underlying mechanisms for the associations of serum leukocytes, haptoglobin, CRP, and IgG with psychiatry disorders remain unclear.
“Possible explanations mainly include blood-brain barrier disruption, microglia activation, neurotransmission impairment, and other interactions between inflammations and neuropathology,” the researchers wrote.
A related paper published online on August 21 in JAMA Psychiatry looked at trajectories of inflammation in childhood and risk for mental and cardiometabolic disorders in adulthood.
This longitudinal cohort study found that having persistently raised levels of inflammation as measured by CRP throughout childhood and adolescence, peaking at age 9 years, were associated with an increased risk of developing psychosis disorder, severe depression, and higher levels of insulin resistance.
Support for Precision Psychiatry
This study is “another strong indication that inflammation plays a role in depression,” Andrew H. Miller, MD, professor of psychiatry and behavioral sciences and director of the behavioral immunology program, Emory University School of Medicine, Atlanta, Georgia, who wasn’t involved in the study, told this news organization.
“The work adds to the mounting data that there exists an inflammatory phenotype of depression that may uniquely respond to treatment and may have a unique trajectory,” Dr. Miller said.
“Eventually the field will want to embrace this novel phenotype and better understand how to recognize it and treat it. This is our entrée into precision psychiatry where we identify the right treatment for the right patient at the right time based on an understanding of the underlying cause of their illness,” Dr. Miller added.
Also weighing in, Alexander B. Niculescu III, MD, PhD, professor of psychiatry and medical neuroscience, Indiana University School of Medicine, Indianapolis, cautioned that these biomarkers are “very nonspecific and are likely related to these subjects that go on to develop psychiatric disorders having more stressful, adverse life trajectories.”
“There are better, more specific blood biomarkers for psychiatric disorders already available,” Dr. Niculescu told this news organization.
His group recently reported that a panel of blood-based biomarkers can distinguish between depression and bipolar disorder, predict a person’s future risk for these disorders, and inform more tailored medication choices.
Notably, they observed a strong circadian clock gene component to mood disorders, which helps explain why some patients’ conditions become worse with seasonal changes. It also explains the sleep alterations that occur among patients with mood disorders, they said.
This study had no commercial funding. Yu Zeng and Dr. Miller had no relevant disclosures. Dr. Niculescu is a cofounder of MindX Sciences and is listed as inventor on a patent application filed by Indiana University.
A version of this article first appeared on Medscape.com.
New research provides more evidence that inflammation may contribute to the development of psychiatric disorders and suggests that measuring certain inflammatory biomarkers may aid in the early identification of individuals at high risk.
Using large-scale datasets, researchers found that elevated levels of certain inflammatory biomarkers, particularly leukocytes, haptoglobin, and C-reactive protein (CRP), and lower levels of anti-inflammatory immunoglobulin G (IgG) were associated with an increased risk for psychiatric disorders.
Individuals with psychiatric disorders had persistently higher levels of leukocytes and haptoglobin, as well as persistently lower levels of IgG, than controls during the 30 years before diagnosis, which suggest “long-term processes and may aid in the identification of individuals at high risk,” the researchers wrote.
In addition, a higher level of leukocytes was consistently associated with increased odds of depression across different methods of Mendelian randomization (MR) analysis, “indicating a possible causal relationship between leukocytes and depression,” they said.
The study, with first author Yu Zeng, MSc, with the Mental Health Center and West China Biomedical Big Data Center, West China Hospital, Sichuan University, Chengdu, China, was published online on August 21 in JAMA Psychiatry.
Inflammatory Phenotype
Individuals with psychiatric disorders have been found to have elevated levels of inflammatory biomarkers, but prospective evidence is limited regarding the association between inflammatory biomarkers and subsequent psychiatric disorders risk.
To investigate further, the researchers employed a “triangulation” approach consisting of an exploration dataset of 585,279 adults in the Swedish AMORIS cohort with no prior psychiatric diagnoses and a measurement of at least one inflammatory biomarker, a validation dataset of 485,620 UK Biobank participants, and genetic and MR analyses using genome-wide association study summary statistics.
In the AMORIS cohort, individuals with a higher than median level of leukocytes (hazard ratio [HR], 1.11), haptoglobin (HR, 1.13), or CRP (HR, 1.02) had an elevated risk for any psychiatric disorder. In contrast, there was an inverse association for IgG level (HR, 0.92).
“The estimates were comparable for depression, anxiety, and stress-related disorders, specifically, and these results were largely validated in the UK Biobank,” the authors reported.
In trajectory analyses, compared with controls, individuals with psychiatric disorders had higher leukocyte and haptoglobin levels and lower IgG up to three decades before being diagnosed.
The MR analysis suggested a possible causal relationship between leukocytes and depression.
The underlying mechanisms for the associations of serum leukocytes, haptoglobin, CRP, and IgG with psychiatry disorders remain unclear.
“Possible explanations mainly include blood-brain barrier disruption, microglia activation, neurotransmission impairment, and other interactions between inflammations and neuropathology,” the researchers wrote.
A related paper published online on August 21 in JAMA Psychiatry looked at trajectories of inflammation in childhood and risk for mental and cardiometabolic disorders in adulthood.
This longitudinal cohort study found that having persistently raised levels of inflammation as measured by CRP throughout childhood and adolescence, peaking at age 9 years, were associated with an increased risk of developing psychosis disorder, severe depression, and higher levels of insulin resistance.
Support for Precision Psychiatry
This study is “another strong indication that inflammation plays a role in depression,” Andrew H. Miller, MD, professor of psychiatry and behavioral sciences and director of the behavioral immunology program, Emory University School of Medicine, Atlanta, Georgia, who wasn’t involved in the study, told this news organization.
“The work adds to the mounting data that there exists an inflammatory phenotype of depression that may uniquely respond to treatment and may have a unique trajectory,” Dr. Miller said.
“Eventually the field will want to embrace this novel phenotype and better understand how to recognize it and treat it. This is our entrée into precision psychiatry where we identify the right treatment for the right patient at the right time based on an understanding of the underlying cause of their illness,” Dr. Miller added.
Also weighing in, Alexander B. Niculescu III, MD, PhD, professor of psychiatry and medical neuroscience, Indiana University School of Medicine, Indianapolis, cautioned that these biomarkers are “very nonspecific and are likely related to these subjects that go on to develop psychiatric disorders having more stressful, adverse life trajectories.”
“There are better, more specific blood biomarkers for psychiatric disorders already available,” Dr. Niculescu told this news organization.
His group recently reported that a panel of blood-based biomarkers can distinguish between depression and bipolar disorder, predict a person’s future risk for these disorders, and inform more tailored medication choices.
Notably, they observed a strong circadian clock gene component to mood disorders, which helps explain why some patients’ conditions become worse with seasonal changes. It also explains the sleep alterations that occur among patients with mood disorders, they said.
This study had no commercial funding. Yu Zeng and Dr. Miller had no relevant disclosures. Dr. Niculescu is a cofounder of MindX Sciences and is listed as inventor on a patent application filed by Indiana University.
A version of this article first appeared on Medscape.com.
New research provides more evidence that inflammation may contribute to the development of psychiatric disorders and suggests that measuring certain inflammatory biomarkers may aid in the early identification of individuals at high risk.
Using large-scale datasets, researchers found that elevated levels of certain inflammatory biomarkers, particularly leukocytes, haptoglobin, and C-reactive protein (CRP), and lower levels of anti-inflammatory immunoglobulin G (IgG) were associated with an increased risk for psychiatric disorders.
Individuals with psychiatric disorders had persistently higher levels of leukocytes and haptoglobin, as well as persistently lower levels of IgG, than controls during the 30 years before diagnosis, which suggest “long-term processes and may aid in the identification of individuals at high risk,” the researchers wrote.
In addition, a higher level of leukocytes was consistently associated with increased odds of depression across different methods of Mendelian randomization (MR) analysis, “indicating a possible causal relationship between leukocytes and depression,” they said.
The study, with first author Yu Zeng, MSc, with the Mental Health Center and West China Biomedical Big Data Center, West China Hospital, Sichuan University, Chengdu, China, was published online on August 21 in JAMA Psychiatry.
Inflammatory Phenotype
Individuals with psychiatric disorders have been found to have elevated levels of inflammatory biomarkers, but prospective evidence is limited regarding the association between inflammatory biomarkers and subsequent psychiatric disorders risk.
To investigate further, the researchers employed a “triangulation” approach consisting of an exploration dataset of 585,279 adults in the Swedish AMORIS cohort with no prior psychiatric diagnoses and a measurement of at least one inflammatory biomarker, a validation dataset of 485,620 UK Biobank participants, and genetic and MR analyses using genome-wide association study summary statistics.
In the AMORIS cohort, individuals with a higher than median level of leukocytes (hazard ratio [HR], 1.11), haptoglobin (HR, 1.13), or CRP (HR, 1.02) had an elevated risk for any psychiatric disorder. In contrast, there was an inverse association for IgG level (HR, 0.92).
“The estimates were comparable for depression, anxiety, and stress-related disorders, specifically, and these results were largely validated in the UK Biobank,” the authors reported.
In trajectory analyses, compared with controls, individuals with psychiatric disorders had higher leukocyte and haptoglobin levels and lower IgG up to three decades before being diagnosed.
The MR analysis suggested a possible causal relationship between leukocytes and depression.
The underlying mechanisms for the associations of serum leukocytes, haptoglobin, CRP, and IgG with psychiatry disorders remain unclear.
“Possible explanations mainly include blood-brain barrier disruption, microglia activation, neurotransmission impairment, and other interactions between inflammations and neuropathology,” the researchers wrote.
A related paper published online on August 21 in JAMA Psychiatry looked at trajectories of inflammation in childhood and risk for mental and cardiometabolic disorders in adulthood.
This longitudinal cohort study found that having persistently raised levels of inflammation as measured by CRP throughout childhood and adolescence, peaking at age 9 years, were associated with an increased risk of developing psychosis disorder, severe depression, and higher levels of insulin resistance.
Support for Precision Psychiatry
This study is “another strong indication that inflammation plays a role in depression,” Andrew H. Miller, MD, professor of psychiatry and behavioral sciences and director of the behavioral immunology program, Emory University School of Medicine, Atlanta, Georgia, who wasn’t involved in the study, told this news organization.
“The work adds to the mounting data that there exists an inflammatory phenotype of depression that may uniquely respond to treatment and may have a unique trajectory,” Dr. Miller said.
“Eventually the field will want to embrace this novel phenotype and better understand how to recognize it and treat it. This is our entrée into precision psychiatry where we identify the right treatment for the right patient at the right time based on an understanding of the underlying cause of their illness,” Dr. Miller added.
Also weighing in, Alexander B. Niculescu III, MD, PhD, professor of psychiatry and medical neuroscience, Indiana University School of Medicine, Indianapolis, cautioned that these biomarkers are “very nonspecific and are likely related to these subjects that go on to develop psychiatric disorders having more stressful, adverse life trajectories.”
“There are better, more specific blood biomarkers for psychiatric disorders already available,” Dr. Niculescu told this news organization.
His group recently reported that a panel of blood-based biomarkers can distinguish between depression and bipolar disorder, predict a person’s future risk for these disorders, and inform more tailored medication choices.
Notably, they observed a strong circadian clock gene component to mood disorders, which helps explain why some patients’ conditions become worse with seasonal changes. It also explains the sleep alterations that occur among patients with mood disorders, they said.
This study had no commercial funding. Yu Zeng and Dr. Miller had no relevant disclosures. Dr. Niculescu is a cofounder of MindX Sciences and is listed as inventor on a patent application filed by Indiana University.
A version of this article first appeared on Medscape.com.
When Childhood Cancer Survivors Face Sexual Challenges
Childhood cancers represent a diverse group of neoplasms, and thanks to advances in treatment, survival rates have improved significantly. Today, more than 80%-85% of children diagnosed with cancer in developed countries survive into adulthood.
This increase in survival has brought new challenges, however. Compared with the general population, childhood cancer survivors (CCS) are at a notably higher risk for early mortality, developing secondary cancers, and experiencing various long-term clinical and psychosocial issues stemming from their disease or its treatment.
Long-term follow-up care for CCS is a complex and evolving field. Despite ongoing efforts to establish global and national guidelines, current evidence indicates that the care and management of these patients remain suboptimal.
The disruptions caused by cancer and its treatment can interfere with normal physiological and psychological development, leading to issues with sexual function. This aspect of health is critical as it influences not just physical well-being but also psychosocial, developmental, and emotional health.
Characteristics and Mechanisms
Sexual functioning encompasses the physiological and psychological aspects of sexual behavior, including desire, arousal, orgasm, sexual pleasure, and overall satisfaction.
As CCS reach adolescence or adulthood, they often face sexual and reproductive issues, particularly as they enter romantic relationships.
Sexual functioning is a complex process that relies on the interaction of various factors, including physiological health, psychosexual development, romantic relationships, body image, and desire.
Despite its importance, the impact of childhood cancer on sexual function is often overlooked, even though cancer and its treatments can have lifelong effects.
Sexual Function in CCS
A recent review aimed to summarize the existing research on sexual function among CCS, highlighting assessment tools, key stages of psychosexual development, common sexual problems, and the prevalence of sexual dysfunction.
The review study included 22 studies published between 2000 and 2022, comprising two qualitative, six cohort, and 14 cross-sectional studies.
Most CCS reached all key stages of psychosexual development at an average age of 29.8 years. Although some milestones were achieved later than is typical, many survivors felt they reached these stages at the appropriate time. Sexual initiation was less common among those who had undergone intensive neurotoxic treatments, such as those diagnosed with brain tumors or leukemia in childhood.
In a cross-sectional study of CCS aged 17-39 years, about one third had never engaged in sexual intercourse, 41.4% reported never experiencing sexual attraction, 44.8% were dissatisfied with their sex lives, and many rarely felt sexually attractive to others. Another study found that common issues among CCS included a lack of interest in sex (30%), difficulty enjoying sex (24%), and difficulty becoming aroused (23%). However, comparing and analyzing these problems was challenging due to the lack of standardized assessment criteria.
The prevalence of sexual dysfunction among CCS ranged from 12.3% to 46.5%. For males, the prevalence ranged from 12.3% to 54.0%, while for females, it ranged from 19.9% to 57.0%.
Factors Influencing Sexual Function
The review identified the following four categories of factors influencing sexual function in CCS: Demographic, treatment-related, psychological, and physiological.
Demographic factors: Gender, age, education level, relationship status, income level, and race all play roles in sexual function.
Female survivors reported more severe sexual dysfunction and poorer sexual health than did male survivors. Age at cancer diagnosis, age at evaluation, and the time since diagnosis were closely linked to sexual experiences. Patients diagnosed with cancer during childhood tended to report better sexual function than those diagnosed during adolescence.
Treatment-related factors: The type of cancer and intensity of treatment, along with surgical history, were significant factors. Surgeries involving the spinal cord or sympathetic nerves, as well as a history of prostate or pelvic surgery, were strongly associated with erectile dysfunction in men. In women, pelvic surgeries and treatments to the pelvic area were commonly linked to sexual dysfunction.
The association between treatment intensity and sexual function was noted across several studies, although the results were not always consistent. For example, testicular radiation above 10 Gy was positively correlated with sexual dysfunction. Women who underwent more intensive treatments were more likely to report issues in multiple areas of sexual function, while men in this group were less likely to have children.
Among female CCS, certain types of cancer, such as germ cell tumors, renal tumors, and leukemia, present a higher risk for sexual dysfunction. Women who had CNS tumors in childhood frequently reported problems like difficulty in sexual arousal, low sexual satisfaction, infrequent sexual activity, and fewer sexual partners, compared with survivors of other cancers. Survivors of acute lymphoblastic leukemia and those who underwent hematopoietic stem cell transplantation (HSCT) also showed varying degrees of impaired sexual function, compared with the general population. The HSCT group showed significant testicular damage, including reduced testicular volumes, low testosterone levels, and low sperm counts.
Psychological factors: These factors, such as emotional distress, play a significant role in sexual dysfunction among CCS. Symptoms like anxiety, nervousness during sexual activity, and depression are commonly reported by those with sexual dysfunction. The connection between body image and sexual function is complex. Many CCS with sexual dysfunction express concern about how others, particularly their partners, perceived their altered body image due to cancer and its treatment.
Physiological factors: In male CCS, low serum testosterone levels and low lean muscle mass are linked to an increased risk for sexual dysfunction. Treatments involving alkylating agents or testicular radiation, and surgery or radiotherapy targeting the genitourinary organs or the hypothalamic-pituitary region, can lead to various physiological and endocrine disorders, contributing to sexual dysfunction. Despite these risks, there is a lack of research evaluating sexual function through the lens of the hypothalamic-pituitary-gonadal axis and neuroendocrine pathways.
This story was translated from Univadis Italy using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Childhood cancers represent a diverse group of neoplasms, and thanks to advances in treatment, survival rates have improved significantly. Today, more than 80%-85% of children diagnosed with cancer in developed countries survive into adulthood.
This increase in survival has brought new challenges, however. Compared with the general population, childhood cancer survivors (CCS) are at a notably higher risk for early mortality, developing secondary cancers, and experiencing various long-term clinical and psychosocial issues stemming from their disease or its treatment.
Long-term follow-up care for CCS is a complex and evolving field. Despite ongoing efforts to establish global and national guidelines, current evidence indicates that the care and management of these patients remain suboptimal.
The disruptions caused by cancer and its treatment can interfere with normal physiological and psychological development, leading to issues with sexual function. This aspect of health is critical as it influences not just physical well-being but also psychosocial, developmental, and emotional health.
Characteristics and Mechanisms
Sexual functioning encompasses the physiological and psychological aspects of sexual behavior, including desire, arousal, orgasm, sexual pleasure, and overall satisfaction.
As CCS reach adolescence or adulthood, they often face sexual and reproductive issues, particularly as they enter romantic relationships.
Sexual functioning is a complex process that relies on the interaction of various factors, including physiological health, psychosexual development, romantic relationships, body image, and desire.
Despite its importance, the impact of childhood cancer on sexual function is often overlooked, even though cancer and its treatments can have lifelong effects.
Sexual Function in CCS
A recent review aimed to summarize the existing research on sexual function among CCS, highlighting assessment tools, key stages of psychosexual development, common sexual problems, and the prevalence of sexual dysfunction.
The review study included 22 studies published between 2000 and 2022, comprising two qualitative, six cohort, and 14 cross-sectional studies.
Most CCS reached all key stages of psychosexual development at an average age of 29.8 years. Although some milestones were achieved later than is typical, many survivors felt they reached these stages at the appropriate time. Sexual initiation was less common among those who had undergone intensive neurotoxic treatments, such as those diagnosed with brain tumors or leukemia in childhood.
In a cross-sectional study of CCS aged 17-39 years, about one third had never engaged in sexual intercourse, 41.4% reported never experiencing sexual attraction, 44.8% were dissatisfied with their sex lives, and many rarely felt sexually attractive to others. Another study found that common issues among CCS included a lack of interest in sex (30%), difficulty enjoying sex (24%), and difficulty becoming aroused (23%). However, comparing and analyzing these problems was challenging due to the lack of standardized assessment criteria.
The prevalence of sexual dysfunction among CCS ranged from 12.3% to 46.5%. For males, the prevalence ranged from 12.3% to 54.0%, while for females, it ranged from 19.9% to 57.0%.
Factors Influencing Sexual Function
The review identified the following four categories of factors influencing sexual function in CCS: Demographic, treatment-related, psychological, and physiological.
Demographic factors: Gender, age, education level, relationship status, income level, and race all play roles in sexual function.
Female survivors reported more severe sexual dysfunction and poorer sexual health than did male survivors. Age at cancer diagnosis, age at evaluation, and the time since diagnosis were closely linked to sexual experiences. Patients diagnosed with cancer during childhood tended to report better sexual function than those diagnosed during adolescence.
Treatment-related factors: The type of cancer and intensity of treatment, along with surgical history, were significant factors. Surgeries involving the spinal cord or sympathetic nerves, as well as a history of prostate or pelvic surgery, were strongly associated with erectile dysfunction in men. In women, pelvic surgeries and treatments to the pelvic area were commonly linked to sexual dysfunction.
The association between treatment intensity and sexual function was noted across several studies, although the results were not always consistent. For example, testicular radiation above 10 Gy was positively correlated with sexual dysfunction. Women who underwent more intensive treatments were more likely to report issues in multiple areas of sexual function, while men in this group were less likely to have children.
Among female CCS, certain types of cancer, such as germ cell tumors, renal tumors, and leukemia, present a higher risk for sexual dysfunction. Women who had CNS tumors in childhood frequently reported problems like difficulty in sexual arousal, low sexual satisfaction, infrequent sexual activity, and fewer sexual partners, compared with survivors of other cancers. Survivors of acute lymphoblastic leukemia and those who underwent hematopoietic stem cell transplantation (HSCT) also showed varying degrees of impaired sexual function, compared with the general population. The HSCT group showed significant testicular damage, including reduced testicular volumes, low testosterone levels, and low sperm counts.
Psychological factors: These factors, such as emotional distress, play a significant role in sexual dysfunction among CCS. Symptoms like anxiety, nervousness during sexual activity, and depression are commonly reported by those with sexual dysfunction. The connection between body image and sexual function is complex. Many CCS with sexual dysfunction express concern about how others, particularly their partners, perceived their altered body image due to cancer and its treatment.
Physiological factors: In male CCS, low serum testosterone levels and low lean muscle mass are linked to an increased risk for sexual dysfunction. Treatments involving alkylating agents or testicular radiation, and surgery or radiotherapy targeting the genitourinary organs or the hypothalamic-pituitary region, can lead to various physiological and endocrine disorders, contributing to sexual dysfunction. Despite these risks, there is a lack of research evaluating sexual function through the lens of the hypothalamic-pituitary-gonadal axis and neuroendocrine pathways.
This story was translated from Univadis Italy using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Childhood cancers represent a diverse group of neoplasms, and thanks to advances in treatment, survival rates have improved significantly. Today, more than 80%-85% of children diagnosed with cancer in developed countries survive into adulthood.
This increase in survival has brought new challenges, however. Compared with the general population, childhood cancer survivors (CCS) are at a notably higher risk for early mortality, developing secondary cancers, and experiencing various long-term clinical and psychosocial issues stemming from their disease or its treatment.
Long-term follow-up care for CCS is a complex and evolving field. Despite ongoing efforts to establish global and national guidelines, current evidence indicates that the care and management of these patients remain suboptimal.
The disruptions caused by cancer and its treatment can interfere with normal physiological and psychological development, leading to issues with sexual function. This aspect of health is critical as it influences not just physical well-being but also psychosocial, developmental, and emotional health.
Characteristics and Mechanisms
Sexual functioning encompasses the physiological and psychological aspects of sexual behavior, including desire, arousal, orgasm, sexual pleasure, and overall satisfaction.
As CCS reach adolescence or adulthood, they often face sexual and reproductive issues, particularly as they enter romantic relationships.
Sexual functioning is a complex process that relies on the interaction of various factors, including physiological health, psychosexual development, romantic relationships, body image, and desire.
Despite its importance, the impact of childhood cancer on sexual function is often overlooked, even though cancer and its treatments can have lifelong effects.
Sexual Function in CCS
A recent review aimed to summarize the existing research on sexual function among CCS, highlighting assessment tools, key stages of psychosexual development, common sexual problems, and the prevalence of sexual dysfunction.
The review study included 22 studies published between 2000 and 2022, comprising two qualitative, six cohort, and 14 cross-sectional studies.
Most CCS reached all key stages of psychosexual development at an average age of 29.8 years. Although some milestones were achieved later than is typical, many survivors felt they reached these stages at the appropriate time. Sexual initiation was less common among those who had undergone intensive neurotoxic treatments, such as those diagnosed with brain tumors or leukemia in childhood.
In a cross-sectional study of CCS aged 17-39 years, about one third had never engaged in sexual intercourse, 41.4% reported never experiencing sexual attraction, 44.8% were dissatisfied with their sex lives, and many rarely felt sexually attractive to others. Another study found that common issues among CCS included a lack of interest in sex (30%), difficulty enjoying sex (24%), and difficulty becoming aroused (23%). However, comparing and analyzing these problems was challenging due to the lack of standardized assessment criteria.
The prevalence of sexual dysfunction among CCS ranged from 12.3% to 46.5%. For males, the prevalence ranged from 12.3% to 54.0%, while for females, it ranged from 19.9% to 57.0%.
Factors Influencing Sexual Function
The review identified the following four categories of factors influencing sexual function in CCS: Demographic, treatment-related, psychological, and physiological.
Demographic factors: Gender, age, education level, relationship status, income level, and race all play roles in sexual function.
Female survivors reported more severe sexual dysfunction and poorer sexual health than did male survivors. Age at cancer diagnosis, age at evaluation, and the time since diagnosis were closely linked to sexual experiences. Patients diagnosed with cancer during childhood tended to report better sexual function than those diagnosed during adolescence.
Treatment-related factors: The type of cancer and intensity of treatment, along with surgical history, were significant factors. Surgeries involving the spinal cord or sympathetic nerves, as well as a history of prostate or pelvic surgery, were strongly associated with erectile dysfunction in men. In women, pelvic surgeries and treatments to the pelvic area were commonly linked to sexual dysfunction.
The association between treatment intensity and sexual function was noted across several studies, although the results were not always consistent. For example, testicular radiation above 10 Gy was positively correlated with sexual dysfunction. Women who underwent more intensive treatments were more likely to report issues in multiple areas of sexual function, while men in this group were less likely to have children.
Among female CCS, certain types of cancer, such as germ cell tumors, renal tumors, and leukemia, present a higher risk for sexual dysfunction. Women who had CNS tumors in childhood frequently reported problems like difficulty in sexual arousal, low sexual satisfaction, infrequent sexual activity, and fewer sexual partners, compared with survivors of other cancers. Survivors of acute lymphoblastic leukemia and those who underwent hematopoietic stem cell transplantation (HSCT) also showed varying degrees of impaired sexual function, compared with the general population. The HSCT group showed significant testicular damage, including reduced testicular volumes, low testosterone levels, and low sperm counts.
Psychological factors: These factors, such as emotional distress, play a significant role in sexual dysfunction among CCS. Symptoms like anxiety, nervousness during sexual activity, and depression are commonly reported by those with sexual dysfunction. The connection between body image and sexual function is complex. Many CCS with sexual dysfunction express concern about how others, particularly their partners, perceived their altered body image due to cancer and its treatment.
Physiological factors: In male CCS, low serum testosterone levels and low lean muscle mass are linked to an increased risk for sexual dysfunction. Treatments involving alkylating agents or testicular radiation, and surgery or radiotherapy targeting the genitourinary organs or the hypothalamic-pituitary region, can lead to various physiological and endocrine disorders, contributing to sexual dysfunction. Despite these risks, there is a lack of research evaluating sexual function through the lens of the hypothalamic-pituitary-gonadal axis and neuroendocrine pathways.
This story was translated from Univadis Italy using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
CBD Use in Pregnant People Double That of Nonpregnant Counterparts
Pregnant women in a large North American sample reported nearly double the rate of cannabidiol (CBD) use compared with nonpregnant women, new data published in a research letter in Obstetrics & Gynecology indicates.
Healthcare providers should be aware of the high rate of CBD use in pregnancy, especially as legal use of cannabis is increasing faster than evidence on outcomes for exposed offspring, note the researchers, led by Devika Bhatia, MD, from the Department of Psychiatry, Colorado School of Medicine, University of Colorado Anschutz Medical Campus in Aurora.
In an accompanying editorial, Torri D. Metz, MD, MS, deputy editor for obstetrics for Obstetrics & Gynecology, writes that the study “is critically important.” She points out that pregnant individuals may perceive that CBD is a safe drug to use in pregnancy, despite there being essentially no data examining whether or not this is the case.
Large Dataset From United States and Canada
Researchers used data from the International Cannabis Policy Study (2019-2021), a repeated cross-sectional survey of people aged 16-65 years in the United States and Canada. There were 66,457 women in the sample, including 1096 pregnant women.
Particularly concerning, the authors write, is the prenatal use of CBD-only products. Those products are advertised to contain only CBD, rather than tetrahydrocannabinol (THC). They point out CBD-only products are often legal in North America and often marketed as supplements.
The prevalence of CBD-only use in pregnant women in the study was 20.4% compared with 11.3% among nonpregnant women, P < .001. The top reason for use by pregnant women was anxiety (58.4%). Other top reasons included depression (40.3%), posttraumatic stress disorder (32.1%), pain (52.3%), headache (35.6%), and nausea or vomiting (31.9%).
“Nonpregnant women were significantly more likely to report using CBD for pain, sleep, general well-being, and ‘other’ physical or mental health reasons, or to not use CBD for mental health,” the authors write, adding that the reasons for CBD use highlight drivers that may be important to address in treating pregnant patients.
Provider Endorsement in Some Cases
Dr. Metz, associate professor of obstetrics and gynecology with the University of Utah Health in Salt Lake City, says in some cases women may be getting endorsement of CBD use from their provider or at least implied support when CBD is prescribed. In the study, pregnant women had 2.33 times greater adjusted odds of having a CBD prescription than nonpregnant women (95% confidence interval, 1.27-2.88).
She points to another cross-sectional study of more than 10,000 participants using PRAMS (Pregnancy Risk Assessment Monitoring System) data that found that “from 2017 to 2019, 63% of pregnant women reported that they were not told to avoid cannabis use in pregnancy, and 8% noted that they were advised to use cannabis by their prenatal care practitioner.”
The American College of Obstetricians and Gynecologists recommends against prescribing cannabis products for pregnant or lactating women.
Studies that have explored THC and its metabolites have shown “a consistent association between cannabis use and decreased fetal growth,” Dr. Metz noted. “There also remain persistent concerns about the long-term neurodevelopmental effects of maternal cannabis use on the fetus and, subsequently, the newborn.”
Limitations of the study include the self-reported responses and participants’ ability to accurately distinguish between CBD-only and THC-containing products.
Because self-reports of CBD use in pregnancy may be drastically underestimated and nonreliable, Dr. Metz writes, development of blood and urine screens to help detect CBD product use “will be helpful in moving the field forward.”
Study senior author David Hammond, PhD, has been a paid expert witness on behalf of public health authorities in response to legal challenges from the cannabis, tobacco, vaping, and food industries. Other authors did not report any potential conflicts. Dr. Metz reports personal fees from Pfizer, and grants from Pfizer for her role as a site principal investigator for SARS-CoV-2 vaccination and for her role as a site PI for RSV vaccination in pregnancy study.
Pregnant women in a large North American sample reported nearly double the rate of cannabidiol (CBD) use compared with nonpregnant women, new data published in a research letter in Obstetrics & Gynecology indicates.
Healthcare providers should be aware of the high rate of CBD use in pregnancy, especially as legal use of cannabis is increasing faster than evidence on outcomes for exposed offspring, note the researchers, led by Devika Bhatia, MD, from the Department of Psychiatry, Colorado School of Medicine, University of Colorado Anschutz Medical Campus in Aurora.
In an accompanying editorial, Torri D. Metz, MD, MS, deputy editor for obstetrics for Obstetrics & Gynecology, writes that the study “is critically important.” She points out that pregnant individuals may perceive that CBD is a safe drug to use in pregnancy, despite there being essentially no data examining whether or not this is the case.
Large Dataset From United States and Canada
Researchers used data from the International Cannabis Policy Study (2019-2021), a repeated cross-sectional survey of people aged 16-65 years in the United States and Canada. There were 66,457 women in the sample, including 1096 pregnant women.
Particularly concerning, the authors write, is the prenatal use of CBD-only products. Those products are advertised to contain only CBD, rather than tetrahydrocannabinol (THC). They point out CBD-only products are often legal in North America and often marketed as supplements.
The prevalence of CBD-only use in pregnant women in the study was 20.4% compared with 11.3% among nonpregnant women, P < .001. The top reason for use by pregnant women was anxiety (58.4%). Other top reasons included depression (40.3%), posttraumatic stress disorder (32.1%), pain (52.3%), headache (35.6%), and nausea or vomiting (31.9%).
“Nonpregnant women were significantly more likely to report using CBD for pain, sleep, general well-being, and ‘other’ physical or mental health reasons, or to not use CBD for mental health,” the authors write, adding that the reasons for CBD use highlight drivers that may be important to address in treating pregnant patients.
Provider Endorsement in Some Cases
Dr. Metz, associate professor of obstetrics and gynecology with the University of Utah Health in Salt Lake City, says in some cases women may be getting endorsement of CBD use from their provider or at least implied support when CBD is prescribed. In the study, pregnant women had 2.33 times greater adjusted odds of having a CBD prescription than nonpregnant women (95% confidence interval, 1.27-2.88).
She points to another cross-sectional study of more than 10,000 participants using PRAMS (Pregnancy Risk Assessment Monitoring System) data that found that “from 2017 to 2019, 63% of pregnant women reported that they were not told to avoid cannabis use in pregnancy, and 8% noted that they were advised to use cannabis by their prenatal care practitioner.”
The American College of Obstetricians and Gynecologists recommends against prescribing cannabis products for pregnant or lactating women.
Studies that have explored THC and its metabolites have shown “a consistent association between cannabis use and decreased fetal growth,” Dr. Metz noted. “There also remain persistent concerns about the long-term neurodevelopmental effects of maternal cannabis use on the fetus and, subsequently, the newborn.”
Limitations of the study include the self-reported responses and participants’ ability to accurately distinguish between CBD-only and THC-containing products.
Because self-reports of CBD use in pregnancy may be drastically underestimated and nonreliable, Dr. Metz writes, development of blood and urine screens to help detect CBD product use “will be helpful in moving the field forward.”
Study senior author David Hammond, PhD, has been a paid expert witness on behalf of public health authorities in response to legal challenges from the cannabis, tobacco, vaping, and food industries. Other authors did not report any potential conflicts. Dr. Metz reports personal fees from Pfizer, and grants from Pfizer for her role as a site principal investigator for SARS-CoV-2 vaccination and for her role as a site PI for RSV vaccination in pregnancy study.
Pregnant women in a large North American sample reported nearly double the rate of cannabidiol (CBD) use compared with nonpregnant women, new data published in a research letter in Obstetrics & Gynecology indicates.
Healthcare providers should be aware of the high rate of CBD use in pregnancy, especially as legal use of cannabis is increasing faster than evidence on outcomes for exposed offspring, note the researchers, led by Devika Bhatia, MD, from the Department of Psychiatry, Colorado School of Medicine, University of Colorado Anschutz Medical Campus in Aurora.
In an accompanying editorial, Torri D. Metz, MD, MS, deputy editor for obstetrics for Obstetrics & Gynecology, writes that the study “is critically important.” She points out that pregnant individuals may perceive that CBD is a safe drug to use in pregnancy, despite there being essentially no data examining whether or not this is the case.
Large Dataset From United States and Canada
Researchers used data from the International Cannabis Policy Study (2019-2021), a repeated cross-sectional survey of people aged 16-65 years in the United States and Canada. There were 66,457 women in the sample, including 1096 pregnant women.
Particularly concerning, the authors write, is the prenatal use of CBD-only products. Those products are advertised to contain only CBD, rather than tetrahydrocannabinol (THC). They point out CBD-only products are often legal in North America and often marketed as supplements.
The prevalence of CBD-only use in pregnant women in the study was 20.4% compared with 11.3% among nonpregnant women, P < .001. The top reason for use by pregnant women was anxiety (58.4%). Other top reasons included depression (40.3%), posttraumatic stress disorder (32.1%), pain (52.3%), headache (35.6%), and nausea or vomiting (31.9%).
“Nonpregnant women were significantly more likely to report using CBD for pain, sleep, general well-being, and ‘other’ physical or mental health reasons, or to not use CBD for mental health,” the authors write, adding that the reasons for CBD use highlight drivers that may be important to address in treating pregnant patients.
Provider Endorsement in Some Cases
Dr. Metz, associate professor of obstetrics and gynecology with the University of Utah Health in Salt Lake City, says in some cases women may be getting endorsement of CBD use from their provider or at least implied support when CBD is prescribed. In the study, pregnant women had 2.33 times greater adjusted odds of having a CBD prescription than nonpregnant women (95% confidence interval, 1.27-2.88).
She points to another cross-sectional study of more than 10,000 participants using PRAMS (Pregnancy Risk Assessment Monitoring System) data that found that “from 2017 to 2019, 63% of pregnant women reported that they were not told to avoid cannabis use in pregnancy, and 8% noted that they were advised to use cannabis by their prenatal care practitioner.”
The American College of Obstetricians and Gynecologists recommends against prescribing cannabis products for pregnant or lactating women.
Studies that have explored THC and its metabolites have shown “a consistent association between cannabis use and decreased fetal growth,” Dr. Metz noted. “There also remain persistent concerns about the long-term neurodevelopmental effects of maternal cannabis use on the fetus and, subsequently, the newborn.”
Limitations of the study include the self-reported responses and participants’ ability to accurately distinguish between CBD-only and THC-containing products.
Because self-reports of CBD use in pregnancy may be drastically underestimated and nonreliable, Dr. Metz writes, development of blood and urine screens to help detect CBD product use “will be helpful in moving the field forward.”
Study senior author David Hammond, PhD, has been a paid expert witness on behalf of public health authorities in response to legal challenges from the cannabis, tobacco, vaping, and food industries. Other authors did not report any potential conflicts. Dr. Metz reports personal fees from Pfizer, and grants from Pfizer for her role as a site principal investigator for SARS-CoV-2 vaccination and for her role as a site PI for RSV vaccination in pregnancy study.
FROM OBSTETRICS & GYNECOLOGY
Navigating Election Anxiety: How Worry Affects the Brain
Once again, America is deeply divided before a national election, with people on each side convinced of the horrors that will be visited upon us if the other side wins.
’Tis the season — and regrettably, not to be jolly but to be worried.
As a neuroscientist, I am especially aware of the deleterious mental and physical impact of chronic worry on our citizenry. That’s because worry is not “all in your head.” We modern humans live in a world of worry which appears to be progressively growing.
Flight or Fight
Worry stems from the brain’s rather remarkable ability to foresee and reflexively respond to threat. Our “fight or flight” brain machinery probably arose in our vertebrate ancestors more than 300 million years ago. The fact that we have machinery akin to that possessed by lizards or tigers or shrews is testimony to its crucial contribution to our species’ survival.
As the phrase “fight or flight” suggests, a brain that senses trouble immediately biases certain body and brain functions. As it shifts into a higher-alert mode, it increases the energy supplies in our blood and supports other changes that facilitate faster and stronger reactions, while it shuts down less essential processes which do not contribute to hiding, fighting, or running like hell.
This hyperreactive response is initiated in the amygdala in the anterior brain, which identifies “what’s happening” as immediately or potentially threatening. The now-activated amygdala generates a response in the hypothalamus that provokes an immediate increase of adrenaline and cortisol in the body, and cortisol and noradrenaline in the brain. Both sharply speed up our physical and neurologic reactivity. In the brain, that is achieved by increasing the level of excitability of neurons across the forebrain. Depending on the perceived level of threat, an excitable brain will be just a little or a lot more “on alert,” just a little or a lot faster to respond, and just a little or a lot better at remembering the specific “warning” events that trigger this lizard-brain response.
Alas, this machinery was designed to be engaged every so often when a potentially dangerous surprise arises in life. When the worry and stress are persistent, the brain experiences a kind of neurologic “burn-out” of its fight versus flight machinery.
Dangers of Nonstop Anxiety and Stress
A consistently stressed-out brain turns down its production and release of noradrenaline, and the brain becomes less attentive, less engaged. This sets the brain on the path to an anxiety (and then a depressive) disorder, and, in the longer term, to cognitive losses in memory and executive control systems, and to emotional distortions that can lead to substance abuse or other addictions.
Our political distress is but one source of persistent worry and stress. Worry is a modern plague. The head counts of individuals seeking psychiatric or psychological health are at an all-time high in the United States. Near-universal low-level stressors, such as 2 years of COVID, insecurities about the changing demands of our professional and private lives, and a deeply divided body politic are unequivocally affecting American brain health.
The brain also collaborates in our body’s response to stress. Its regulation of hormonal responses and its autonomic nervous system’s mediated responses contribute to elevated blood sugar levels, to craving high-sugar foods, to elevated blood pressure, and to weaker immune responses. This all contributes to higher risks for cardiovascular and other dietary- and immune system–related disease. And ultimately, to shorter lifespans.
Strategies to Address Neurologic Changes Arising From Chronic Stress
There are many things you can try to bring your worry back to a manageable (and even productive) level.
- Engage in a “reset” strategy several times a day to bring your amygdala and locus coeruleus back under control. It takes a minute (or five) of calm, positive meditation to take your brain to a happy, optimistic place. Or use a mindfulness exercise to quiet down that overactive amygdala.
- Talk to people. Keeping your worries to yourself can compound them. Hashing through your concerns with a family member, friend, professional coach, or therapist can help put them in perspective and may allow you to come up with strategies to identify and neurologically respond to your sources of stress.
- Exercise, both physically and mentally. Do what works for you, whether it’s a run, a long walk, pumping iron, playing racquetball — anything that promotes physical release. Exercise your brain too. Engage in a project or activity that is mentally demanding. Personally, I like to garden and do online brain exercises. There’s nothing quite like yanking out weeds or hitting a new personal best at a cognitive exercise for me to notch a sense of accomplishment to counterbalance the unresolved issues driving my worry.
- Accept the uncertainty. Life is full of uncertainty. To paraphrase from Yale theologian Reinhold Niebuhr’s “Serenity Prayer”: Have the serenity to accept what you cannot help, the courage to change what you can, and the wisdom to recognize one from the other.
And, please, be assured that you’ll make it through this election season.
Dr. Merzenich, professor emeritus, Department of Neuroscience, University of California San Francisco, disclosed ties with Posit Science. He is often credited with discovering lifelong plasticity, with being the first to harness plasticity for human benefit (in his co-invention of the cochlear implant), and for pioneering the field of plasticity-based computerized brain exercise. He is a Kavli Laureate in Neuroscience, and he has been honored by each of the US National Academies of Sciences, Engineering, and Medicine. He may be most widely known for a series of specials on the brain on public television. His current focus is BrainHQ, a brain exercise app.
A version of this article appeared on Medscape.com.
Once again, America is deeply divided before a national election, with people on each side convinced of the horrors that will be visited upon us if the other side wins.
’Tis the season — and regrettably, not to be jolly but to be worried.
As a neuroscientist, I am especially aware of the deleterious mental and physical impact of chronic worry on our citizenry. That’s because worry is not “all in your head.” We modern humans live in a world of worry which appears to be progressively growing.
Flight or Fight
Worry stems from the brain’s rather remarkable ability to foresee and reflexively respond to threat. Our “fight or flight” brain machinery probably arose in our vertebrate ancestors more than 300 million years ago. The fact that we have machinery akin to that possessed by lizards or tigers or shrews is testimony to its crucial contribution to our species’ survival.
As the phrase “fight or flight” suggests, a brain that senses trouble immediately biases certain body and brain functions. As it shifts into a higher-alert mode, it increases the energy supplies in our blood and supports other changes that facilitate faster and stronger reactions, while it shuts down less essential processes which do not contribute to hiding, fighting, or running like hell.
This hyperreactive response is initiated in the amygdala in the anterior brain, which identifies “what’s happening” as immediately or potentially threatening. The now-activated amygdala generates a response in the hypothalamus that provokes an immediate increase of adrenaline and cortisol in the body, and cortisol and noradrenaline in the brain. Both sharply speed up our physical and neurologic reactivity. In the brain, that is achieved by increasing the level of excitability of neurons across the forebrain. Depending on the perceived level of threat, an excitable brain will be just a little or a lot more “on alert,” just a little or a lot faster to respond, and just a little or a lot better at remembering the specific “warning” events that trigger this lizard-brain response.
Alas, this machinery was designed to be engaged every so often when a potentially dangerous surprise arises in life. When the worry and stress are persistent, the brain experiences a kind of neurologic “burn-out” of its fight versus flight machinery.
Dangers of Nonstop Anxiety and Stress
A consistently stressed-out brain turns down its production and release of noradrenaline, and the brain becomes less attentive, less engaged. This sets the brain on the path to an anxiety (and then a depressive) disorder, and, in the longer term, to cognitive losses in memory and executive control systems, and to emotional distortions that can lead to substance abuse or other addictions.
Our political distress is but one source of persistent worry and stress. Worry is a modern plague. The head counts of individuals seeking psychiatric or psychological health are at an all-time high in the United States. Near-universal low-level stressors, such as 2 years of COVID, insecurities about the changing demands of our professional and private lives, and a deeply divided body politic are unequivocally affecting American brain health.
The brain also collaborates in our body’s response to stress. Its regulation of hormonal responses and its autonomic nervous system’s mediated responses contribute to elevated blood sugar levels, to craving high-sugar foods, to elevated blood pressure, and to weaker immune responses. This all contributes to higher risks for cardiovascular and other dietary- and immune system–related disease. And ultimately, to shorter lifespans.
Strategies to Address Neurologic Changes Arising From Chronic Stress
There are many things you can try to bring your worry back to a manageable (and even productive) level.
- Engage in a “reset” strategy several times a day to bring your amygdala and locus coeruleus back under control. It takes a minute (or five) of calm, positive meditation to take your brain to a happy, optimistic place. Or use a mindfulness exercise to quiet down that overactive amygdala.
- Talk to people. Keeping your worries to yourself can compound them. Hashing through your concerns with a family member, friend, professional coach, or therapist can help put them in perspective and may allow you to come up with strategies to identify and neurologically respond to your sources of stress.
- Exercise, both physically and mentally. Do what works for you, whether it’s a run, a long walk, pumping iron, playing racquetball — anything that promotes physical release. Exercise your brain too. Engage in a project or activity that is mentally demanding. Personally, I like to garden and do online brain exercises. There’s nothing quite like yanking out weeds or hitting a new personal best at a cognitive exercise for me to notch a sense of accomplishment to counterbalance the unresolved issues driving my worry.
- Accept the uncertainty. Life is full of uncertainty. To paraphrase from Yale theologian Reinhold Niebuhr’s “Serenity Prayer”: Have the serenity to accept what you cannot help, the courage to change what you can, and the wisdom to recognize one from the other.
And, please, be assured that you’ll make it through this election season.
Dr. Merzenich, professor emeritus, Department of Neuroscience, University of California San Francisco, disclosed ties with Posit Science. He is often credited with discovering lifelong plasticity, with being the first to harness plasticity for human benefit (in his co-invention of the cochlear implant), and for pioneering the field of plasticity-based computerized brain exercise. He is a Kavli Laureate in Neuroscience, and he has been honored by each of the US National Academies of Sciences, Engineering, and Medicine. He may be most widely known for a series of specials on the brain on public television. His current focus is BrainHQ, a brain exercise app.
A version of this article appeared on Medscape.com.
Once again, America is deeply divided before a national election, with people on each side convinced of the horrors that will be visited upon us if the other side wins.
’Tis the season — and regrettably, not to be jolly but to be worried.
As a neuroscientist, I am especially aware of the deleterious mental and physical impact of chronic worry on our citizenry. That’s because worry is not “all in your head.” We modern humans live in a world of worry which appears to be progressively growing.
Flight or Fight
Worry stems from the brain’s rather remarkable ability to foresee and reflexively respond to threat. Our “fight or flight” brain machinery probably arose in our vertebrate ancestors more than 300 million years ago. The fact that we have machinery akin to that possessed by lizards or tigers or shrews is testimony to its crucial contribution to our species’ survival.
As the phrase “fight or flight” suggests, a brain that senses trouble immediately biases certain body and brain functions. As it shifts into a higher-alert mode, it increases the energy supplies in our blood and supports other changes that facilitate faster and stronger reactions, while it shuts down less essential processes which do not contribute to hiding, fighting, or running like hell.
This hyperreactive response is initiated in the amygdala in the anterior brain, which identifies “what’s happening” as immediately or potentially threatening. The now-activated amygdala generates a response in the hypothalamus that provokes an immediate increase of adrenaline and cortisol in the body, and cortisol and noradrenaline in the brain. Both sharply speed up our physical and neurologic reactivity. In the brain, that is achieved by increasing the level of excitability of neurons across the forebrain. Depending on the perceived level of threat, an excitable brain will be just a little or a lot more “on alert,” just a little or a lot faster to respond, and just a little or a lot better at remembering the specific “warning” events that trigger this lizard-brain response.
Alas, this machinery was designed to be engaged every so often when a potentially dangerous surprise arises in life. When the worry and stress are persistent, the brain experiences a kind of neurologic “burn-out” of its fight versus flight machinery.
Dangers of Nonstop Anxiety and Stress
A consistently stressed-out brain turns down its production and release of noradrenaline, and the brain becomes less attentive, less engaged. This sets the brain on the path to an anxiety (and then a depressive) disorder, and, in the longer term, to cognitive losses in memory and executive control systems, and to emotional distortions that can lead to substance abuse or other addictions.
Our political distress is but one source of persistent worry and stress. Worry is a modern plague. The head counts of individuals seeking psychiatric or psychological health are at an all-time high in the United States. Near-universal low-level stressors, such as 2 years of COVID, insecurities about the changing demands of our professional and private lives, and a deeply divided body politic are unequivocally affecting American brain health.
The brain also collaborates in our body’s response to stress. Its regulation of hormonal responses and its autonomic nervous system’s mediated responses contribute to elevated blood sugar levels, to craving high-sugar foods, to elevated blood pressure, and to weaker immune responses. This all contributes to higher risks for cardiovascular and other dietary- and immune system–related disease. And ultimately, to shorter lifespans.
Strategies to Address Neurologic Changes Arising From Chronic Stress
There are many things you can try to bring your worry back to a manageable (and even productive) level.
- Engage in a “reset” strategy several times a day to bring your amygdala and locus coeruleus back under control. It takes a minute (or five) of calm, positive meditation to take your brain to a happy, optimistic place. Or use a mindfulness exercise to quiet down that overactive amygdala.
- Talk to people. Keeping your worries to yourself can compound them. Hashing through your concerns with a family member, friend, professional coach, or therapist can help put them in perspective and may allow you to come up with strategies to identify and neurologically respond to your sources of stress.
- Exercise, both physically and mentally. Do what works for you, whether it’s a run, a long walk, pumping iron, playing racquetball — anything that promotes physical release. Exercise your brain too. Engage in a project or activity that is mentally demanding. Personally, I like to garden and do online brain exercises. There’s nothing quite like yanking out weeds or hitting a new personal best at a cognitive exercise for me to notch a sense of accomplishment to counterbalance the unresolved issues driving my worry.
- Accept the uncertainty. Life is full of uncertainty. To paraphrase from Yale theologian Reinhold Niebuhr’s “Serenity Prayer”: Have the serenity to accept what you cannot help, the courage to change what you can, and the wisdom to recognize one from the other.
And, please, be assured that you’ll make it through this election season.
Dr. Merzenich, professor emeritus, Department of Neuroscience, University of California San Francisco, disclosed ties with Posit Science. He is often credited with discovering lifelong plasticity, with being the first to harness plasticity for human benefit (in his co-invention of the cochlear implant), and for pioneering the field of plasticity-based computerized brain exercise. He is a Kavli Laureate in Neuroscience, and he has been honored by each of the US National Academies of Sciences, Engineering, and Medicine. He may be most widely known for a series of specials on the brain on public television. His current focus is BrainHQ, a brain exercise app.
A version of this article appeared on Medscape.com.
More Access to Perinatal Mental Healthcare Needed
Despite federal legislation improving healthcare access, concerted efforts are still needed to increase evidence-based treatment for maternal perinatal mental health issues, a large study of commercially insured mothers suggested. It found that federal legislation had variable and suboptimal effect on mental health services use by delivering mothers.
In the cross-sectional study, published in JAMA Network Open, psychotherapy receipt increased somewhat during 2007-2019 among all mothers and among those diagnosed with perinatal mood and anxiety disorders (PMADs). The timeline encompassed periods before and after passage of the Mental Health Parity and Addiction Equity Act (MHPAEA) of 2008 and the Patient Protection and Affordable Care Act (ACA) of 2010.
The investigators, led by Kara Zivin, PhD, MS, MFA, a professor of psychiatry in the University of Michigan’s School of Public Health at Ann Arbor, found the results varied by policy and between the overall delivering population and the PMAD population. “We did not find a statistically significant immediate change associated with the MHPAEA or ACA in the overall delivering population, except for a steady increase in delivering women who received any psychotherapy after ACA,” Dr. Zivin and colleagues wrote.
The researchers looked at private insurance data for 837,316 deliveries among 716,052 women (64.2% White), ages 15-44 (mean 31.2), to assess changes in psychotherapy visits in the year before and after delivery. They also estimated per-visit out-of-pocket costs for the ACA in 2014 and the MHPAEA in 2010.
In the PMAD population, the MHPAEA was associated with an immediate increase in psychotherapy receipt of 0.72% (95% CI, 0.26%-1.18%; P = .002), followed by a sustained decrease of 0.05% (95% CI, 0.09%-0.02%; P = .001).
In both populations, the ACA was associated with immediate and sustained monthly increases in use of 0.77% (95% CI, 0.26%-1.27%; P = .003) and 0.07% (95% CI, 0.02%-0.12%; P = .005), respectively.
Post MHPAEA, both populations experienced a slight decrease in per-visit monthly out-of-pocket costs, while after the ACA they saw an immediate and steady monthly increase in these.
Although both policies expanded access to any psychotherapy, the greater number of people receiving visits coincided with fewer visits per person, the authors noted. “One hypothesis suggests that the number of available mental health clinicians may not have increased enough to meet the new demand; future research should better characterize this trend,” they wrote.
In addition, a lower standard cost per visit may have dampened the incentive to increase the number of mental health clinicians, they conjectured. These factors could explain why the PMAD group appeared to experience a decrease in the proportion receiving any psychotherapy after the MHPAEA’s implementation.
The findings should be reviewed in the context of the current mental health burden, the authors wrote, in which the shortage of mental health professionals means that less than 30% of mental healthcare needs are being met.
They called for more measures to mitigate the excess burden of PMADs.
This study was funded by the National Institutes of Health. Dr. Zivin had no conflicts of interest. Coauthor Dr. Dalton reported personal fees from Merck, the Society of Family Planning, Up to Date, and The Medical Letter outside of the submitted work.
Despite federal legislation improving healthcare access, concerted efforts are still needed to increase evidence-based treatment for maternal perinatal mental health issues, a large study of commercially insured mothers suggested. It found that federal legislation had variable and suboptimal effect on mental health services use by delivering mothers.
In the cross-sectional study, published in JAMA Network Open, psychotherapy receipt increased somewhat during 2007-2019 among all mothers and among those diagnosed with perinatal mood and anxiety disorders (PMADs). The timeline encompassed periods before and after passage of the Mental Health Parity and Addiction Equity Act (MHPAEA) of 2008 and the Patient Protection and Affordable Care Act (ACA) of 2010.
The investigators, led by Kara Zivin, PhD, MS, MFA, a professor of psychiatry in the University of Michigan’s School of Public Health at Ann Arbor, found the results varied by policy and between the overall delivering population and the PMAD population. “We did not find a statistically significant immediate change associated with the MHPAEA or ACA in the overall delivering population, except for a steady increase in delivering women who received any psychotherapy after ACA,” Dr. Zivin and colleagues wrote.
The researchers looked at private insurance data for 837,316 deliveries among 716,052 women (64.2% White), ages 15-44 (mean 31.2), to assess changes in psychotherapy visits in the year before and after delivery. They also estimated per-visit out-of-pocket costs for the ACA in 2014 and the MHPAEA in 2010.
In the PMAD population, the MHPAEA was associated with an immediate increase in psychotherapy receipt of 0.72% (95% CI, 0.26%-1.18%; P = .002), followed by a sustained decrease of 0.05% (95% CI, 0.09%-0.02%; P = .001).
In both populations, the ACA was associated with immediate and sustained monthly increases in use of 0.77% (95% CI, 0.26%-1.27%; P = .003) and 0.07% (95% CI, 0.02%-0.12%; P = .005), respectively.
Post MHPAEA, both populations experienced a slight decrease in per-visit monthly out-of-pocket costs, while after the ACA they saw an immediate and steady monthly increase in these.
Although both policies expanded access to any psychotherapy, the greater number of people receiving visits coincided with fewer visits per person, the authors noted. “One hypothesis suggests that the number of available mental health clinicians may not have increased enough to meet the new demand; future research should better characterize this trend,” they wrote.
In addition, a lower standard cost per visit may have dampened the incentive to increase the number of mental health clinicians, they conjectured. These factors could explain why the PMAD group appeared to experience a decrease in the proportion receiving any psychotherapy after the MHPAEA’s implementation.
The findings should be reviewed in the context of the current mental health burden, the authors wrote, in which the shortage of mental health professionals means that less than 30% of mental healthcare needs are being met.
They called for more measures to mitigate the excess burden of PMADs.
This study was funded by the National Institutes of Health. Dr. Zivin had no conflicts of interest. Coauthor Dr. Dalton reported personal fees from Merck, the Society of Family Planning, Up to Date, and The Medical Letter outside of the submitted work.
Despite federal legislation improving healthcare access, concerted efforts are still needed to increase evidence-based treatment for maternal perinatal mental health issues, a large study of commercially insured mothers suggested. It found that federal legislation had variable and suboptimal effect on mental health services use by delivering mothers.
In the cross-sectional study, published in JAMA Network Open, psychotherapy receipt increased somewhat during 2007-2019 among all mothers and among those diagnosed with perinatal mood and anxiety disorders (PMADs). The timeline encompassed periods before and after passage of the Mental Health Parity and Addiction Equity Act (MHPAEA) of 2008 and the Patient Protection and Affordable Care Act (ACA) of 2010.
The investigators, led by Kara Zivin, PhD, MS, MFA, a professor of psychiatry in the University of Michigan’s School of Public Health at Ann Arbor, found the results varied by policy and between the overall delivering population and the PMAD population. “We did not find a statistically significant immediate change associated with the MHPAEA or ACA in the overall delivering population, except for a steady increase in delivering women who received any psychotherapy after ACA,” Dr. Zivin and colleagues wrote.
The researchers looked at private insurance data for 837,316 deliveries among 716,052 women (64.2% White), ages 15-44 (mean 31.2), to assess changes in psychotherapy visits in the year before and after delivery. They also estimated per-visit out-of-pocket costs for the ACA in 2014 and the MHPAEA in 2010.
In the PMAD population, the MHPAEA was associated with an immediate increase in psychotherapy receipt of 0.72% (95% CI, 0.26%-1.18%; P = .002), followed by a sustained decrease of 0.05% (95% CI, 0.09%-0.02%; P = .001).
In both populations, the ACA was associated with immediate and sustained monthly increases in use of 0.77% (95% CI, 0.26%-1.27%; P = .003) and 0.07% (95% CI, 0.02%-0.12%; P = .005), respectively.
Post MHPAEA, both populations experienced a slight decrease in per-visit monthly out-of-pocket costs, while after the ACA they saw an immediate and steady monthly increase in these.
Although both policies expanded access to any psychotherapy, the greater number of people receiving visits coincided with fewer visits per person, the authors noted. “One hypothesis suggests that the number of available mental health clinicians may not have increased enough to meet the new demand; future research should better characterize this trend,” they wrote.
In addition, a lower standard cost per visit may have dampened the incentive to increase the number of mental health clinicians, they conjectured. These factors could explain why the PMAD group appeared to experience a decrease in the proportion receiving any psychotherapy after the MHPAEA’s implementation.
The findings should be reviewed in the context of the current mental health burden, the authors wrote, in which the shortage of mental health professionals means that less than 30% of mental healthcare needs are being met.
They called for more measures to mitigate the excess burden of PMADs.
This study was funded by the National Institutes of Health. Dr. Zivin had no conflicts of interest. Coauthor Dr. Dalton reported personal fees from Merck, the Society of Family Planning, Up to Date, and The Medical Letter outside of the submitted work.
FROM JAMA NETWORK NEWS
How Clinicians Can Help Patients Navigate Psychedelics/Microdosing
Peter Grinspoon, MD, has some advice for clinicians when patients ask questions about microdosing of psychedelics: Keep the lines of communication open — and don’t be judgmental.
“If you’re dismissive or critical or sound like you’re judging them, then the patients just clam up,” said Dr. Grinspoon, a professor of medicine at Harvard Medical School and a primary care physician at Massachusetts General Hospital, both in Boston.
Psychedelic drugs are still illegal in the majority of states despite the growth of public interest in and use of these substances. That growth is evidenced by a flurry of workshops, reports, law enforcement seizures, and pressure by Congressional members for the Food and Drug Administration to approve new psychedelic drugs, just in the past year.
A recent study in JAMA Health Forum showed a nearly 14-fold increase in Google searches — from 7.9 to 105.6 per 10 million nationwide — for the term “microdosing” and related wording, between 2015 and 2023.
Two states — Oregon and Colorado — have decriminalized certain psychedelic drugs and are in various stages of establishing regulations and centers for prospective clients. Almost two dozen localities, like Ann Arbor, Michigan, have decriminalized psychedelic drugs. A handful of states have active legislation to decriminalize use, while others have bills that never made it out of committee.
But no definitive studies have reported that microdosing produces positive mental effects at a higher rate than placebo, according to Dr. Grinspoon. So
“We’re in this renaissance where everybody is idealizing these medications, as opposed to 20 years ago when we were in the war on drugs and everybody was dismissing them,” Dr. Grinspoon said. “The truth is somewhere in between.”
The Science
Microdosing is defined as taking doses of 1/5 to 1/20 of the conventional recreational amount, which might include a dried psilocybin mushroom, lysergic acid diethylamide, or 3,4-methylenedioxymethamphetamine. But even that much may be neither effective nor safe.
Dr. Grinspoon said clinicians should tell patients that psychedelics may cause harm, although the drugs are relatively nontoxic and are not addictive. An illegally obtained psilocybin could cause negative reactions, especially if the drug has been adulterated with other substances and if the actual dose is higher than what was indicated by the seller.
He noted that people have different reactions to psychedelics, just as they have to prescription medications. He cited one example of a woman who microdosed and could not sleep for 2 weeks afterward. Only recently have randomized, double-blinded studies begun on benefits and harms.
Researchers have also begun investigating whether long-term microdosing of psilocybin could lead to valvular heart disease (VHD), said Kevin Yang, MD, a psychiatry resident at the University of California San Diego School of Medicine. A recent review of evidence concluded that microdosing various psychedelics over a period of months can lead to drug-induced VHD.
“It’s extremely important to emphasize with patients that not only do we not know if it works or not, we also don’t really know how safe it is,” Dr. Yang said.
Dr. Yang also said clinicians should consider referring patients to a mental health professional, and especially those that may have expertise in psychedelic therapies.
One of those experts is Rachel Yehuda, PhD, director of the Center for Psychedelic Psychotherapy and Trauma Research at Icahn School of Medicine at Mount Sinai in New York City. She said therapists should be able to assess the patient’s perceived need for microdosing and “invite reflections about why current approaches are falling short.”
“I would also not actively discourage it either but remain curious until both of you have a better understanding of the reasons for seeking this out and potential alternative strategies for obtaining more therapeutic benefits,” she said. “I think it is really important to study the effects of both micro- and macrodosing of psychedelics but not move in advance of the data.”
Navigating Legality
Recent ballot measures in Oregon and Colorado directed the states to develop regulated and licensed psilocybin-assisted therapy centers for legal “trips.” Oregon’s first center was opened in 2023, and Colorado is now developing its own licensing model.
According to the Oregon Health Authority, the centers are not medical facilities, and prescription or referral from a medical professional is not required.
The Oregon Academy of Family Physicians (OAFP) has yet to release guidance to clinicians on how to talk to their patients about these drugs or potential interest in visiting a licensed therapy center.
However, Betsy Boyd-Flynn, executive director of OAFP, said the organization is working on continuing medical education for what the average family physician needs to know if a patient asks about use.
“We suspect that many of our members have interest and want to learn more,” she said.
Dr. Grinspoon said clinicians should talk with patients about legality during these conversations.
“The big question I get is: ‘I really want to try microdosing, but how do I obtain the mushrooms?’ ” he said. “You can’t really as a physician tell them to do anything illegal. So you tell them to be safe, be careful, and to use their judgment.”
Patients who want to pursue microdosing who do not live in Oregon have two legal and safe options, Dr. Grinspoon said: Enroll in a clinical study or find a facility in a state or country — such as Oregon or Jamaica — that offers microdosing with psilocybin.
Clinicians also should warn their patients that the consequences of obtaining illicit psilocybin could exacerbate the mental health stresses they are seeking to alleviate.
“It’s going to get worse if they get tangled up with law enforcement or take something that’s contaminated and they get real sick,” he said.
Lisa Gillespie contributed reporting to this story. A version of this article appeared on Medscape.com.
Peter Grinspoon, MD, has some advice for clinicians when patients ask questions about microdosing of psychedelics: Keep the lines of communication open — and don’t be judgmental.
“If you’re dismissive or critical or sound like you’re judging them, then the patients just clam up,” said Dr. Grinspoon, a professor of medicine at Harvard Medical School and a primary care physician at Massachusetts General Hospital, both in Boston.
Psychedelic drugs are still illegal in the majority of states despite the growth of public interest in and use of these substances. That growth is evidenced by a flurry of workshops, reports, law enforcement seizures, and pressure by Congressional members for the Food and Drug Administration to approve new psychedelic drugs, just in the past year.
A recent study in JAMA Health Forum showed a nearly 14-fold increase in Google searches — from 7.9 to 105.6 per 10 million nationwide — for the term “microdosing” and related wording, between 2015 and 2023.
Two states — Oregon and Colorado — have decriminalized certain psychedelic drugs and are in various stages of establishing regulations and centers for prospective clients. Almost two dozen localities, like Ann Arbor, Michigan, have decriminalized psychedelic drugs. A handful of states have active legislation to decriminalize use, while others have bills that never made it out of committee.
But no definitive studies have reported that microdosing produces positive mental effects at a higher rate than placebo, according to Dr. Grinspoon. So
“We’re in this renaissance where everybody is idealizing these medications, as opposed to 20 years ago when we were in the war on drugs and everybody was dismissing them,” Dr. Grinspoon said. “The truth is somewhere in between.”
The Science
Microdosing is defined as taking doses of 1/5 to 1/20 of the conventional recreational amount, which might include a dried psilocybin mushroom, lysergic acid diethylamide, or 3,4-methylenedioxymethamphetamine. But even that much may be neither effective nor safe.
Dr. Grinspoon said clinicians should tell patients that psychedelics may cause harm, although the drugs are relatively nontoxic and are not addictive. An illegally obtained psilocybin could cause negative reactions, especially if the drug has been adulterated with other substances and if the actual dose is higher than what was indicated by the seller.
He noted that people have different reactions to psychedelics, just as they have to prescription medications. He cited one example of a woman who microdosed and could not sleep for 2 weeks afterward. Only recently have randomized, double-blinded studies begun on benefits and harms.
Researchers have also begun investigating whether long-term microdosing of psilocybin could lead to valvular heart disease (VHD), said Kevin Yang, MD, a psychiatry resident at the University of California San Diego School of Medicine. A recent review of evidence concluded that microdosing various psychedelics over a period of months can lead to drug-induced VHD.
“It’s extremely important to emphasize with patients that not only do we not know if it works or not, we also don’t really know how safe it is,” Dr. Yang said.
Dr. Yang also said clinicians should consider referring patients to a mental health professional, and especially those that may have expertise in psychedelic therapies.
One of those experts is Rachel Yehuda, PhD, director of the Center for Psychedelic Psychotherapy and Trauma Research at Icahn School of Medicine at Mount Sinai in New York City. She said therapists should be able to assess the patient’s perceived need for microdosing and “invite reflections about why current approaches are falling short.”
“I would also not actively discourage it either but remain curious until both of you have a better understanding of the reasons for seeking this out and potential alternative strategies for obtaining more therapeutic benefits,” she said. “I think it is really important to study the effects of both micro- and macrodosing of psychedelics but not move in advance of the data.”
Navigating Legality
Recent ballot measures in Oregon and Colorado directed the states to develop regulated and licensed psilocybin-assisted therapy centers for legal “trips.” Oregon’s first center was opened in 2023, and Colorado is now developing its own licensing model.
According to the Oregon Health Authority, the centers are not medical facilities, and prescription or referral from a medical professional is not required.
The Oregon Academy of Family Physicians (OAFP) has yet to release guidance to clinicians on how to talk to their patients about these drugs or potential interest in visiting a licensed therapy center.
However, Betsy Boyd-Flynn, executive director of OAFP, said the organization is working on continuing medical education for what the average family physician needs to know if a patient asks about use.
“We suspect that many of our members have interest and want to learn more,” she said.
Dr. Grinspoon said clinicians should talk with patients about legality during these conversations.
“The big question I get is: ‘I really want to try microdosing, but how do I obtain the mushrooms?’ ” he said. “You can’t really as a physician tell them to do anything illegal. So you tell them to be safe, be careful, and to use their judgment.”
Patients who want to pursue microdosing who do not live in Oregon have two legal and safe options, Dr. Grinspoon said: Enroll in a clinical study or find a facility in a state or country — such as Oregon or Jamaica — that offers microdosing with psilocybin.
Clinicians also should warn their patients that the consequences of obtaining illicit psilocybin could exacerbate the mental health stresses they are seeking to alleviate.
“It’s going to get worse if they get tangled up with law enforcement or take something that’s contaminated and they get real sick,” he said.
Lisa Gillespie contributed reporting to this story. A version of this article appeared on Medscape.com.
Peter Grinspoon, MD, has some advice for clinicians when patients ask questions about microdosing of psychedelics: Keep the lines of communication open — and don’t be judgmental.
“If you’re dismissive or critical or sound like you’re judging them, then the patients just clam up,” said Dr. Grinspoon, a professor of medicine at Harvard Medical School and a primary care physician at Massachusetts General Hospital, both in Boston.
Psychedelic drugs are still illegal in the majority of states despite the growth of public interest in and use of these substances. That growth is evidenced by a flurry of workshops, reports, law enforcement seizures, and pressure by Congressional members for the Food and Drug Administration to approve new psychedelic drugs, just in the past year.
A recent study in JAMA Health Forum showed a nearly 14-fold increase in Google searches — from 7.9 to 105.6 per 10 million nationwide — for the term “microdosing” and related wording, between 2015 and 2023.
Two states — Oregon and Colorado — have decriminalized certain psychedelic drugs and are in various stages of establishing regulations and centers for prospective clients. Almost two dozen localities, like Ann Arbor, Michigan, have decriminalized psychedelic drugs. A handful of states have active legislation to decriminalize use, while others have bills that never made it out of committee.
But no definitive studies have reported that microdosing produces positive mental effects at a higher rate than placebo, according to Dr. Grinspoon. So
“We’re in this renaissance where everybody is idealizing these medications, as opposed to 20 years ago when we were in the war on drugs and everybody was dismissing them,” Dr. Grinspoon said. “The truth is somewhere in between.”
The Science
Microdosing is defined as taking doses of 1/5 to 1/20 of the conventional recreational amount, which might include a dried psilocybin mushroom, lysergic acid diethylamide, or 3,4-methylenedioxymethamphetamine. But even that much may be neither effective nor safe.
Dr. Grinspoon said clinicians should tell patients that psychedelics may cause harm, although the drugs are relatively nontoxic and are not addictive. An illegally obtained psilocybin could cause negative reactions, especially if the drug has been adulterated with other substances and if the actual dose is higher than what was indicated by the seller.
He noted that people have different reactions to psychedelics, just as they have to prescription medications. He cited one example of a woman who microdosed and could not sleep for 2 weeks afterward. Only recently have randomized, double-blinded studies begun on benefits and harms.
Researchers have also begun investigating whether long-term microdosing of psilocybin could lead to valvular heart disease (VHD), said Kevin Yang, MD, a psychiatry resident at the University of California San Diego School of Medicine. A recent review of evidence concluded that microdosing various psychedelics over a period of months can lead to drug-induced VHD.
“It’s extremely important to emphasize with patients that not only do we not know if it works or not, we also don’t really know how safe it is,” Dr. Yang said.
Dr. Yang also said clinicians should consider referring patients to a mental health professional, and especially those that may have expertise in psychedelic therapies.
One of those experts is Rachel Yehuda, PhD, director of the Center for Psychedelic Psychotherapy and Trauma Research at Icahn School of Medicine at Mount Sinai in New York City. She said therapists should be able to assess the patient’s perceived need for microdosing and “invite reflections about why current approaches are falling short.”
“I would also not actively discourage it either but remain curious until both of you have a better understanding of the reasons for seeking this out and potential alternative strategies for obtaining more therapeutic benefits,” she said. “I think it is really important to study the effects of both micro- and macrodosing of psychedelics but not move in advance of the data.”
Navigating Legality
Recent ballot measures in Oregon and Colorado directed the states to develop regulated and licensed psilocybin-assisted therapy centers for legal “trips.” Oregon’s first center was opened in 2023, and Colorado is now developing its own licensing model.
According to the Oregon Health Authority, the centers are not medical facilities, and prescription or referral from a medical professional is not required.
The Oregon Academy of Family Physicians (OAFP) has yet to release guidance to clinicians on how to talk to their patients about these drugs or potential interest in visiting a licensed therapy center.
However, Betsy Boyd-Flynn, executive director of OAFP, said the organization is working on continuing medical education for what the average family physician needs to know if a patient asks about use.
“We suspect that many of our members have interest and want to learn more,” she said.
Dr. Grinspoon said clinicians should talk with patients about legality during these conversations.
“The big question I get is: ‘I really want to try microdosing, but how do I obtain the mushrooms?’ ” he said. “You can’t really as a physician tell them to do anything illegal. So you tell them to be safe, be careful, and to use their judgment.”
Patients who want to pursue microdosing who do not live in Oregon have two legal and safe options, Dr. Grinspoon said: Enroll in a clinical study or find a facility in a state or country — such as Oregon or Jamaica — that offers microdosing with psilocybin.
Clinicians also should warn their patients that the consequences of obtaining illicit psilocybin could exacerbate the mental health stresses they are seeking to alleviate.
“It’s going to get worse if they get tangled up with law enforcement or take something that’s contaminated and they get real sick,” he said.
Lisa Gillespie contributed reporting to this story. A version of this article appeared on Medscape.com.
Anxiety Linked to a Threefold Increased Risk for Dementia
TOPLINE:
, new research shows.
METHODOLOGY:
- A total of 2132 participants aged 55-85 years (mean age, 76 years) were recruited from the Hunter Community Study. Of these, 53% were women.
- Participants were assessed over three different waves, 5 years apart. Demographic and health-related data were captured at wave 1.
- Researchers used the Kessler Psychological Distress Scale (K10) to measure anxiety at two points: Baseline (wave 1) and first follow-up (wave 2), with a 5-year interval between them. Anxiety was classified as chronic if present during both waves, resolved if only present at wave 1, and new if only appearing at wave 2.
- The primary outcome, incident all-cause dementia, during the follow-up period (maximum 13 years after baseline) was identified using the International Classification of Disease-10 codes.
TAKEAWAY:
- Out of 2132 cognitively healthy participants, 64 developed dementia, with an average time to diagnosis of 10 years. Chronic anxiety was linked to a 2.8-fold increased risk for dementia, while new-onset anxiety was associated with a 3.2-fold increased risk (P = .01).
- Participants younger than 70 years with chronic anxiety had a 4.6-fold increased risk for dementia (P = .03), and those with new-onset anxiety had a 7.2 times higher risk for dementia (P = .004).
- There was no significant risk for dementia in participants with anxiety that had resolved.
- Investigators speculated that individuals with anxiety were more likely to engage in unhealthy lifestyle behaviors, such as poor diet and smoking, which can lead to cardiovascular disease — a condition strongly associated with dementia.
IN PRACTICE:
“This prospective cohort study used causal inference methods to explore the role of anxiety in promoting the development of dementia,” lead author Kay Khaing, MMed, The University of Newcastle, Australia, wrote in a press release. “The findings suggest that anxiety may be a new risk factor to target in the prevention of dementia and also indicate that treating anxiety may reduce this risk.”
SOURCE:
Kay Khaing, MMed, of The University of Newcastle, Australia, led the study, which was published online in the Journal of the American Geriatrics Society.
LIMITATIONS:
Anxiety was measured using K10, which assessed symptoms experienced in the most recent 4 weeks, raising concerns about its accuracy over the entire observation period. The authors acknowledged that despite using a combination of the total K10 score and the anxiety subscale, the overlap of anxiety and depression might not be fully disentangled, leading to residual confounding by depression. Additionally, 33% of participants were lost to follow-up, and those lost had higher anxiety rates at baseline, potentially leading to missing cases of dementia and affecting the effect estimate.
DISCLOSURES:
This study did not report any funding or conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article appeared on Medscape.com.
TOPLINE:
, new research shows.
METHODOLOGY:
- A total of 2132 participants aged 55-85 years (mean age, 76 years) were recruited from the Hunter Community Study. Of these, 53% were women.
- Participants were assessed over three different waves, 5 years apart. Demographic and health-related data were captured at wave 1.
- Researchers used the Kessler Psychological Distress Scale (K10) to measure anxiety at two points: Baseline (wave 1) and first follow-up (wave 2), with a 5-year interval between them. Anxiety was classified as chronic if present during both waves, resolved if only present at wave 1, and new if only appearing at wave 2.
- The primary outcome, incident all-cause dementia, during the follow-up period (maximum 13 years after baseline) was identified using the International Classification of Disease-10 codes.
TAKEAWAY:
- Out of 2132 cognitively healthy participants, 64 developed dementia, with an average time to diagnosis of 10 years. Chronic anxiety was linked to a 2.8-fold increased risk for dementia, while new-onset anxiety was associated with a 3.2-fold increased risk (P = .01).
- Participants younger than 70 years with chronic anxiety had a 4.6-fold increased risk for dementia (P = .03), and those with new-onset anxiety had a 7.2 times higher risk for dementia (P = .004).
- There was no significant risk for dementia in participants with anxiety that had resolved.
- Investigators speculated that individuals with anxiety were more likely to engage in unhealthy lifestyle behaviors, such as poor diet and smoking, which can lead to cardiovascular disease — a condition strongly associated with dementia.
IN PRACTICE:
“This prospective cohort study used causal inference methods to explore the role of anxiety in promoting the development of dementia,” lead author Kay Khaing, MMed, The University of Newcastle, Australia, wrote in a press release. “The findings suggest that anxiety may be a new risk factor to target in the prevention of dementia and also indicate that treating anxiety may reduce this risk.”
SOURCE:
Kay Khaing, MMed, of The University of Newcastle, Australia, led the study, which was published online in the Journal of the American Geriatrics Society.
LIMITATIONS:
Anxiety was measured using K10, which assessed symptoms experienced in the most recent 4 weeks, raising concerns about its accuracy over the entire observation period. The authors acknowledged that despite using a combination of the total K10 score and the anxiety subscale, the overlap of anxiety and depression might not be fully disentangled, leading to residual confounding by depression. Additionally, 33% of participants were lost to follow-up, and those lost had higher anxiety rates at baseline, potentially leading to missing cases of dementia and affecting the effect estimate.
DISCLOSURES:
This study did not report any funding or conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article appeared on Medscape.com.
TOPLINE:
, new research shows.
METHODOLOGY:
- A total of 2132 participants aged 55-85 years (mean age, 76 years) were recruited from the Hunter Community Study. Of these, 53% were women.
- Participants were assessed over three different waves, 5 years apart. Demographic and health-related data were captured at wave 1.
- Researchers used the Kessler Psychological Distress Scale (K10) to measure anxiety at two points: Baseline (wave 1) and first follow-up (wave 2), with a 5-year interval between them. Anxiety was classified as chronic if present during both waves, resolved if only present at wave 1, and new if only appearing at wave 2.
- The primary outcome, incident all-cause dementia, during the follow-up period (maximum 13 years after baseline) was identified using the International Classification of Disease-10 codes.
TAKEAWAY:
- Out of 2132 cognitively healthy participants, 64 developed dementia, with an average time to diagnosis of 10 years. Chronic anxiety was linked to a 2.8-fold increased risk for dementia, while new-onset anxiety was associated with a 3.2-fold increased risk (P = .01).
- Participants younger than 70 years with chronic anxiety had a 4.6-fold increased risk for dementia (P = .03), and those with new-onset anxiety had a 7.2 times higher risk for dementia (P = .004).
- There was no significant risk for dementia in participants with anxiety that had resolved.
- Investigators speculated that individuals with anxiety were more likely to engage in unhealthy lifestyle behaviors, such as poor diet and smoking, which can lead to cardiovascular disease — a condition strongly associated with dementia.
IN PRACTICE:
“This prospective cohort study used causal inference methods to explore the role of anxiety in promoting the development of dementia,” lead author Kay Khaing, MMed, The University of Newcastle, Australia, wrote in a press release. “The findings suggest that anxiety may be a new risk factor to target in the prevention of dementia and also indicate that treating anxiety may reduce this risk.”
SOURCE:
Kay Khaing, MMed, of The University of Newcastle, Australia, led the study, which was published online in the Journal of the American Geriatrics Society.
LIMITATIONS:
Anxiety was measured using K10, which assessed symptoms experienced in the most recent 4 weeks, raising concerns about its accuracy over the entire observation period. The authors acknowledged that despite using a combination of the total K10 score and the anxiety subscale, the overlap of anxiety and depression might not be fully disentangled, leading to residual confounding by depression. Additionally, 33% of participants were lost to follow-up, and those lost had higher anxiety rates at baseline, potentially leading to missing cases of dementia and affecting the effect estimate.
DISCLOSURES:
This study did not report any funding or conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article appeared on Medscape.com.
Can Addressing Depression Reduce Chemo Toxicity in Older Adults?
TOPLINE:
METHODOLOGY:
- Researchers conducted a secondary analysis of a randomized controlled trial to evaluate whether greater reductions in grade 3 chemotherapy-related toxicities occurred with geriatric assessment-driven interventions vs standard care.
- A total of 605 patients aged 65 years and older with any stage of solid malignancy were included, with 402 randomized to the intervention arm and 203 to the standard-of-care arm.
- Mental health was assessed using the Mental Health Inventory 13, and chemotherapy toxicity was graded by the National Cancer Institute Common Terminology Criteria for Adverse Events, version 4.0.
- Patients in the intervention arm received recommendations from a multidisciplinary team based on their baseline GA, while those in the standard-of-care arm received only the baseline assessment results.
- The study was conducted at City of Hope National Medical Center in Duarte, California, and patients were followed throughout treatment or for up to 6 months from starting chemotherapy.
TAKEAWAY:
- According to the authors, patients with depression had increased chemotherapy toxicity in the standard-of-care arm (70.7% vs 54.3%; P = .02) but not in the GA-driven intervention arm (54.3% vs 48.5%; P = .27).
- The association between depression and chemotherapy toxicity was also seen after adjustment for the Cancer and Aging Research Group toxicity score (odds ratio, [OR], 1.98; 95% CI, 1.07-3.65) and for demographic, disease, and treatment factors (OR, 2.00; 95% CI, 1.03-3.85).
- No significant association was found between anxiety and chemotherapy toxicity in either the standard-of-care arm (univariate OR, 1.07; 95% CI, 0.61-1.88) or the GA-driven intervention arm (univariate OR, 1.15; 95% CI, 0.78-1.71).
- The authors stated that depression was associated with increased odds of hematologic-only toxicities (OR, 2.50; 95% CI, 1.13-5.56) in the standard-of-care arm.
- An analysis of a small subgroup found associations between elevated anxiety symptoms and increased risk for hematologic and nonhematologic chemotherapy toxicities.
IN PRACTICE:
“The current study showed that elevated depression symptoms are associated with increased risk of severe chemotherapy toxicities in older adults with cancer. This risk was mitigated in those in the GA intervention arm, which suggests that addressing elevated depression symptoms may lower the risk of toxicities,” the authors wrote. “Overall, elevated anxiety symptoms were not associated with risk for severe chemotherapy toxicity.”
SOURCE:
Reena V. Jayani, MD, MSCI, of Vanderbilt University Medical Center in Nashville, Tennessee, was the first and corresponding author for this paper. This study was published online August 4, 2024, in Cancer.
LIMITATIONS:
The thresholds for depression and anxiety used in the Mental Health Inventory 13 were based on an English-speaking population, which may not be fully applicable to Chinese- and Spanish-speaking patients included in the study. Depression and anxiety were not evaluated by a mental health professional or with a structured interview to assess formal diagnostic criteria. Psychiatric medication used at the time of baseline GA was not included in the analysis. The study is a secondary analysis of a randomized controlled trial, and it is not known which components of the interventions affected mental health.
DISCLOSURES:
This research project was supported by the UniHealth Foundation, the City of Hope Center for Cancer and Aging, and the National Institutes of Health. One coauthor disclosed receiving institutional research funding from AstraZeneca and Brooklyn ImmunoTherapeutics and consulting for multiple pharmaceutical companies, including AbbVie, Adagene, and Bayer HealthCare Pharmaceuticals. William Dale, MD, PhD, of City of Hope National Medical Center, served as senior author and a principal investigator. Additional disclosures are noted in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- Researchers conducted a secondary analysis of a randomized controlled trial to evaluate whether greater reductions in grade 3 chemotherapy-related toxicities occurred with geriatric assessment-driven interventions vs standard care.
- A total of 605 patients aged 65 years and older with any stage of solid malignancy were included, with 402 randomized to the intervention arm and 203 to the standard-of-care arm.
- Mental health was assessed using the Mental Health Inventory 13, and chemotherapy toxicity was graded by the National Cancer Institute Common Terminology Criteria for Adverse Events, version 4.0.
- Patients in the intervention arm received recommendations from a multidisciplinary team based on their baseline GA, while those in the standard-of-care arm received only the baseline assessment results.
- The study was conducted at City of Hope National Medical Center in Duarte, California, and patients were followed throughout treatment or for up to 6 months from starting chemotherapy.
TAKEAWAY:
- According to the authors, patients with depression had increased chemotherapy toxicity in the standard-of-care arm (70.7% vs 54.3%; P = .02) but not in the GA-driven intervention arm (54.3% vs 48.5%; P = .27).
- The association between depression and chemotherapy toxicity was also seen after adjustment for the Cancer and Aging Research Group toxicity score (odds ratio, [OR], 1.98; 95% CI, 1.07-3.65) and for demographic, disease, and treatment factors (OR, 2.00; 95% CI, 1.03-3.85).
- No significant association was found between anxiety and chemotherapy toxicity in either the standard-of-care arm (univariate OR, 1.07; 95% CI, 0.61-1.88) or the GA-driven intervention arm (univariate OR, 1.15; 95% CI, 0.78-1.71).
- The authors stated that depression was associated with increased odds of hematologic-only toxicities (OR, 2.50; 95% CI, 1.13-5.56) in the standard-of-care arm.
- An analysis of a small subgroup found associations between elevated anxiety symptoms and increased risk for hematologic and nonhematologic chemotherapy toxicities.
IN PRACTICE:
“The current study showed that elevated depression symptoms are associated with increased risk of severe chemotherapy toxicities in older adults with cancer. This risk was mitigated in those in the GA intervention arm, which suggests that addressing elevated depression symptoms may lower the risk of toxicities,” the authors wrote. “Overall, elevated anxiety symptoms were not associated with risk for severe chemotherapy toxicity.”
SOURCE:
Reena V. Jayani, MD, MSCI, of Vanderbilt University Medical Center in Nashville, Tennessee, was the first and corresponding author for this paper. This study was published online August 4, 2024, in Cancer.
LIMITATIONS:
The thresholds for depression and anxiety used in the Mental Health Inventory 13 were based on an English-speaking population, which may not be fully applicable to Chinese- and Spanish-speaking patients included in the study. Depression and anxiety were not evaluated by a mental health professional or with a structured interview to assess formal diagnostic criteria. Psychiatric medication used at the time of baseline GA was not included in the analysis. The study is a secondary analysis of a randomized controlled trial, and it is not known which components of the interventions affected mental health.
DISCLOSURES:
This research project was supported by the UniHealth Foundation, the City of Hope Center for Cancer and Aging, and the National Institutes of Health. One coauthor disclosed receiving institutional research funding from AstraZeneca and Brooklyn ImmunoTherapeutics and consulting for multiple pharmaceutical companies, including AbbVie, Adagene, and Bayer HealthCare Pharmaceuticals. William Dale, MD, PhD, of City of Hope National Medical Center, served as senior author and a principal investigator. Additional disclosures are noted in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- Researchers conducted a secondary analysis of a randomized controlled trial to evaluate whether greater reductions in grade 3 chemotherapy-related toxicities occurred with geriatric assessment-driven interventions vs standard care.
- A total of 605 patients aged 65 years and older with any stage of solid malignancy were included, with 402 randomized to the intervention arm and 203 to the standard-of-care arm.
- Mental health was assessed using the Mental Health Inventory 13, and chemotherapy toxicity was graded by the National Cancer Institute Common Terminology Criteria for Adverse Events, version 4.0.
- Patients in the intervention arm received recommendations from a multidisciplinary team based on their baseline GA, while those in the standard-of-care arm received only the baseline assessment results.
- The study was conducted at City of Hope National Medical Center in Duarte, California, and patients were followed throughout treatment or for up to 6 months from starting chemotherapy.
TAKEAWAY:
- According to the authors, patients with depression had increased chemotherapy toxicity in the standard-of-care arm (70.7% vs 54.3%; P = .02) but not in the GA-driven intervention arm (54.3% vs 48.5%; P = .27).
- The association between depression and chemotherapy toxicity was also seen after adjustment for the Cancer and Aging Research Group toxicity score (odds ratio, [OR], 1.98; 95% CI, 1.07-3.65) and for demographic, disease, and treatment factors (OR, 2.00; 95% CI, 1.03-3.85).
- No significant association was found between anxiety and chemotherapy toxicity in either the standard-of-care arm (univariate OR, 1.07; 95% CI, 0.61-1.88) or the GA-driven intervention arm (univariate OR, 1.15; 95% CI, 0.78-1.71).
- The authors stated that depression was associated with increased odds of hematologic-only toxicities (OR, 2.50; 95% CI, 1.13-5.56) in the standard-of-care arm.
- An analysis of a small subgroup found associations between elevated anxiety symptoms and increased risk for hematologic and nonhematologic chemotherapy toxicities.
IN PRACTICE:
“The current study showed that elevated depression symptoms are associated with increased risk of severe chemotherapy toxicities in older adults with cancer. This risk was mitigated in those in the GA intervention arm, which suggests that addressing elevated depression symptoms may lower the risk of toxicities,” the authors wrote. “Overall, elevated anxiety symptoms were not associated with risk for severe chemotherapy toxicity.”
SOURCE:
Reena V. Jayani, MD, MSCI, of Vanderbilt University Medical Center in Nashville, Tennessee, was the first and corresponding author for this paper. This study was published online August 4, 2024, in Cancer.
LIMITATIONS:
The thresholds for depression and anxiety used in the Mental Health Inventory 13 were based on an English-speaking population, which may not be fully applicable to Chinese- and Spanish-speaking patients included in the study. Depression and anxiety were not evaluated by a mental health professional or with a structured interview to assess formal diagnostic criteria. Psychiatric medication used at the time of baseline GA was not included in the analysis. The study is a secondary analysis of a randomized controlled trial, and it is not known which components of the interventions affected mental health.
DISCLOSURES:
This research project was supported by the UniHealth Foundation, the City of Hope Center for Cancer and Aging, and the National Institutes of Health. One coauthor disclosed receiving institutional research funding from AstraZeneca and Brooklyn ImmunoTherapeutics and consulting for multiple pharmaceutical companies, including AbbVie, Adagene, and Bayer HealthCare Pharmaceuticals. William Dale, MD, PhD, of City of Hope National Medical Center, served as senior author and a principal investigator. Additional disclosures are noted in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.