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Metformin fails as early COVID-19 treatment but shows potential
Neither metformin, ivermectin, or fluvoxamine had any impact on reducing disease severity, hospitalization, or death from COVID-19, according to results from more than 1,000 overweight or obese adult patients in the COVID-OUT randomized trial.
However, metformin showed some potential in a secondary analysis.
Early treatment to prevent severe disease remains a goal in managing the ongoing COVID-19 pandemic, and biophysical modeling suggested that metformin, ivermectin, and fluvoxamine may serve as antivirals to help reduce severe disease in COVID-19 patients, Carolyn T. Bramante, MD, of the University of Minnesota, Minneapolis, and colleagues wrote.
“We started enrolling patients at the end of December 2020,” Dr. Bramante said in an interview. “At that time, even though vaccine data were coming out, we thought it was important to test early outpatient treatment with widely available safe medications with no interactions, because the virus would evolve and vaccine availability may be limited.”
In a study published in the New England Journal of Medicine, the researchers used a two-by-three factorial design to test the ability of metformin, ivermectin, and fluvoxamine to prevent severe COVID-19 infection in nonhospitalized adults aged 30-85 years. A total of 1,431 patients at six U.S. sites were enrolled within 3 days of a confirmed infection and less than 7 days after the start of symptoms, then randomized to one of six groups: metformin plus fluvoxamine; metformin plus ivermectin; metformin plus placebo; placebo plus fluvoxamine; placebo plus ivermectin; and placebo plus placebo.
A total of 1,323 patients were included in the primary analysis. The median age of the patients was 46 years, 56% were female (of whom 6% were pregnant), and all individuals met criteria for overweight or obesity. About half (52%) of the patients had been vaccinated against COVID-19.
The primary endpoint was a composite of hypoxemia, ED visit, hospitalization, or death. The analyses were adjusted for COVID-19 vaccination and other trial medications. Overall, the adjusted odds ratios of any primary event, compared with placebo, was 0.84 for metformin (P = .19), 1.05 for ivermectin (P = .78), and 0.94 for fluvoxamine (P = .75).
The researchers also conducted a prespecified secondary analysis of components of the primary endpoint. In this analysis, the aORs for an ED visit, hospitalization, or death was 0.58 for metformin, 1.39 for ivermectin, and 1.17 for fluvoxamine. The aORs for hospitalization or death were 0.47, 0.73, and 1.11 for metformin, ivermectin, and fluvoxamine, respectively. No medication-related serious adverse events were reported with any of the drugs during the study period.
The possible benefit for prevention of severe COVID-19 with metformin was a prespecified secondary endpoint, and therefore not definitive until more research has been completed, the researchers said. Metformin has demonstrated anti-inflammatory actions in previous studies, and has shown protective effects against COVID-19 lung injury in animal studies.
Previous observational studies also have shown an association between metformin use and less severe COVID-19 in patients already taking metformin. “The proposed mechanisms of action against COVID-19 for metformin include anti-inflammatory and antiviral activity and the prevention of hyperglycemia during acute illness,” they added.
The study findings were limited by several factors including the population age range and focus on overweight and obese patients, which may limit generalizability, the researchers noted. Other limitations include the disproportionately small percentage of Black and Latino patients and the potential lack of accuracy in identifying hypoxemia via home oxygen monitors.
However, the results demonstrate that none of the three repurposed drugs – metformin, ivermectin, and fluvoxamine – prevented primary events or reduced symptom severity in COVID-19, compared with placebos, the researchers concluded.
“Metformin had several streams of evidence supporting its use: in vitro, in silico [computer modeled], observational, and in tissue. We were not surprised to see that it reduced emergency department visits, hospitalization, and death,” Dr. Bramante said in an interview.
The take-home message for clinicians is to continue to look to guideline committees for direction on COVID-19 treatments, but to continue to consider metformin along with other treatments, she said.
“All research should be replicated, whether the primary outcome is positive or negative,” Dr. Bramante emphasized. “In this case, when our positive outcome was negative and secondary outcome was positive, a confirmatory trial for metformin is particularly important.”
Ineffective drugs are inefficient use of resources
“The results of the COVID-OUT trial provide persuasive additional data that increase the confidence and degree of certainty that fluvoxamine and ivermectin are not effective in preventing progression to severe disease,” wrote Salim S. Abdool Karim, MB, and Nikita Devnarain, PhD, of the Centre for the AIDS Programme of Research in South Africa, Durban, in an accompanying editorial.
At the start of the study, in 2020, data on the use of the three drugs to prevent severe COVID-19 were “either unavailable or equivocal,” they said. Since then, accumulating data support the current study findings of the nonefficacy of ivermectin and fluvoxamine, and the World Health Organization has advised against their use for COVID-19, although the WHO has not provided guidance for the use of metformin.
The authors called on clinicians to stop using ivermectin and fluvoxamine to treat COVID-19 patients.
“With respect to clinical decisions about COVID-19 treatment, some drug choices, especially those that have negative [World Health Organization] recommendations, are clearly wrong,” they wrote. “In keeping with evidence-based medical practice, patients with COVID-19 must be treated with efficacious medications; they deserve nothing less.”
The study was supported by the Parsemus Foundation, Rainwater Charitable Foundation, Fast Grants, and UnitedHealth Group Foundation. The fluvoxamine placebo tablets were donated by Apotex Pharmaceuticals. The ivermectin placebo and active tablets were donated by Edenbridge Pharmaceuticals. Lead author Dr. Bramante was supported the National Center for Advancing Translational Sciences and the National Institute of Diabetes and Digestive and Kidney Diseases. The researchers had no financial conflicts to disclose. Dr. Abdool Karim serves as a member of the World Health Organization Science Council. Dr. Devnarain had no financial conflicts to disclose.
Neither metformin, ivermectin, or fluvoxamine had any impact on reducing disease severity, hospitalization, or death from COVID-19, according to results from more than 1,000 overweight or obese adult patients in the COVID-OUT randomized trial.
However, metformin showed some potential in a secondary analysis.
Early treatment to prevent severe disease remains a goal in managing the ongoing COVID-19 pandemic, and biophysical modeling suggested that metformin, ivermectin, and fluvoxamine may serve as antivirals to help reduce severe disease in COVID-19 patients, Carolyn T. Bramante, MD, of the University of Minnesota, Minneapolis, and colleagues wrote.
“We started enrolling patients at the end of December 2020,” Dr. Bramante said in an interview. “At that time, even though vaccine data were coming out, we thought it was important to test early outpatient treatment with widely available safe medications with no interactions, because the virus would evolve and vaccine availability may be limited.”
In a study published in the New England Journal of Medicine, the researchers used a two-by-three factorial design to test the ability of metformin, ivermectin, and fluvoxamine to prevent severe COVID-19 infection in nonhospitalized adults aged 30-85 years. A total of 1,431 patients at six U.S. sites were enrolled within 3 days of a confirmed infection and less than 7 days after the start of symptoms, then randomized to one of six groups: metformin plus fluvoxamine; metformin plus ivermectin; metformin plus placebo; placebo plus fluvoxamine; placebo plus ivermectin; and placebo plus placebo.
A total of 1,323 patients were included in the primary analysis. The median age of the patients was 46 years, 56% were female (of whom 6% were pregnant), and all individuals met criteria for overweight or obesity. About half (52%) of the patients had been vaccinated against COVID-19.
The primary endpoint was a composite of hypoxemia, ED visit, hospitalization, or death. The analyses were adjusted for COVID-19 vaccination and other trial medications. Overall, the adjusted odds ratios of any primary event, compared with placebo, was 0.84 for metformin (P = .19), 1.05 for ivermectin (P = .78), and 0.94 for fluvoxamine (P = .75).
The researchers also conducted a prespecified secondary analysis of components of the primary endpoint. In this analysis, the aORs for an ED visit, hospitalization, or death was 0.58 for metformin, 1.39 for ivermectin, and 1.17 for fluvoxamine. The aORs for hospitalization or death were 0.47, 0.73, and 1.11 for metformin, ivermectin, and fluvoxamine, respectively. No medication-related serious adverse events were reported with any of the drugs during the study period.
The possible benefit for prevention of severe COVID-19 with metformin was a prespecified secondary endpoint, and therefore not definitive until more research has been completed, the researchers said. Metformin has demonstrated anti-inflammatory actions in previous studies, and has shown protective effects against COVID-19 lung injury in animal studies.
Previous observational studies also have shown an association between metformin use and less severe COVID-19 in patients already taking metformin. “The proposed mechanisms of action against COVID-19 for metformin include anti-inflammatory and antiviral activity and the prevention of hyperglycemia during acute illness,” they added.
The study findings were limited by several factors including the population age range and focus on overweight and obese patients, which may limit generalizability, the researchers noted. Other limitations include the disproportionately small percentage of Black and Latino patients and the potential lack of accuracy in identifying hypoxemia via home oxygen monitors.
However, the results demonstrate that none of the three repurposed drugs – metformin, ivermectin, and fluvoxamine – prevented primary events or reduced symptom severity in COVID-19, compared with placebos, the researchers concluded.
“Metformin had several streams of evidence supporting its use: in vitro, in silico [computer modeled], observational, and in tissue. We were not surprised to see that it reduced emergency department visits, hospitalization, and death,” Dr. Bramante said in an interview.
The take-home message for clinicians is to continue to look to guideline committees for direction on COVID-19 treatments, but to continue to consider metformin along with other treatments, she said.
“All research should be replicated, whether the primary outcome is positive or negative,” Dr. Bramante emphasized. “In this case, when our positive outcome was negative and secondary outcome was positive, a confirmatory trial for metformin is particularly important.”
Ineffective drugs are inefficient use of resources
“The results of the COVID-OUT trial provide persuasive additional data that increase the confidence and degree of certainty that fluvoxamine and ivermectin are not effective in preventing progression to severe disease,” wrote Salim S. Abdool Karim, MB, and Nikita Devnarain, PhD, of the Centre for the AIDS Programme of Research in South Africa, Durban, in an accompanying editorial.
At the start of the study, in 2020, data on the use of the three drugs to prevent severe COVID-19 were “either unavailable or equivocal,” they said. Since then, accumulating data support the current study findings of the nonefficacy of ivermectin and fluvoxamine, and the World Health Organization has advised against their use for COVID-19, although the WHO has not provided guidance for the use of metformin.
The authors called on clinicians to stop using ivermectin and fluvoxamine to treat COVID-19 patients.
“With respect to clinical decisions about COVID-19 treatment, some drug choices, especially those that have negative [World Health Organization] recommendations, are clearly wrong,” they wrote. “In keeping with evidence-based medical practice, patients with COVID-19 must be treated with efficacious medications; they deserve nothing less.”
The study was supported by the Parsemus Foundation, Rainwater Charitable Foundation, Fast Grants, and UnitedHealth Group Foundation. The fluvoxamine placebo tablets were donated by Apotex Pharmaceuticals. The ivermectin placebo and active tablets were donated by Edenbridge Pharmaceuticals. Lead author Dr. Bramante was supported the National Center for Advancing Translational Sciences and the National Institute of Diabetes and Digestive and Kidney Diseases. The researchers had no financial conflicts to disclose. Dr. Abdool Karim serves as a member of the World Health Organization Science Council. Dr. Devnarain had no financial conflicts to disclose.
Neither metformin, ivermectin, or fluvoxamine had any impact on reducing disease severity, hospitalization, or death from COVID-19, according to results from more than 1,000 overweight or obese adult patients in the COVID-OUT randomized trial.
However, metformin showed some potential in a secondary analysis.
Early treatment to prevent severe disease remains a goal in managing the ongoing COVID-19 pandemic, and biophysical modeling suggested that metformin, ivermectin, and fluvoxamine may serve as antivirals to help reduce severe disease in COVID-19 patients, Carolyn T. Bramante, MD, of the University of Minnesota, Minneapolis, and colleagues wrote.
“We started enrolling patients at the end of December 2020,” Dr. Bramante said in an interview. “At that time, even though vaccine data were coming out, we thought it was important to test early outpatient treatment with widely available safe medications with no interactions, because the virus would evolve and vaccine availability may be limited.”
In a study published in the New England Journal of Medicine, the researchers used a two-by-three factorial design to test the ability of metformin, ivermectin, and fluvoxamine to prevent severe COVID-19 infection in nonhospitalized adults aged 30-85 years. A total of 1,431 patients at six U.S. sites were enrolled within 3 days of a confirmed infection and less than 7 days after the start of symptoms, then randomized to one of six groups: metformin plus fluvoxamine; metformin plus ivermectin; metformin plus placebo; placebo plus fluvoxamine; placebo plus ivermectin; and placebo plus placebo.
A total of 1,323 patients were included in the primary analysis. The median age of the patients was 46 years, 56% were female (of whom 6% were pregnant), and all individuals met criteria for overweight or obesity. About half (52%) of the patients had been vaccinated against COVID-19.
The primary endpoint was a composite of hypoxemia, ED visit, hospitalization, or death. The analyses were adjusted for COVID-19 vaccination and other trial medications. Overall, the adjusted odds ratios of any primary event, compared with placebo, was 0.84 for metformin (P = .19), 1.05 for ivermectin (P = .78), and 0.94 for fluvoxamine (P = .75).
The researchers also conducted a prespecified secondary analysis of components of the primary endpoint. In this analysis, the aORs for an ED visit, hospitalization, or death was 0.58 for metformin, 1.39 for ivermectin, and 1.17 for fluvoxamine. The aORs for hospitalization or death were 0.47, 0.73, and 1.11 for metformin, ivermectin, and fluvoxamine, respectively. No medication-related serious adverse events were reported with any of the drugs during the study period.
The possible benefit for prevention of severe COVID-19 with metformin was a prespecified secondary endpoint, and therefore not definitive until more research has been completed, the researchers said. Metformin has demonstrated anti-inflammatory actions in previous studies, and has shown protective effects against COVID-19 lung injury in animal studies.
Previous observational studies also have shown an association between metformin use and less severe COVID-19 in patients already taking metformin. “The proposed mechanisms of action against COVID-19 for metformin include anti-inflammatory and antiviral activity and the prevention of hyperglycemia during acute illness,” they added.
The study findings were limited by several factors including the population age range and focus on overweight and obese patients, which may limit generalizability, the researchers noted. Other limitations include the disproportionately small percentage of Black and Latino patients and the potential lack of accuracy in identifying hypoxemia via home oxygen monitors.
However, the results demonstrate that none of the three repurposed drugs – metformin, ivermectin, and fluvoxamine – prevented primary events or reduced symptom severity in COVID-19, compared with placebos, the researchers concluded.
“Metformin had several streams of evidence supporting its use: in vitro, in silico [computer modeled], observational, and in tissue. We were not surprised to see that it reduced emergency department visits, hospitalization, and death,” Dr. Bramante said in an interview.
The take-home message for clinicians is to continue to look to guideline committees for direction on COVID-19 treatments, but to continue to consider metformin along with other treatments, she said.
“All research should be replicated, whether the primary outcome is positive or negative,” Dr. Bramante emphasized. “In this case, when our positive outcome was negative and secondary outcome was positive, a confirmatory trial for metformin is particularly important.”
Ineffective drugs are inefficient use of resources
“The results of the COVID-OUT trial provide persuasive additional data that increase the confidence and degree of certainty that fluvoxamine and ivermectin are not effective in preventing progression to severe disease,” wrote Salim S. Abdool Karim, MB, and Nikita Devnarain, PhD, of the Centre for the AIDS Programme of Research in South Africa, Durban, in an accompanying editorial.
At the start of the study, in 2020, data on the use of the three drugs to prevent severe COVID-19 were “either unavailable or equivocal,” they said. Since then, accumulating data support the current study findings of the nonefficacy of ivermectin and fluvoxamine, and the World Health Organization has advised against their use for COVID-19, although the WHO has not provided guidance for the use of metformin.
The authors called on clinicians to stop using ivermectin and fluvoxamine to treat COVID-19 patients.
“With respect to clinical decisions about COVID-19 treatment, some drug choices, especially those that have negative [World Health Organization] recommendations, are clearly wrong,” they wrote. “In keeping with evidence-based medical practice, patients with COVID-19 must be treated with efficacious medications; they deserve nothing less.”
The study was supported by the Parsemus Foundation, Rainwater Charitable Foundation, Fast Grants, and UnitedHealth Group Foundation. The fluvoxamine placebo tablets were donated by Apotex Pharmaceuticals. The ivermectin placebo and active tablets were donated by Edenbridge Pharmaceuticals. Lead author Dr. Bramante was supported the National Center for Advancing Translational Sciences and the National Institute of Diabetes and Digestive and Kidney Diseases. The researchers had no financial conflicts to disclose. Dr. Abdool Karim serves as a member of the World Health Organization Science Council. Dr. Devnarain had no financial conflicts to disclose.
FROM THE NEW ENGLAND JOURNAL OF MEDICINE
Large genetic study links 72 genes to autism spectrum disorders
according to a study published in Nature Genetics. The findings, based on analysis of more than 150,000 people’s genetics, arose from a collaboration of five research groups whose work included comparisons of ASD cohorts with separate cohorts of individuals with developmental delay or schizophrenia.
“We know that many genes, when mutated, contribute to autism,” and this study brought together “multiple types of mutations in a wide array of samples to get a much richer sense of the genes and genetic architecture involved in autism and other neurodevelopmental conditions,” co–senior author Joseph D. Buxbaum, PhD, director of the Seaver Autism Center for Research and Treatment at Mount Sinai and a professor at the Icahn School of Medicine at Mount Sinai, both in New York, said in a prepared statement. “This is significant in that we now have more insights as to the biology of the brain changes that underlie autism and more potential targets for treatment.”
Glen Elliott, PhD, MD, a clinical professor of psychiatry at Stanford (Calif.) University who was not involved in the study, said the paper is important paper for informing clinicians of where the basic research is headed. “We’re still in for a long road” before it bears fruit in terms of therapeutics. The value of studies like these, that investigate which genes are most associated with ASD, is that they may lead toward understanding the pathways in the brain that give rise to certain symptoms of ASD, which can then become therapeutic targets, Dr. Elliott said.
Investigating large cohorts
The researchers analyzed genetic exome sequencing data from 33 ASD cohorts with a total of 63,237 people and then compared these data with another cohort of people with developmental delay and a cohort of people with schizophrenia. The combined ASD cohorts included 15,036 individuals with ASD, 28,522 parents, and 5,492 unaffected siblings. The remaining participants were 5,591 people with ASD and 8,597 matched controls from case control studies.
In the ASD cohorts, the researchers identified 72 genes that were associated with ASD. De novo variants were eight times more likely in cases (4%) than in controls (0.5%). Ten genes occurred at least twice in ASD cases but never occurred in unaffected siblings.
Then the researchers integrated these ASD genetic data with a cohort of 91,605 people that included 31,058 people with developmental delay and their parents. Substantial overlap with gene mutations existed between these two cohorts: 70.1% of the genes related to developmental delay appeared linked to risk for ASD, and 86.6% of genes associated with ASD risk also had associations with developmental delay. Overall, the researchers identified 373 genes strongly associated with ASD and/or developmental delay and 664 genes with a likely association.
“Isolating genes that exert a greater effect on ASD than they do on other developmental delays has remained challenging due to the frequent comorbidity of these phenotypes,” wrote lead author Jack M. Fu, of Massachusetts General Hospital and Harvard Medical School, both in Boston, and colleagues. “Still, an estimated 13.4% of the transmission and de novo association–ASD genes show little evidence for association in the developmental delay cohort.”
ASD, developmental delay, and schizophrenia
When the researchers compared the cells where the genetic mutations occurred in fetal brains, they found that genes associated with developmental delay more often occurred in less differentiated cell types – less mature cells in the developmental process. Gene mutations associated with ASD, on the other hand, occurred in more mature cell types, particularly in maturing excitatory neurons and related cells.
”Our results are consistent with developmental delay-predominant genes being expressed earlier in development and in less differentiated cells than ASD-predominant genes,” they wrote.
The researchers also compared the specific gene mutations found in these two cohorts with a previously published set of 244 genes associated with schizophrenia. Of these, 234 genes are among those with a transmission and de novo association to ASD and/or developmental delay. Of the 72 genes linked to ASD, eight appear in the set of genes linked to schizophrenia, and 61 were associated with developmental delay, though these two subsets do not overlap each other much.
“The ASD-schizophrenia overlap was significantly enriched, while the developmental delay-schizophrenia overlap was not,” they reported. ”Together, these data suggest that one subset of ASD risk genes may overlap developmental delay while a different subset overlaps schizophrenia.”
Chasing therapy targets by backtracking through genes
The findings are a substantial step forward in understanding the potential genetic contribution to ASD, but they also highlight the challenges of eventually trying to use this information in a clinically meaningful way.
“Given the substantial overlap between the genes implicated in neurodevelopmental disorders writ large and those implicated directly in ASD, disentangling the relative impact of individual genes on neurodevelopment and phenotypic spectra is a daunting yet important challenge,” the researchers wrote. “To identify the key neurobiological features of ASD will likely require convergence of evidence from many ASD genes and studies.”
Dr. Elliott said the biggest takeaway from this study is a better understanding of how the paradigm has shifted away from finding “one gene” for autism or a cure based on genetics and more toward understanding the pathophysiology of symptoms that can point to therapies for better management of the condition.
“Basic researchers have completely changed the strategy for trying to understand the biology of major disorders,” including, in this case, autism, Dr. Elliott said. “The intent is to try to find the underlying systems [in the brain] by backtracking through genes. Meanwhile, given that scientists have made substantial progress in identifying genes that have specific effects on brain development, “the hope is that will mesh with this kind of research, to begin to identify systems that might ultimately be targets for treating.”
The end goal is to be able to offer targeted approaches, based on the pathways causing a symptom, which can be linked backward to a gene.
”So this is not going to offer an immediate cure – it’s probably not going to offer a cure at all – but it may actually lead to much more targeted medications than we currently have for specific types of symptoms within the autism spectrum,” Dr. Elliott said. “What they’re trying to do, ultimately, is to say, when this system is really badly affected because of a genetic abnormality, even though that genetic abnormality is very rare, it leads to these specific kinds of symptoms. If we can find out the neuroregulators underlying that change, then that would be the target, even if that gene were not present.”
The research was funded by the Simons Foundation for Autism Research Initiative, the SPARK project, the National Human Genome Research Institute Home, the National Institute of Mental Health, the National Institute of Child Health and Development, AMED, and the Beatrice and Samuel Seaver Foundation. Five authors reported financial disclosures linked to Desitin, Roche, BioMarin, BrigeBio Pharma, Illumina, Levo Therapeutics, and Microsoft.
according to a study published in Nature Genetics. The findings, based on analysis of more than 150,000 people’s genetics, arose from a collaboration of five research groups whose work included comparisons of ASD cohorts with separate cohorts of individuals with developmental delay or schizophrenia.
“We know that many genes, when mutated, contribute to autism,” and this study brought together “multiple types of mutations in a wide array of samples to get a much richer sense of the genes and genetic architecture involved in autism and other neurodevelopmental conditions,” co–senior author Joseph D. Buxbaum, PhD, director of the Seaver Autism Center for Research and Treatment at Mount Sinai and a professor at the Icahn School of Medicine at Mount Sinai, both in New York, said in a prepared statement. “This is significant in that we now have more insights as to the biology of the brain changes that underlie autism and more potential targets for treatment.”
Glen Elliott, PhD, MD, a clinical professor of psychiatry at Stanford (Calif.) University who was not involved in the study, said the paper is important paper for informing clinicians of where the basic research is headed. “We’re still in for a long road” before it bears fruit in terms of therapeutics. The value of studies like these, that investigate which genes are most associated with ASD, is that they may lead toward understanding the pathways in the brain that give rise to certain symptoms of ASD, which can then become therapeutic targets, Dr. Elliott said.
Investigating large cohorts
The researchers analyzed genetic exome sequencing data from 33 ASD cohorts with a total of 63,237 people and then compared these data with another cohort of people with developmental delay and a cohort of people with schizophrenia. The combined ASD cohorts included 15,036 individuals with ASD, 28,522 parents, and 5,492 unaffected siblings. The remaining participants were 5,591 people with ASD and 8,597 matched controls from case control studies.
In the ASD cohorts, the researchers identified 72 genes that were associated with ASD. De novo variants were eight times more likely in cases (4%) than in controls (0.5%). Ten genes occurred at least twice in ASD cases but never occurred in unaffected siblings.
Then the researchers integrated these ASD genetic data with a cohort of 91,605 people that included 31,058 people with developmental delay and their parents. Substantial overlap with gene mutations existed between these two cohorts: 70.1% of the genes related to developmental delay appeared linked to risk for ASD, and 86.6% of genes associated with ASD risk also had associations with developmental delay. Overall, the researchers identified 373 genes strongly associated with ASD and/or developmental delay and 664 genes with a likely association.
“Isolating genes that exert a greater effect on ASD than they do on other developmental delays has remained challenging due to the frequent comorbidity of these phenotypes,” wrote lead author Jack M. Fu, of Massachusetts General Hospital and Harvard Medical School, both in Boston, and colleagues. “Still, an estimated 13.4% of the transmission and de novo association–ASD genes show little evidence for association in the developmental delay cohort.”
ASD, developmental delay, and schizophrenia
When the researchers compared the cells where the genetic mutations occurred in fetal brains, they found that genes associated with developmental delay more often occurred in less differentiated cell types – less mature cells in the developmental process. Gene mutations associated with ASD, on the other hand, occurred in more mature cell types, particularly in maturing excitatory neurons and related cells.
”Our results are consistent with developmental delay-predominant genes being expressed earlier in development and in less differentiated cells than ASD-predominant genes,” they wrote.
The researchers also compared the specific gene mutations found in these two cohorts with a previously published set of 244 genes associated with schizophrenia. Of these, 234 genes are among those with a transmission and de novo association to ASD and/or developmental delay. Of the 72 genes linked to ASD, eight appear in the set of genes linked to schizophrenia, and 61 were associated with developmental delay, though these two subsets do not overlap each other much.
“The ASD-schizophrenia overlap was significantly enriched, while the developmental delay-schizophrenia overlap was not,” they reported. ”Together, these data suggest that one subset of ASD risk genes may overlap developmental delay while a different subset overlaps schizophrenia.”
Chasing therapy targets by backtracking through genes
The findings are a substantial step forward in understanding the potential genetic contribution to ASD, but they also highlight the challenges of eventually trying to use this information in a clinically meaningful way.
“Given the substantial overlap between the genes implicated in neurodevelopmental disorders writ large and those implicated directly in ASD, disentangling the relative impact of individual genes on neurodevelopment and phenotypic spectra is a daunting yet important challenge,” the researchers wrote. “To identify the key neurobiological features of ASD will likely require convergence of evidence from many ASD genes and studies.”
Dr. Elliott said the biggest takeaway from this study is a better understanding of how the paradigm has shifted away from finding “one gene” for autism or a cure based on genetics and more toward understanding the pathophysiology of symptoms that can point to therapies for better management of the condition.
“Basic researchers have completely changed the strategy for trying to understand the biology of major disorders,” including, in this case, autism, Dr. Elliott said. “The intent is to try to find the underlying systems [in the brain] by backtracking through genes. Meanwhile, given that scientists have made substantial progress in identifying genes that have specific effects on brain development, “the hope is that will mesh with this kind of research, to begin to identify systems that might ultimately be targets for treating.”
The end goal is to be able to offer targeted approaches, based on the pathways causing a symptom, which can be linked backward to a gene.
”So this is not going to offer an immediate cure – it’s probably not going to offer a cure at all – but it may actually lead to much more targeted medications than we currently have for specific types of symptoms within the autism spectrum,” Dr. Elliott said. “What they’re trying to do, ultimately, is to say, when this system is really badly affected because of a genetic abnormality, even though that genetic abnormality is very rare, it leads to these specific kinds of symptoms. If we can find out the neuroregulators underlying that change, then that would be the target, even if that gene were not present.”
The research was funded by the Simons Foundation for Autism Research Initiative, the SPARK project, the National Human Genome Research Institute Home, the National Institute of Mental Health, the National Institute of Child Health and Development, AMED, and the Beatrice and Samuel Seaver Foundation. Five authors reported financial disclosures linked to Desitin, Roche, BioMarin, BrigeBio Pharma, Illumina, Levo Therapeutics, and Microsoft.
according to a study published in Nature Genetics. The findings, based on analysis of more than 150,000 people’s genetics, arose from a collaboration of five research groups whose work included comparisons of ASD cohorts with separate cohorts of individuals with developmental delay or schizophrenia.
“We know that many genes, when mutated, contribute to autism,” and this study brought together “multiple types of mutations in a wide array of samples to get a much richer sense of the genes and genetic architecture involved in autism and other neurodevelopmental conditions,” co–senior author Joseph D. Buxbaum, PhD, director of the Seaver Autism Center for Research and Treatment at Mount Sinai and a professor at the Icahn School of Medicine at Mount Sinai, both in New York, said in a prepared statement. “This is significant in that we now have more insights as to the biology of the brain changes that underlie autism and more potential targets for treatment.”
Glen Elliott, PhD, MD, a clinical professor of psychiatry at Stanford (Calif.) University who was not involved in the study, said the paper is important paper for informing clinicians of where the basic research is headed. “We’re still in for a long road” before it bears fruit in terms of therapeutics. The value of studies like these, that investigate which genes are most associated with ASD, is that they may lead toward understanding the pathways in the brain that give rise to certain symptoms of ASD, which can then become therapeutic targets, Dr. Elliott said.
Investigating large cohorts
The researchers analyzed genetic exome sequencing data from 33 ASD cohorts with a total of 63,237 people and then compared these data with another cohort of people with developmental delay and a cohort of people with schizophrenia. The combined ASD cohorts included 15,036 individuals with ASD, 28,522 parents, and 5,492 unaffected siblings. The remaining participants were 5,591 people with ASD and 8,597 matched controls from case control studies.
In the ASD cohorts, the researchers identified 72 genes that were associated with ASD. De novo variants were eight times more likely in cases (4%) than in controls (0.5%). Ten genes occurred at least twice in ASD cases but never occurred in unaffected siblings.
Then the researchers integrated these ASD genetic data with a cohort of 91,605 people that included 31,058 people with developmental delay and their parents. Substantial overlap with gene mutations existed between these two cohorts: 70.1% of the genes related to developmental delay appeared linked to risk for ASD, and 86.6% of genes associated with ASD risk also had associations with developmental delay. Overall, the researchers identified 373 genes strongly associated with ASD and/or developmental delay and 664 genes with a likely association.
“Isolating genes that exert a greater effect on ASD than they do on other developmental delays has remained challenging due to the frequent comorbidity of these phenotypes,” wrote lead author Jack M. Fu, of Massachusetts General Hospital and Harvard Medical School, both in Boston, and colleagues. “Still, an estimated 13.4% of the transmission and de novo association–ASD genes show little evidence for association in the developmental delay cohort.”
ASD, developmental delay, and schizophrenia
When the researchers compared the cells where the genetic mutations occurred in fetal brains, they found that genes associated with developmental delay more often occurred in less differentiated cell types – less mature cells in the developmental process. Gene mutations associated with ASD, on the other hand, occurred in more mature cell types, particularly in maturing excitatory neurons and related cells.
”Our results are consistent with developmental delay-predominant genes being expressed earlier in development and in less differentiated cells than ASD-predominant genes,” they wrote.
The researchers also compared the specific gene mutations found in these two cohorts with a previously published set of 244 genes associated with schizophrenia. Of these, 234 genes are among those with a transmission and de novo association to ASD and/or developmental delay. Of the 72 genes linked to ASD, eight appear in the set of genes linked to schizophrenia, and 61 were associated with developmental delay, though these two subsets do not overlap each other much.
“The ASD-schizophrenia overlap was significantly enriched, while the developmental delay-schizophrenia overlap was not,” they reported. ”Together, these data suggest that one subset of ASD risk genes may overlap developmental delay while a different subset overlaps schizophrenia.”
Chasing therapy targets by backtracking through genes
The findings are a substantial step forward in understanding the potential genetic contribution to ASD, but they also highlight the challenges of eventually trying to use this information in a clinically meaningful way.
“Given the substantial overlap between the genes implicated in neurodevelopmental disorders writ large and those implicated directly in ASD, disentangling the relative impact of individual genes on neurodevelopment and phenotypic spectra is a daunting yet important challenge,” the researchers wrote. “To identify the key neurobiological features of ASD will likely require convergence of evidence from many ASD genes and studies.”
Dr. Elliott said the biggest takeaway from this study is a better understanding of how the paradigm has shifted away from finding “one gene” for autism or a cure based on genetics and more toward understanding the pathophysiology of symptoms that can point to therapies for better management of the condition.
“Basic researchers have completely changed the strategy for trying to understand the biology of major disorders,” including, in this case, autism, Dr. Elliott said. “The intent is to try to find the underlying systems [in the brain] by backtracking through genes. Meanwhile, given that scientists have made substantial progress in identifying genes that have specific effects on brain development, “the hope is that will mesh with this kind of research, to begin to identify systems that might ultimately be targets for treating.”
The end goal is to be able to offer targeted approaches, based on the pathways causing a symptom, which can be linked backward to a gene.
”So this is not going to offer an immediate cure – it’s probably not going to offer a cure at all – but it may actually lead to much more targeted medications than we currently have for specific types of symptoms within the autism spectrum,” Dr. Elliott said. “What they’re trying to do, ultimately, is to say, when this system is really badly affected because of a genetic abnormality, even though that genetic abnormality is very rare, it leads to these specific kinds of symptoms. If we can find out the neuroregulators underlying that change, then that would be the target, even if that gene were not present.”
The research was funded by the Simons Foundation for Autism Research Initiative, the SPARK project, the National Human Genome Research Institute Home, the National Institute of Mental Health, the National Institute of Child Health and Development, AMED, and the Beatrice and Samuel Seaver Foundation. Five authors reported financial disclosures linked to Desitin, Roche, BioMarin, BrigeBio Pharma, Illumina, Levo Therapeutics, and Microsoft.
FROM NATURE GENETICS
No fish can escape this net ... of COVID testing
Something about this COVID testing smells fishy
The Chinese have been challenging America’s political and economic hegemony (yes, we did have to look that one up – you’re rude to ask) for some time, but now they’ve gone too far. Are we going to just sit here and let China do something more ridiculous than us in response to COVID? No way!
Here’s the deal: The government of the Chinese coastal city of Xiamen has decided that it’s not just the workers on returning fishing boats who have the potential to introduce COVID to the rest of the population. The fish also present a problem. So when the authorities say that everyone needs to be tested before they can enter the city, they mean everyone.
An employee of the municipal ocean development bureau told local media that “all people in Xiamen City need nucleic acid testing, and the fish catches must be tested as well,” according to the Guardian, which also said that “TV news reports showed officials swabbing the mouths of fish and the underside of crabs.”
In the words of George Takei: “Oh my.”
Hold on there a second, George Takei, because we here in the good old US of A have still got Los Angeles, where COVID testing also has taken a nonhuman turn. The LA County public health department recently announced that pets are now eligible for a free SARS-CoV-2 test through veterinarians and other animal care facilities.
“Our goal is to test many different species of animals including wildlife (deer, bats, raccoons), pets (dogs, cats, hamsters, pocket pets), marine mammals (seals), and more,” Veterinary Public Health announced.
Hegemony restored.
Not even God could save them from worms
The Dark Ages may not have been as dark and violent as many people think, but there’s no denying that life in medieval Europe kind of sucked. The only real alternative to serfdom was a job with the Catholic Church. Medieval friars, for example, lived in stone buildings, had access to fresh fruits and vegetables, and even had latrines and running water. Luxuries compared with the life of the average peasant.
So why then, despite having access to more modern sanitation and amenities, did the friars have so many gut parasites? That’s the question raised by a group of researchers from the University of Cambridge, who conducted a study of 19 medieval friars buried at a local friary (Oh, doesn’t your town have one of those?) and 25 local people buried at a nonreligious cemetery during a similar time period. Of those 19 friars, 11 were infected with worms and parasites, compared with just 8 of 25 townspeople.
This doesn’t make a lot of sense. The friars had a good life by old-time standards: They had basic sanitation down and a solid diet. These things should lead to a healthier population. The problem, the researchers found, is two pronged and a vicious cycle. First off, the friars had plenty of fresh food, but they used human feces to fertilize their produce. There’s a reason modern practice for human waste fertilization is to let the waste compost for 6 months: The waiting period allows the parasites a chance to kindly die off, which prevents reinfection.
Secondly, the friars’ diet of fresh fruits and vegetables mixed together into a salad, while appealing to our modern-day sensibilities, was not a great choice. By comparison, laypeople tended to eat a boiled mishmash of whatever they could find, and while that’s kind of gross, the key here is that their food was cooked. And heat kills parasites. The uncooked salads did no such thing, so the monks ate infected food, expelled infected poop, and grew more infected food with their infected poop.
Once the worms arrived, they never left, making them the worst kind of house guest. Read the room, worms, take your dinner and move on. You don’t have to go home, but you can’t stay here.
What’s a shared genotype between friends?
Do you find it hard to tell the difference between Katy Perry and Zooey Deschanel? They look alike, but they’re not related. Or are they? According to new research, people who look and act very similar but are not related may share DNA.
“Our study provides a rare insight into human likeness by showing that people with extreme look-alike faces share common genotypes, whereas they are discordant at the epigenome and microbiome levels,” senior author Manel Esteller of the Josep Carreras Leukemia Research Institute in Barcelona said in a written statement. “Genomics clusters them together, and the rest sets them apart.”
The Internet has been a great source in being able to find look-alikes. The research team found photos of doppelgangers photographed by François Brunelle, a Canadian artist. Using facial recognition algorithms, the investigators were able to measure likeness between the each pair of look-alikes. The participants also completed a questionnaire about lifestyle and provided a saliva sample.
The results showed that the look-alikes had similar genotypes but different DNA methylation and microbiome landscapes. The look-alikes also seemed to have similarities in weight, height, and behaviors such as smoking, proving that doppelgangers not only look alike but also share common interests.
Next time someone tells you that you look like their best friend Steve, you won’t have to wonder much what Steve is like.
The secret to a good relationship? It’s a secret
Strong relationships are built on honesty and trust, right? Being open with your partner and/or friends is usually a good practice for keeping the relationship healthy, but the latest evidence suggests that maybe you shouldn’t share everything.
According to the first known study on the emotional, behavioral, and relational aspect of consumer behavior, not disclosing certain purchases to your partner can actually be a good thing for the relationship. How? Well, it all has to do with guilt.
In a series of studies, the researchers asked couples about their secret consumptions. The most commonly hidden thing by far was a product (65%).
“We found that 90% of people have recently kept everyday consumer behaviors a secret from a close other – like a friend or spouse – even though they also report that they don’t think their partner would care if they knew about it,” Kelley Gullo Wight, one of the study’s two lead authors, said in a written statement.
Keeping a hidden stash of chocolate produces guilt, which the researchers found to be the key factor, making the perpetrator want to do more in the relationship to ease that sense of betrayal or dishonesty. They called it a “greater relationship investment,” meaning the person is more likely to do a little extra for their partner, like shell out more money for the next anniversary gift or yield to watching their partner’s favorite program.
So don’t feel too bad about that secret Amazon purchase. As long as the other person doesn’t see the box, nobody has to know. Your relationship can only improve.
Something about this COVID testing smells fishy
The Chinese have been challenging America’s political and economic hegemony (yes, we did have to look that one up – you’re rude to ask) for some time, but now they’ve gone too far. Are we going to just sit here and let China do something more ridiculous than us in response to COVID? No way!
Here’s the deal: The government of the Chinese coastal city of Xiamen has decided that it’s not just the workers on returning fishing boats who have the potential to introduce COVID to the rest of the population. The fish also present a problem. So when the authorities say that everyone needs to be tested before they can enter the city, they mean everyone.
An employee of the municipal ocean development bureau told local media that “all people in Xiamen City need nucleic acid testing, and the fish catches must be tested as well,” according to the Guardian, which also said that “TV news reports showed officials swabbing the mouths of fish and the underside of crabs.”
In the words of George Takei: “Oh my.”
Hold on there a second, George Takei, because we here in the good old US of A have still got Los Angeles, where COVID testing also has taken a nonhuman turn. The LA County public health department recently announced that pets are now eligible for a free SARS-CoV-2 test through veterinarians and other animal care facilities.
“Our goal is to test many different species of animals including wildlife (deer, bats, raccoons), pets (dogs, cats, hamsters, pocket pets), marine mammals (seals), and more,” Veterinary Public Health announced.
Hegemony restored.
Not even God could save them from worms
The Dark Ages may not have been as dark and violent as many people think, but there’s no denying that life in medieval Europe kind of sucked. The only real alternative to serfdom was a job with the Catholic Church. Medieval friars, for example, lived in stone buildings, had access to fresh fruits and vegetables, and even had latrines and running water. Luxuries compared with the life of the average peasant.
So why then, despite having access to more modern sanitation and amenities, did the friars have so many gut parasites? That’s the question raised by a group of researchers from the University of Cambridge, who conducted a study of 19 medieval friars buried at a local friary (Oh, doesn’t your town have one of those?) and 25 local people buried at a nonreligious cemetery during a similar time period. Of those 19 friars, 11 were infected with worms and parasites, compared with just 8 of 25 townspeople.
This doesn’t make a lot of sense. The friars had a good life by old-time standards: They had basic sanitation down and a solid diet. These things should lead to a healthier population. The problem, the researchers found, is two pronged and a vicious cycle. First off, the friars had plenty of fresh food, but they used human feces to fertilize their produce. There’s a reason modern practice for human waste fertilization is to let the waste compost for 6 months: The waiting period allows the parasites a chance to kindly die off, which prevents reinfection.
Secondly, the friars’ diet of fresh fruits and vegetables mixed together into a salad, while appealing to our modern-day sensibilities, was not a great choice. By comparison, laypeople tended to eat a boiled mishmash of whatever they could find, and while that’s kind of gross, the key here is that their food was cooked. And heat kills parasites. The uncooked salads did no such thing, so the monks ate infected food, expelled infected poop, and grew more infected food with their infected poop.
Once the worms arrived, they never left, making them the worst kind of house guest. Read the room, worms, take your dinner and move on. You don’t have to go home, but you can’t stay here.
What’s a shared genotype between friends?
Do you find it hard to tell the difference between Katy Perry and Zooey Deschanel? They look alike, but they’re not related. Or are they? According to new research, people who look and act very similar but are not related may share DNA.
“Our study provides a rare insight into human likeness by showing that people with extreme look-alike faces share common genotypes, whereas they are discordant at the epigenome and microbiome levels,” senior author Manel Esteller of the Josep Carreras Leukemia Research Institute in Barcelona said in a written statement. “Genomics clusters them together, and the rest sets them apart.”
The Internet has been a great source in being able to find look-alikes. The research team found photos of doppelgangers photographed by François Brunelle, a Canadian artist. Using facial recognition algorithms, the investigators were able to measure likeness between the each pair of look-alikes. The participants also completed a questionnaire about lifestyle and provided a saliva sample.
The results showed that the look-alikes had similar genotypes but different DNA methylation and microbiome landscapes. The look-alikes also seemed to have similarities in weight, height, and behaviors such as smoking, proving that doppelgangers not only look alike but also share common interests.
Next time someone tells you that you look like their best friend Steve, you won’t have to wonder much what Steve is like.
The secret to a good relationship? It’s a secret
Strong relationships are built on honesty and trust, right? Being open with your partner and/or friends is usually a good practice for keeping the relationship healthy, but the latest evidence suggests that maybe you shouldn’t share everything.
According to the first known study on the emotional, behavioral, and relational aspect of consumer behavior, not disclosing certain purchases to your partner can actually be a good thing for the relationship. How? Well, it all has to do with guilt.
In a series of studies, the researchers asked couples about their secret consumptions. The most commonly hidden thing by far was a product (65%).
“We found that 90% of people have recently kept everyday consumer behaviors a secret from a close other – like a friend or spouse – even though they also report that they don’t think their partner would care if they knew about it,” Kelley Gullo Wight, one of the study’s two lead authors, said in a written statement.
Keeping a hidden stash of chocolate produces guilt, which the researchers found to be the key factor, making the perpetrator want to do more in the relationship to ease that sense of betrayal or dishonesty. They called it a “greater relationship investment,” meaning the person is more likely to do a little extra for their partner, like shell out more money for the next anniversary gift or yield to watching their partner’s favorite program.
So don’t feel too bad about that secret Amazon purchase. As long as the other person doesn’t see the box, nobody has to know. Your relationship can only improve.
Something about this COVID testing smells fishy
The Chinese have been challenging America’s political and economic hegemony (yes, we did have to look that one up – you’re rude to ask) for some time, but now they’ve gone too far. Are we going to just sit here and let China do something more ridiculous than us in response to COVID? No way!
Here’s the deal: The government of the Chinese coastal city of Xiamen has decided that it’s not just the workers on returning fishing boats who have the potential to introduce COVID to the rest of the population. The fish also present a problem. So when the authorities say that everyone needs to be tested before they can enter the city, they mean everyone.
An employee of the municipal ocean development bureau told local media that “all people in Xiamen City need nucleic acid testing, and the fish catches must be tested as well,” according to the Guardian, which also said that “TV news reports showed officials swabbing the mouths of fish and the underside of crabs.”
In the words of George Takei: “Oh my.”
Hold on there a second, George Takei, because we here in the good old US of A have still got Los Angeles, where COVID testing also has taken a nonhuman turn. The LA County public health department recently announced that pets are now eligible for a free SARS-CoV-2 test through veterinarians and other animal care facilities.
“Our goal is to test many different species of animals including wildlife (deer, bats, raccoons), pets (dogs, cats, hamsters, pocket pets), marine mammals (seals), and more,” Veterinary Public Health announced.
Hegemony restored.
Not even God could save them from worms
The Dark Ages may not have been as dark and violent as many people think, but there’s no denying that life in medieval Europe kind of sucked. The only real alternative to serfdom was a job with the Catholic Church. Medieval friars, for example, lived in stone buildings, had access to fresh fruits and vegetables, and even had latrines and running water. Luxuries compared with the life of the average peasant.
So why then, despite having access to more modern sanitation and amenities, did the friars have so many gut parasites? That’s the question raised by a group of researchers from the University of Cambridge, who conducted a study of 19 medieval friars buried at a local friary (Oh, doesn’t your town have one of those?) and 25 local people buried at a nonreligious cemetery during a similar time period. Of those 19 friars, 11 were infected with worms and parasites, compared with just 8 of 25 townspeople.
This doesn’t make a lot of sense. The friars had a good life by old-time standards: They had basic sanitation down and a solid diet. These things should lead to a healthier population. The problem, the researchers found, is two pronged and a vicious cycle. First off, the friars had plenty of fresh food, but they used human feces to fertilize their produce. There’s a reason modern practice for human waste fertilization is to let the waste compost for 6 months: The waiting period allows the parasites a chance to kindly die off, which prevents reinfection.
Secondly, the friars’ diet of fresh fruits and vegetables mixed together into a salad, while appealing to our modern-day sensibilities, was not a great choice. By comparison, laypeople tended to eat a boiled mishmash of whatever they could find, and while that’s kind of gross, the key here is that their food was cooked. And heat kills parasites. The uncooked salads did no such thing, so the monks ate infected food, expelled infected poop, and grew more infected food with their infected poop.
Once the worms arrived, they never left, making them the worst kind of house guest. Read the room, worms, take your dinner and move on. You don’t have to go home, but you can’t stay here.
What’s a shared genotype between friends?
Do you find it hard to tell the difference between Katy Perry and Zooey Deschanel? They look alike, but they’re not related. Or are they? According to new research, people who look and act very similar but are not related may share DNA.
“Our study provides a rare insight into human likeness by showing that people with extreme look-alike faces share common genotypes, whereas they are discordant at the epigenome and microbiome levels,” senior author Manel Esteller of the Josep Carreras Leukemia Research Institute in Barcelona said in a written statement. “Genomics clusters them together, and the rest sets them apart.”
The Internet has been a great source in being able to find look-alikes. The research team found photos of doppelgangers photographed by François Brunelle, a Canadian artist. Using facial recognition algorithms, the investigators were able to measure likeness between the each pair of look-alikes. The participants also completed a questionnaire about lifestyle and provided a saliva sample.
The results showed that the look-alikes had similar genotypes but different DNA methylation and microbiome landscapes. The look-alikes also seemed to have similarities in weight, height, and behaviors such as smoking, proving that doppelgangers not only look alike but also share common interests.
Next time someone tells you that you look like their best friend Steve, you won’t have to wonder much what Steve is like.
The secret to a good relationship? It’s a secret
Strong relationships are built on honesty and trust, right? Being open with your partner and/or friends is usually a good practice for keeping the relationship healthy, but the latest evidence suggests that maybe you shouldn’t share everything.
According to the first known study on the emotional, behavioral, and relational aspect of consumer behavior, not disclosing certain purchases to your partner can actually be a good thing for the relationship. How? Well, it all has to do with guilt.
In a series of studies, the researchers asked couples about their secret consumptions. The most commonly hidden thing by far was a product (65%).
“We found that 90% of people have recently kept everyday consumer behaviors a secret from a close other – like a friend or spouse – even though they also report that they don’t think their partner would care if they knew about it,” Kelley Gullo Wight, one of the study’s two lead authors, said in a written statement.
Keeping a hidden stash of chocolate produces guilt, which the researchers found to be the key factor, making the perpetrator want to do more in the relationship to ease that sense of betrayal or dishonesty. They called it a “greater relationship investment,” meaning the person is more likely to do a little extra for their partner, like shell out more money for the next anniversary gift or yield to watching their partner’s favorite program.
So don’t feel too bad about that secret Amazon purchase. As long as the other person doesn’t see the box, nobody has to know. Your relationship can only improve.
Pfizer seeks approval for updated COVID booster
Pfizer has sent an application to the Food and Drug Administration for emergency use authorization of its updated COVID-19 booster vaccine for the fall of 2022, the company announced on Aug. 22.
The vaccine, which is adapted for the BA.4 and BA.5 Omicron variants, would be meant for ages 12 and older. If authorized by the FDA, the doses could ship as soon as September.
“Having rapidly scaled up production, we are positioned to immediately begin distribution of the bivalent Omicron BA.4/BA.5 boosters, if authorized, to help protect individuals and families as we prepare for potential fall and winter surges,” Albert Bourla, PhD, Pfizer’s chairman and CEO, said in the statement.
Earlier this year, the FDA ordered vaccine makers such as Pfizer and Moderna to update their shots to target BA.4 and BA.5, which are better at escaping immunity from earlier vaccines and previous infections.
The United States has a contract to buy 105 million of the Pfizer doses and 66 million of the Moderna doses, according to The Associated Press. Moderna is expected to file its FDA application soon as well.
The new shots target both the original spike protein on the coronavirus and the spike mutations carried by BA.4 and BA.5. For now, BA.5 is causing 89% of new infections in the United States, followed by BA.4.6 with 6.3% and BA.4 with 4.3%, according to the latest Centers for Disease Control and Prevention data.
There’s no way to tell if BA.5 will still be the dominant strain this winter or if new variant will replace it, the AP reported. But public health officials have supported the updated boosters as a way to target the most recent strains and increase immunity again.
On Aug. 15, Great Britain became the first country to authorize another one of Moderna’s updated vaccines, which adds protection against BA.1, or the original Omicron strain that became dominant in the winter of 2021-2022. European regulators are considering this shot, the AP reported, but the United States opted not to use this version since new Omicron variants have become dominant.
To approve the latest Pfizer shot, the FDA will rely on scientific testing of prior updates to the vaccine, rather than the newest boosters, to decide whether to fast-track the updated shots for fall, the AP reported. This method is like how flu vaccines are updated each year without large studies that take months.
Previously, Pfizer announced results from a study that found the earlier Omicron update significantly boosted antibodies capable of fighting the BA.1 variant and provided some protection against BA.4 and BA.5. The company’s latest FDA application contains that data and animal testing on the newest booster, the AP reported.
Pfizer will start a trial using the BA.4/BA.5 booster in coming weeks to get more data on how well the latest shot works. Moderna has begun a similar study.
The full results from these studies won’t be available before a fall booster campaign, which is why the FDA and public health officials have called for an updated shot to be ready for distribution in September.
“It’s clear that none of these vaccines are going to completely prevent infection,” Rachel Presti, MD, a researcher with the Moderna trial and an infectious diseases specialist at Washington University in St. Louis, told the AP.
But previous studies of variant booster candidates have shown that “you still get a broader immune response giving a variant booster than giving the same booster,” she said.
A version of this article first appeared on WebMD.com.
Pfizer has sent an application to the Food and Drug Administration for emergency use authorization of its updated COVID-19 booster vaccine for the fall of 2022, the company announced on Aug. 22.
The vaccine, which is adapted for the BA.4 and BA.5 Omicron variants, would be meant for ages 12 and older. If authorized by the FDA, the doses could ship as soon as September.
“Having rapidly scaled up production, we are positioned to immediately begin distribution of the bivalent Omicron BA.4/BA.5 boosters, if authorized, to help protect individuals and families as we prepare for potential fall and winter surges,” Albert Bourla, PhD, Pfizer’s chairman and CEO, said in the statement.
Earlier this year, the FDA ordered vaccine makers such as Pfizer and Moderna to update their shots to target BA.4 and BA.5, which are better at escaping immunity from earlier vaccines and previous infections.
The United States has a contract to buy 105 million of the Pfizer doses and 66 million of the Moderna doses, according to The Associated Press. Moderna is expected to file its FDA application soon as well.
The new shots target both the original spike protein on the coronavirus and the spike mutations carried by BA.4 and BA.5. For now, BA.5 is causing 89% of new infections in the United States, followed by BA.4.6 with 6.3% and BA.4 with 4.3%, according to the latest Centers for Disease Control and Prevention data.
There’s no way to tell if BA.5 will still be the dominant strain this winter or if new variant will replace it, the AP reported. But public health officials have supported the updated boosters as a way to target the most recent strains and increase immunity again.
On Aug. 15, Great Britain became the first country to authorize another one of Moderna’s updated vaccines, which adds protection against BA.1, or the original Omicron strain that became dominant in the winter of 2021-2022. European regulators are considering this shot, the AP reported, but the United States opted not to use this version since new Omicron variants have become dominant.
To approve the latest Pfizer shot, the FDA will rely on scientific testing of prior updates to the vaccine, rather than the newest boosters, to decide whether to fast-track the updated shots for fall, the AP reported. This method is like how flu vaccines are updated each year without large studies that take months.
Previously, Pfizer announced results from a study that found the earlier Omicron update significantly boosted antibodies capable of fighting the BA.1 variant and provided some protection against BA.4 and BA.5. The company’s latest FDA application contains that data and animal testing on the newest booster, the AP reported.
Pfizer will start a trial using the BA.4/BA.5 booster in coming weeks to get more data on how well the latest shot works. Moderna has begun a similar study.
The full results from these studies won’t be available before a fall booster campaign, which is why the FDA and public health officials have called for an updated shot to be ready for distribution in September.
“It’s clear that none of these vaccines are going to completely prevent infection,” Rachel Presti, MD, a researcher with the Moderna trial and an infectious diseases specialist at Washington University in St. Louis, told the AP.
But previous studies of variant booster candidates have shown that “you still get a broader immune response giving a variant booster than giving the same booster,” she said.
A version of this article first appeared on WebMD.com.
Pfizer has sent an application to the Food and Drug Administration for emergency use authorization of its updated COVID-19 booster vaccine for the fall of 2022, the company announced on Aug. 22.
The vaccine, which is adapted for the BA.4 and BA.5 Omicron variants, would be meant for ages 12 and older. If authorized by the FDA, the doses could ship as soon as September.
“Having rapidly scaled up production, we are positioned to immediately begin distribution of the bivalent Omicron BA.4/BA.5 boosters, if authorized, to help protect individuals and families as we prepare for potential fall and winter surges,” Albert Bourla, PhD, Pfizer’s chairman and CEO, said in the statement.
Earlier this year, the FDA ordered vaccine makers such as Pfizer and Moderna to update their shots to target BA.4 and BA.5, which are better at escaping immunity from earlier vaccines and previous infections.
The United States has a contract to buy 105 million of the Pfizer doses and 66 million of the Moderna doses, according to The Associated Press. Moderna is expected to file its FDA application soon as well.
The new shots target both the original spike protein on the coronavirus and the spike mutations carried by BA.4 and BA.5. For now, BA.5 is causing 89% of new infections in the United States, followed by BA.4.6 with 6.3% and BA.4 with 4.3%, according to the latest Centers for Disease Control and Prevention data.
There’s no way to tell if BA.5 will still be the dominant strain this winter or if new variant will replace it, the AP reported. But public health officials have supported the updated boosters as a way to target the most recent strains and increase immunity again.
On Aug. 15, Great Britain became the first country to authorize another one of Moderna’s updated vaccines, which adds protection against BA.1, or the original Omicron strain that became dominant in the winter of 2021-2022. European regulators are considering this shot, the AP reported, but the United States opted not to use this version since new Omicron variants have become dominant.
To approve the latest Pfizer shot, the FDA will rely on scientific testing of prior updates to the vaccine, rather than the newest boosters, to decide whether to fast-track the updated shots for fall, the AP reported. This method is like how flu vaccines are updated each year without large studies that take months.
Previously, Pfizer announced results from a study that found the earlier Omicron update significantly boosted antibodies capable of fighting the BA.1 variant and provided some protection against BA.4 and BA.5. The company’s latest FDA application contains that data and animal testing on the newest booster, the AP reported.
Pfizer will start a trial using the BA.4/BA.5 booster in coming weeks to get more data on how well the latest shot works. Moderna has begun a similar study.
The full results from these studies won’t be available before a fall booster campaign, which is why the FDA and public health officials have called for an updated shot to be ready for distribution in September.
“It’s clear that none of these vaccines are going to completely prevent infection,” Rachel Presti, MD, a researcher with the Moderna trial and an infectious diseases specialist at Washington University in St. Louis, told the AP.
But previous studies of variant booster candidates have shown that “you still get a broader immune response giving a variant booster than giving the same booster,” she said.
A version of this article first appeared on WebMD.com.
Children and COVID: New cases fall again, ED rates rebound for some
The 7-day average percentage of ED visits with diagnosed COVID, which had reached a post-Omicron high of 3.5% in late July for those aged 12-15, began to fall and was down to 3.0% on Aug. 12. That trend reversed, however, and the rate was up to 3.6% on Aug. 19, the last date for which data are available from the Centers for Disease Control and Prevention.
That change of COVID fortunes cannot yet be seen for all children. The 7-day average ED visit rate for those aged 0-11 years peaked at 6.8% during the last week of July and has continued to fall, dropping from 5.7% on Aug. 12 to 5.1% on Aug. 19. Children aged 16-17 years seem to be taking a middle path: Their ED-visit rate declined from late July into mid-August but held steady over the last week, according to the CDC’s COVID Data Tracker.
There is a hint of the same trend regarding new admissions among children aged 0-17 years. The national rate, which had declined in recent weeks, ticked up from 0.42 to 0.43 new admissions per 100,000 population over the last week of available data, the CDC said.
Weekly cases fall below 80,000
New cases in general were down by 8.5% from the previous week, dropping from 87,902 for the week of Aug. 5-11 to 79,525 for Aug. 12-18. That marked the second straight week with fewer cases after a 4-week period that saw weekly totals increase from almost 68,000 to nearly 97,000, according to a report from the American Academy of Pediatrics and the Children’s Hospital Association.
The AAP and CHA put the cumulative number of child COVID-19 cases at just under 14.4 million since the pandemic began, which represents 18.4% of cases among all ages. The CDC estimates that there have been almost 14.7 million cases in children aged 0-17 years, as well as 1,750 deaths, of which 14 were reported in the last week (Aug. 16-22).
The CDC age subgroups indicate that children aged 0-4 years have experienced fewer cases (2.9 million) than children aged 5-11 years (5.6 million cases) and 12-15 (3.0 million cases) but more deaths: 548 so far, versus 432 for 5- to 11-year-olds and 437 for 12- to 15-year-olds, the COVID Data Tracker shows. Those aged 0-4 make up 6% of the total U.S. population, compared with 8.7% and 5.1%, respectively, for the older children.
Most younger children still not vaccinated
Although it may not qualify as a big push to vaccinate children before the start of the new school year, first-time vaccinations did rise somewhat in late July and August for children aged 5-17 years. Among children younger than 5 years, though, initial doses of the vaccine fell during the second full week of August, especially in 2- to 4-year-olds, based on the CDC data.
Through almost 2 months of vaccine eligibility, 4.8% of children under age 5 have received at least one dose and 0.9% are fully vaccinated as of Aug. 17. The current rates are 37.8% (one dose) and 30.4% (completed) for those aged 5-11 and 70.5% and 60.3% for 12- to 17-year-olds.
The 7-day average percentage of ED visits with diagnosed COVID, which had reached a post-Omicron high of 3.5% in late July for those aged 12-15, began to fall and was down to 3.0% on Aug. 12. That trend reversed, however, and the rate was up to 3.6% on Aug. 19, the last date for which data are available from the Centers for Disease Control and Prevention.
That change of COVID fortunes cannot yet be seen for all children. The 7-day average ED visit rate for those aged 0-11 years peaked at 6.8% during the last week of July and has continued to fall, dropping from 5.7% on Aug. 12 to 5.1% on Aug. 19. Children aged 16-17 years seem to be taking a middle path: Their ED-visit rate declined from late July into mid-August but held steady over the last week, according to the CDC’s COVID Data Tracker.
There is a hint of the same trend regarding new admissions among children aged 0-17 years. The national rate, which had declined in recent weeks, ticked up from 0.42 to 0.43 new admissions per 100,000 population over the last week of available data, the CDC said.
Weekly cases fall below 80,000
New cases in general were down by 8.5% from the previous week, dropping from 87,902 for the week of Aug. 5-11 to 79,525 for Aug. 12-18. That marked the second straight week with fewer cases after a 4-week period that saw weekly totals increase from almost 68,000 to nearly 97,000, according to a report from the American Academy of Pediatrics and the Children’s Hospital Association.
The AAP and CHA put the cumulative number of child COVID-19 cases at just under 14.4 million since the pandemic began, which represents 18.4% of cases among all ages. The CDC estimates that there have been almost 14.7 million cases in children aged 0-17 years, as well as 1,750 deaths, of which 14 were reported in the last week (Aug. 16-22).
The CDC age subgroups indicate that children aged 0-4 years have experienced fewer cases (2.9 million) than children aged 5-11 years (5.6 million cases) and 12-15 (3.0 million cases) but more deaths: 548 so far, versus 432 for 5- to 11-year-olds and 437 for 12- to 15-year-olds, the COVID Data Tracker shows. Those aged 0-4 make up 6% of the total U.S. population, compared with 8.7% and 5.1%, respectively, for the older children.
Most younger children still not vaccinated
Although it may not qualify as a big push to vaccinate children before the start of the new school year, first-time vaccinations did rise somewhat in late July and August for children aged 5-17 years. Among children younger than 5 years, though, initial doses of the vaccine fell during the second full week of August, especially in 2- to 4-year-olds, based on the CDC data.
Through almost 2 months of vaccine eligibility, 4.8% of children under age 5 have received at least one dose and 0.9% are fully vaccinated as of Aug. 17. The current rates are 37.8% (one dose) and 30.4% (completed) for those aged 5-11 and 70.5% and 60.3% for 12- to 17-year-olds.
The 7-day average percentage of ED visits with diagnosed COVID, which had reached a post-Omicron high of 3.5% in late July for those aged 12-15, began to fall and was down to 3.0% on Aug. 12. That trend reversed, however, and the rate was up to 3.6% on Aug. 19, the last date for which data are available from the Centers for Disease Control and Prevention.
That change of COVID fortunes cannot yet be seen for all children. The 7-day average ED visit rate for those aged 0-11 years peaked at 6.8% during the last week of July and has continued to fall, dropping from 5.7% on Aug. 12 to 5.1% on Aug. 19. Children aged 16-17 years seem to be taking a middle path: Their ED-visit rate declined from late July into mid-August but held steady over the last week, according to the CDC’s COVID Data Tracker.
There is a hint of the same trend regarding new admissions among children aged 0-17 years. The national rate, which had declined in recent weeks, ticked up from 0.42 to 0.43 new admissions per 100,000 population over the last week of available data, the CDC said.
Weekly cases fall below 80,000
New cases in general were down by 8.5% from the previous week, dropping from 87,902 for the week of Aug. 5-11 to 79,525 for Aug. 12-18. That marked the second straight week with fewer cases after a 4-week period that saw weekly totals increase from almost 68,000 to nearly 97,000, according to a report from the American Academy of Pediatrics and the Children’s Hospital Association.
The AAP and CHA put the cumulative number of child COVID-19 cases at just under 14.4 million since the pandemic began, which represents 18.4% of cases among all ages. The CDC estimates that there have been almost 14.7 million cases in children aged 0-17 years, as well as 1,750 deaths, of which 14 were reported in the last week (Aug. 16-22).
The CDC age subgroups indicate that children aged 0-4 years have experienced fewer cases (2.9 million) than children aged 5-11 years (5.6 million cases) and 12-15 (3.0 million cases) but more deaths: 548 so far, versus 432 for 5- to 11-year-olds and 437 for 12- to 15-year-olds, the COVID Data Tracker shows. Those aged 0-4 make up 6% of the total U.S. population, compared with 8.7% and 5.1%, respectively, for the older children.
Most younger children still not vaccinated
Although it may not qualify as a big push to vaccinate children before the start of the new school year, first-time vaccinations did rise somewhat in late July and August for children aged 5-17 years. Among children younger than 5 years, though, initial doses of the vaccine fell during the second full week of August, especially in 2- to 4-year-olds, based on the CDC data.
Through almost 2 months of vaccine eligibility, 4.8% of children under age 5 have received at least one dose and 0.9% are fully vaccinated as of Aug. 17. The current rates are 37.8% (one dose) and 30.4% (completed) for those aged 5-11 and 70.5% and 60.3% for 12- to 17-year-olds.
How does not getting enough sleep affect the developing brain?
Children who do not get enough sleep for one night can be cranky, groggy, or meltdown prone the next day.
Over time, though, insufficient sleep may impair neurodevelopment in ways that can be measured on brain scans and tests long term, a new study shows.
Research published in The Lancet Child & Adolescent Health found that 9- and 10-year-olds who do not get at least 9 hours of sleep most nights tend to have less gray matter and smaller areas of the brain responsible for attention, memory, and inhibition control, relative to children who do get enough sleep.
The researchers also found a relationship between insufficient sleep and disrupted connections between the basal ganglia and cortical regions of the brain. These disruptions appeared to be linked to depression, thought problems, and impairments in crystallized intelligence, a type of intelligence that depends on memory.
The overall patterns persisted 2 years later, even as those who got enough sleep at baseline gradually slept less over time, while those who were not getting enough sleep to begin with continued to sleep about the same amount, the researchers reported.
The results bolster the case for delaying school start times, as California recently did, according one researcher who was not involved in the study.
The ABCD Study
To examine how insufficient sleep affects children’s mental health, cognition, brain function, and brain structure over 2 years, Ze Wang, PhD, professor of diagnostic radiology and nuclear medicine at the University of Maryland, Baltimore, and colleagues analyzed data from the ongoing Adolescent Brain Cognitive Development (ABCD) Study. The ABCD Study is tracking the biologic and behavioral development of more than 11,000 children in the United States who were recruited for the study when they were 9 or 10 years old.
For their new analysis, Dr. Wang’s group focused on 6,042 participants: 3,021 children with insufficient sleep who were matched with an equal number of participants who were similar in many respects, including sex, socioeconomic status, and puberty status, except they got at least 9 hours of sleep. They also looked at outcomes 2 years later from 749 of the matched pairs who had results available.
The investigators determined sleep duration based on how parents answered the question: “How many hours of sleep does your child get on most nights in the past 6 months?” Possible answers included at least 9 hours, 8-9 hours, 7-8 hours, 5-7 hours, or less than 5 hours. They also looked at functional and structural MRI scans, test results, and responses to questionnaires.
Negative effects of inadequate sleep were spread over “several different domains including brain structure, function, cognition, behavior, and mental health,” Dr. Wang said.
The strength of the relationship between sleep duration and the various outcomes was “modest” and based on group averages, he said. So, a given child who does not sleep for 9 hours most nights won’t necessarily perform worse than a child who gets enough sleep.
Still, modest effects may accumulate and have lasting consequences, Dr. Wang said.
Crystallized intelligence
The researchers looked at 42 behavioral outcomes, 32 of which were significantly different between the groups. Four outcomes in particular – depression, thought problems, performance on a picture-vocabulary test, and crystallized intelligence – were areas where insufficient sleep seemed to have a larger negative effect.
Sleep duration’s relationship with crystallized intelligence was twice that for fluid intelligence, which does not depend on memory.
“Sleep affects memory,” Dr. Wang said. “Crystallized intelligence depends on learned skills and knowledge, which are memory. In this sense, sleep is related to crystallized intelligence.”
One limitation of the study is that some parents may not accurately report how much sleep their child gets, Dr. Wang acknowledged. Children may be awake when parents think they are asleep, for example.
And although the results show getting 9 hours of sleep may help neurocognitive development, it’s also possible that excessive amounts of sleep could be problematic, the study authors wrote.
Further experiments are needed to prove that insufficient sleep – and not some other, unaccounted for factor – causes the observed impairments in neurodevelopment.
To promote healthy sleep, parents should keep a strict routine for their children, such as a regular bedtime and no electronic devices in the bedroom, Dr. Wang suggested. More physical activity during the day also should help.
If children have high levels of stress and depression, “finding the source is critical,” he said. Likewise, clinicians should consider how mental health can affect their patients’ sleep.
More to healthy sleep than duration
“This study both aligns with and advances existing research on the importance of sufficient sleep for child well-being,” said Ariel A. Williamson, PhD, DBSM, a psychologist and pediatric sleep expert in the department of child and adolescent psychiatry and behavioral sciences at Children’s Hospital of Philadelphia and assistant professor of psychiatry and pediatrics at University of Pennsylvania, also in Philadelphia.
The researchers used rigorous propensity score matching, longitudinal data, and brain imaging, which are “innovative methods that provide more evidence on potential mechanisms linking insufficient sleep and child outcomes,” said Dr. Williamson, who was not involved in the study.
While the investigators focused on sleep duration, child sleep health is multidimensional and includes other elements like timing and perception of sleep quality, Dr. Williamson noted. “For example, some research shows that having a sleep schedule that varies night to night is linked to poor child outcomes.”
Dr. Williamson tells families and clinicians that “sleep is a pillar of health,” equal to diet and exercise. That said, sleep recommendations need to fit within a family’s life – taking into account after school activities and late-night homework sessions. But extending sleep by just “20-30 minutes can make a meaningful difference for daytime functioning,” Dr. Williamson said.
Start school later?
Researchers have only relatively recently begun to understand how insufficient sleep affects adolescent neurocognitive development long term, and this study provides “crucial evidence” about the consequences, Lydia Gabriela Speyer, PhD, said in an editorial published with the study. Dr. Speyer is affiliated with the department of psychology at the University of Cambridge (England).
“Given the novel finding that insufficient sleep is associated with changes in brain structure and connectivity that are long-lasting, early intervention is crucial because such neural changes are probably not reversible and might consequently affect adolescents’ development into adulthood,” Dr. Speyer wrote.
Delaying school start times could be one way to help kids get more sleep. The American Academy of Pediatrics and the American Academy of Sleep Medicine recommend that middle schools and high schools start no earlier than 8:30 a.m. to better align with students’ circadian rhythm, Dr. Speyer noted.
As it is in the United States, most schools start closer to 8 a.m. In California, though, a law that went into effect on July 1 prohibits high schools from starting before 8:30 a.m. Other states are weighing similar legislation.
The research was supported by the National Institutes of Health. Dr. Wang and his coauthors and Dr. Speyer had no conflict of interest disclosures. Dr. Williamson is a sleep expert for the Pediatric Sleep Council (www.babysleep.com), which provides free information about early childhood sleep, but she does not receive compensation for this role.
Children who do not get enough sleep for one night can be cranky, groggy, or meltdown prone the next day.
Over time, though, insufficient sleep may impair neurodevelopment in ways that can be measured on brain scans and tests long term, a new study shows.
Research published in The Lancet Child & Adolescent Health found that 9- and 10-year-olds who do not get at least 9 hours of sleep most nights tend to have less gray matter and smaller areas of the brain responsible for attention, memory, and inhibition control, relative to children who do get enough sleep.
The researchers also found a relationship between insufficient sleep and disrupted connections between the basal ganglia and cortical regions of the brain. These disruptions appeared to be linked to depression, thought problems, and impairments in crystallized intelligence, a type of intelligence that depends on memory.
The overall patterns persisted 2 years later, even as those who got enough sleep at baseline gradually slept less over time, while those who were not getting enough sleep to begin with continued to sleep about the same amount, the researchers reported.
The results bolster the case for delaying school start times, as California recently did, according one researcher who was not involved in the study.
The ABCD Study
To examine how insufficient sleep affects children’s mental health, cognition, brain function, and brain structure over 2 years, Ze Wang, PhD, professor of diagnostic radiology and nuclear medicine at the University of Maryland, Baltimore, and colleagues analyzed data from the ongoing Adolescent Brain Cognitive Development (ABCD) Study. The ABCD Study is tracking the biologic and behavioral development of more than 11,000 children in the United States who were recruited for the study when they were 9 or 10 years old.
For their new analysis, Dr. Wang’s group focused on 6,042 participants: 3,021 children with insufficient sleep who were matched with an equal number of participants who were similar in many respects, including sex, socioeconomic status, and puberty status, except they got at least 9 hours of sleep. They also looked at outcomes 2 years later from 749 of the matched pairs who had results available.
The investigators determined sleep duration based on how parents answered the question: “How many hours of sleep does your child get on most nights in the past 6 months?” Possible answers included at least 9 hours, 8-9 hours, 7-8 hours, 5-7 hours, or less than 5 hours. They also looked at functional and structural MRI scans, test results, and responses to questionnaires.
Negative effects of inadequate sleep were spread over “several different domains including brain structure, function, cognition, behavior, and mental health,” Dr. Wang said.
The strength of the relationship between sleep duration and the various outcomes was “modest” and based on group averages, he said. So, a given child who does not sleep for 9 hours most nights won’t necessarily perform worse than a child who gets enough sleep.
Still, modest effects may accumulate and have lasting consequences, Dr. Wang said.
Crystallized intelligence
The researchers looked at 42 behavioral outcomes, 32 of which were significantly different between the groups. Four outcomes in particular – depression, thought problems, performance on a picture-vocabulary test, and crystallized intelligence – were areas where insufficient sleep seemed to have a larger negative effect.
Sleep duration’s relationship with crystallized intelligence was twice that for fluid intelligence, which does not depend on memory.
“Sleep affects memory,” Dr. Wang said. “Crystallized intelligence depends on learned skills and knowledge, which are memory. In this sense, sleep is related to crystallized intelligence.”
One limitation of the study is that some parents may not accurately report how much sleep their child gets, Dr. Wang acknowledged. Children may be awake when parents think they are asleep, for example.
And although the results show getting 9 hours of sleep may help neurocognitive development, it’s also possible that excessive amounts of sleep could be problematic, the study authors wrote.
Further experiments are needed to prove that insufficient sleep – and not some other, unaccounted for factor – causes the observed impairments in neurodevelopment.
To promote healthy sleep, parents should keep a strict routine for their children, such as a regular bedtime and no electronic devices in the bedroom, Dr. Wang suggested. More physical activity during the day also should help.
If children have high levels of stress and depression, “finding the source is critical,” he said. Likewise, clinicians should consider how mental health can affect their patients’ sleep.
More to healthy sleep than duration
“This study both aligns with and advances existing research on the importance of sufficient sleep for child well-being,” said Ariel A. Williamson, PhD, DBSM, a psychologist and pediatric sleep expert in the department of child and adolescent psychiatry and behavioral sciences at Children’s Hospital of Philadelphia and assistant professor of psychiatry and pediatrics at University of Pennsylvania, also in Philadelphia.
The researchers used rigorous propensity score matching, longitudinal data, and brain imaging, which are “innovative methods that provide more evidence on potential mechanisms linking insufficient sleep and child outcomes,” said Dr. Williamson, who was not involved in the study.
While the investigators focused on sleep duration, child sleep health is multidimensional and includes other elements like timing and perception of sleep quality, Dr. Williamson noted. “For example, some research shows that having a sleep schedule that varies night to night is linked to poor child outcomes.”
Dr. Williamson tells families and clinicians that “sleep is a pillar of health,” equal to diet and exercise. That said, sleep recommendations need to fit within a family’s life – taking into account after school activities and late-night homework sessions. But extending sleep by just “20-30 minutes can make a meaningful difference for daytime functioning,” Dr. Williamson said.
Start school later?
Researchers have only relatively recently begun to understand how insufficient sleep affects adolescent neurocognitive development long term, and this study provides “crucial evidence” about the consequences, Lydia Gabriela Speyer, PhD, said in an editorial published with the study. Dr. Speyer is affiliated with the department of psychology at the University of Cambridge (England).
“Given the novel finding that insufficient sleep is associated with changes in brain structure and connectivity that are long-lasting, early intervention is crucial because such neural changes are probably not reversible and might consequently affect adolescents’ development into adulthood,” Dr. Speyer wrote.
Delaying school start times could be one way to help kids get more sleep. The American Academy of Pediatrics and the American Academy of Sleep Medicine recommend that middle schools and high schools start no earlier than 8:30 a.m. to better align with students’ circadian rhythm, Dr. Speyer noted.
As it is in the United States, most schools start closer to 8 a.m. In California, though, a law that went into effect on July 1 prohibits high schools from starting before 8:30 a.m. Other states are weighing similar legislation.
The research was supported by the National Institutes of Health. Dr. Wang and his coauthors and Dr. Speyer had no conflict of interest disclosures. Dr. Williamson is a sleep expert for the Pediatric Sleep Council (www.babysleep.com), which provides free information about early childhood sleep, but she does not receive compensation for this role.
Children who do not get enough sleep for one night can be cranky, groggy, or meltdown prone the next day.
Over time, though, insufficient sleep may impair neurodevelopment in ways that can be measured on brain scans and tests long term, a new study shows.
Research published in The Lancet Child & Adolescent Health found that 9- and 10-year-olds who do not get at least 9 hours of sleep most nights tend to have less gray matter and smaller areas of the brain responsible for attention, memory, and inhibition control, relative to children who do get enough sleep.
The researchers also found a relationship between insufficient sleep and disrupted connections between the basal ganglia and cortical regions of the brain. These disruptions appeared to be linked to depression, thought problems, and impairments in crystallized intelligence, a type of intelligence that depends on memory.
The overall patterns persisted 2 years later, even as those who got enough sleep at baseline gradually slept less over time, while those who were not getting enough sleep to begin with continued to sleep about the same amount, the researchers reported.
The results bolster the case for delaying school start times, as California recently did, according one researcher who was not involved in the study.
The ABCD Study
To examine how insufficient sleep affects children’s mental health, cognition, brain function, and brain structure over 2 years, Ze Wang, PhD, professor of diagnostic radiology and nuclear medicine at the University of Maryland, Baltimore, and colleagues analyzed data from the ongoing Adolescent Brain Cognitive Development (ABCD) Study. The ABCD Study is tracking the biologic and behavioral development of more than 11,000 children in the United States who were recruited for the study when they were 9 or 10 years old.
For their new analysis, Dr. Wang’s group focused on 6,042 participants: 3,021 children with insufficient sleep who were matched with an equal number of participants who were similar in many respects, including sex, socioeconomic status, and puberty status, except they got at least 9 hours of sleep. They also looked at outcomes 2 years later from 749 of the matched pairs who had results available.
The investigators determined sleep duration based on how parents answered the question: “How many hours of sleep does your child get on most nights in the past 6 months?” Possible answers included at least 9 hours, 8-9 hours, 7-8 hours, 5-7 hours, or less than 5 hours. They also looked at functional and structural MRI scans, test results, and responses to questionnaires.
Negative effects of inadequate sleep were spread over “several different domains including brain structure, function, cognition, behavior, and mental health,” Dr. Wang said.
The strength of the relationship between sleep duration and the various outcomes was “modest” and based on group averages, he said. So, a given child who does not sleep for 9 hours most nights won’t necessarily perform worse than a child who gets enough sleep.
Still, modest effects may accumulate and have lasting consequences, Dr. Wang said.
Crystallized intelligence
The researchers looked at 42 behavioral outcomes, 32 of which were significantly different between the groups. Four outcomes in particular – depression, thought problems, performance on a picture-vocabulary test, and crystallized intelligence – were areas where insufficient sleep seemed to have a larger negative effect.
Sleep duration’s relationship with crystallized intelligence was twice that for fluid intelligence, which does not depend on memory.
“Sleep affects memory,” Dr. Wang said. “Crystallized intelligence depends on learned skills and knowledge, which are memory. In this sense, sleep is related to crystallized intelligence.”
One limitation of the study is that some parents may not accurately report how much sleep their child gets, Dr. Wang acknowledged. Children may be awake when parents think they are asleep, for example.
And although the results show getting 9 hours of sleep may help neurocognitive development, it’s also possible that excessive amounts of sleep could be problematic, the study authors wrote.
Further experiments are needed to prove that insufficient sleep – and not some other, unaccounted for factor – causes the observed impairments in neurodevelopment.
To promote healthy sleep, parents should keep a strict routine for their children, such as a regular bedtime and no electronic devices in the bedroom, Dr. Wang suggested. More physical activity during the day also should help.
If children have high levels of stress and depression, “finding the source is critical,” he said. Likewise, clinicians should consider how mental health can affect their patients’ sleep.
More to healthy sleep than duration
“This study both aligns with and advances existing research on the importance of sufficient sleep for child well-being,” said Ariel A. Williamson, PhD, DBSM, a psychologist and pediatric sleep expert in the department of child and adolescent psychiatry and behavioral sciences at Children’s Hospital of Philadelphia and assistant professor of psychiatry and pediatrics at University of Pennsylvania, also in Philadelphia.
The researchers used rigorous propensity score matching, longitudinal data, and brain imaging, which are “innovative methods that provide more evidence on potential mechanisms linking insufficient sleep and child outcomes,” said Dr. Williamson, who was not involved in the study.
While the investigators focused on sleep duration, child sleep health is multidimensional and includes other elements like timing and perception of sleep quality, Dr. Williamson noted. “For example, some research shows that having a sleep schedule that varies night to night is linked to poor child outcomes.”
Dr. Williamson tells families and clinicians that “sleep is a pillar of health,” equal to diet and exercise. That said, sleep recommendations need to fit within a family’s life – taking into account after school activities and late-night homework sessions. But extending sleep by just “20-30 minutes can make a meaningful difference for daytime functioning,” Dr. Williamson said.
Start school later?
Researchers have only relatively recently begun to understand how insufficient sleep affects adolescent neurocognitive development long term, and this study provides “crucial evidence” about the consequences, Lydia Gabriela Speyer, PhD, said in an editorial published with the study. Dr. Speyer is affiliated with the department of psychology at the University of Cambridge (England).
“Given the novel finding that insufficient sleep is associated with changes in brain structure and connectivity that are long-lasting, early intervention is crucial because such neural changes are probably not reversible and might consequently affect adolescents’ development into adulthood,” Dr. Speyer wrote.
Delaying school start times could be one way to help kids get more sleep. The American Academy of Pediatrics and the American Academy of Sleep Medicine recommend that middle schools and high schools start no earlier than 8:30 a.m. to better align with students’ circadian rhythm, Dr. Speyer noted.
As it is in the United States, most schools start closer to 8 a.m. In California, though, a law that went into effect on July 1 prohibits high schools from starting before 8:30 a.m. Other states are weighing similar legislation.
The research was supported by the National Institutes of Health. Dr. Wang and his coauthors and Dr. Speyer had no conflict of interest disclosures. Dr. Williamson is a sleep expert for the Pediatric Sleep Council (www.babysleep.com), which provides free information about early childhood sleep, but she does not receive compensation for this role.
FROM THE LANCET CHILD & ADOLESCENT HEALTH
Consider essential oil allergy in patient with dermatitis
PORTLAND, ORE. – When patients present to Brandon L. Adler, MD, with dermatitis on the eyelid, face, or neck, he routinely asks them if they apply essential oils on their skin, or if they have an essential oil diffuser or nebulizer in their home.
“The answer is frequently ‘yes,’ ” Dr. Adler, clinical assistant professor of dermatology at the University of Southern California, Los Angeles, said at the annual meeting of the Pacific Dermatologic Association. “Essential oils are widely used throughout the wellness industry. They are contained in personal care products, beauty products, natural cleaning products, and they’re being diffused by our patients into the air. More than 75 essential oils are reported to cause allergic contact dermatitis.”
“Linalool is most classically associated with lavender, while limonene is associated with citrus, but they’re found in many different plants,” said Dr. Adler, who directs USC’s contact dermatitis clinic. “On their own, linalool and limonene are not particularly allergenic; they’re not a big deal in the patch test clinic. The problem comes when we add air to the mix, because they oxidize to hydroperoxides of linalool and limonene. These are quite potent allergens.”
According to the most recent North American Contact Dermatitis Group data, 8.9% of patients undergoing patch testing tested positive to linalool hydroperoxides and 2.6% were positive to limonene hydroperoxides.
Dr. Adler discussed the case of a female massage therapist who presented with refractory hand dermatitis and was on methotrexate and dupilumab at the time of consultation but was still symptomatic. She patch-tested positive to limonene and linalool hydroperoxides as well as multiple essential oils that she had been using with her clients, ranging from sacred frankincense oil to basil oil, and she was advised to massage using only coconut or vegetable oils.
Essential oil allergy may also be related to cannabis allergy. According to Dr. Adler, allergic contact dermatitis to cannabis has been rarely reported, but in an analysis of 103 commercial topical cannabinoid preparations that he published with Vincent DeLeo, MD, also with USC, 84% contained a NACDG allergen, frequently essential oils.
More recently, Dr. Adler and colleagues reported the case of a 40-year-old woman who was referred for patch testing for nummular dermatitis that wasn’t responding to treatment. The patient was found to be using topical cannabis and also grew cannabis at home. “She asked to be patch-tested to her homegrown cannabis and had a strong positive patch test to the cannabis, linalool and limonene hydroperoxides, and other essential oils,” Dr. Adler recalled. “We sent her cannabis sample for analysis at a commercial lab and found that it contained limonene and other allergenic terpene chemicals.
“We’re just starting to unravel what this means in terms of our patients and how to manage them, but many are using topical cannabis and topical CBD. I suspect this is a lot less rare than we realize.”
Another recent case from Europe reported allergic contact dermatitis to Cannabis sativa (hemp) seed oil following topical application, with positive patch testing.
Dr. Adler disclosed that he has received research grants from the American Contact Dermatitis Society. He is also an investigator for AbbVie and a consultant for the Skin Research Institute.
PORTLAND, ORE. – When patients present to Brandon L. Adler, MD, with dermatitis on the eyelid, face, or neck, he routinely asks them if they apply essential oils on their skin, or if they have an essential oil diffuser or nebulizer in their home.
“The answer is frequently ‘yes,’ ” Dr. Adler, clinical assistant professor of dermatology at the University of Southern California, Los Angeles, said at the annual meeting of the Pacific Dermatologic Association. “Essential oils are widely used throughout the wellness industry. They are contained in personal care products, beauty products, natural cleaning products, and they’re being diffused by our patients into the air. More than 75 essential oils are reported to cause allergic contact dermatitis.”
“Linalool is most classically associated with lavender, while limonene is associated with citrus, but they’re found in many different plants,” said Dr. Adler, who directs USC’s contact dermatitis clinic. “On their own, linalool and limonene are not particularly allergenic; they’re not a big deal in the patch test clinic. The problem comes when we add air to the mix, because they oxidize to hydroperoxides of linalool and limonene. These are quite potent allergens.”
According to the most recent North American Contact Dermatitis Group data, 8.9% of patients undergoing patch testing tested positive to linalool hydroperoxides and 2.6% were positive to limonene hydroperoxides.
Dr. Adler discussed the case of a female massage therapist who presented with refractory hand dermatitis and was on methotrexate and dupilumab at the time of consultation but was still symptomatic. She patch-tested positive to limonene and linalool hydroperoxides as well as multiple essential oils that she had been using with her clients, ranging from sacred frankincense oil to basil oil, and she was advised to massage using only coconut or vegetable oils.
Essential oil allergy may also be related to cannabis allergy. According to Dr. Adler, allergic contact dermatitis to cannabis has been rarely reported, but in an analysis of 103 commercial topical cannabinoid preparations that he published with Vincent DeLeo, MD, also with USC, 84% contained a NACDG allergen, frequently essential oils.
More recently, Dr. Adler and colleagues reported the case of a 40-year-old woman who was referred for patch testing for nummular dermatitis that wasn’t responding to treatment. The patient was found to be using topical cannabis and also grew cannabis at home. “She asked to be patch-tested to her homegrown cannabis and had a strong positive patch test to the cannabis, linalool and limonene hydroperoxides, and other essential oils,” Dr. Adler recalled. “We sent her cannabis sample for analysis at a commercial lab and found that it contained limonene and other allergenic terpene chemicals.
“We’re just starting to unravel what this means in terms of our patients and how to manage them, but many are using topical cannabis and topical CBD. I suspect this is a lot less rare than we realize.”
Another recent case from Europe reported allergic contact dermatitis to Cannabis sativa (hemp) seed oil following topical application, with positive patch testing.
Dr. Adler disclosed that he has received research grants from the American Contact Dermatitis Society. He is also an investigator for AbbVie and a consultant for the Skin Research Institute.
PORTLAND, ORE. – When patients present to Brandon L. Adler, MD, with dermatitis on the eyelid, face, or neck, he routinely asks them if they apply essential oils on their skin, or if they have an essential oil diffuser or nebulizer in their home.
“The answer is frequently ‘yes,’ ” Dr. Adler, clinical assistant professor of dermatology at the University of Southern California, Los Angeles, said at the annual meeting of the Pacific Dermatologic Association. “Essential oils are widely used throughout the wellness industry. They are contained in personal care products, beauty products, natural cleaning products, and they’re being diffused by our patients into the air. More than 75 essential oils are reported to cause allergic contact dermatitis.”
“Linalool is most classically associated with lavender, while limonene is associated with citrus, but they’re found in many different plants,” said Dr. Adler, who directs USC’s contact dermatitis clinic. “On their own, linalool and limonene are not particularly allergenic; they’re not a big deal in the patch test clinic. The problem comes when we add air to the mix, because they oxidize to hydroperoxides of linalool and limonene. These are quite potent allergens.”
According to the most recent North American Contact Dermatitis Group data, 8.9% of patients undergoing patch testing tested positive to linalool hydroperoxides and 2.6% were positive to limonene hydroperoxides.
Dr. Adler discussed the case of a female massage therapist who presented with refractory hand dermatitis and was on methotrexate and dupilumab at the time of consultation but was still symptomatic. She patch-tested positive to limonene and linalool hydroperoxides as well as multiple essential oils that she had been using with her clients, ranging from sacred frankincense oil to basil oil, and she was advised to massage using only coconut or vegetable oils.
Essential oil allergy may also be related to cannabis allergy. According to Dr. Adler, allergic contact dermatitis to cannabis has been rarely reported, but in an analysis of 103 commercial topical cannabinoid preparations that he published with Vincent DeLeo, MD, also with USC, 84% contained a NACDG allergen, frequently essential oils.
More recently, Dr. Adler and colleagues reported the case of a 40-year-old woman who was referred for patch testing for nummular dermatitis that wasn’t responding to treatment. The patient was found to be using topical cannabis and also grew cannabis at home. “She asked to be patch-tested to her homegrown cannabis and had a strong positive patch test to the cannabis, linalool and limonene hydroperoxides, and other essential oils,” Dr. Adler recalled. “We sent her cannabis sample for analysis at a commercial lab and found that it contained limonene and other allergenic terpene chemicals.
“We’re just starting to unravel what this means in terms of our patients and how to manage them, but many are using topical cannabis and topical CBD. I suspect this is a lot less rare than we realize.”
Another recent case from Europe reported allergic contact dermatitis to Cannabis sativa (hemp) seed oil following topical application, with positive patch testing.
Dr. Adler disclosed that he has received research grants from the American Contact Dermatitis Society. He is also an investigator for AbbVie and a consultant for the Skin Research Institute.
AT PDA 2022
Leukemia rates two to three times higher in children born near fracking
Children born near fracking and other “unconventional” drilling sites are at two to three times greater risk of developing childhood leukemia, according to new research.
The study, published in the journal Environmental Health Perspectives, compared proximity of homes to unconventional oil and gas development (UOGD) sites and risk of the most common form of childhood leukemia, acute lymphoblastic leukemia (ALL).
Researchers looked at 405 children aged 2-7 diagnosed with ALL in Pennsylvania from 2009 to 2017. These children were compared to a control group of 2,080 without the disease matched on the year of birth.
“Unconventional oil and gas development can both use and release chemicals that have been linked to cancer,” study coauthor Nicole Deziel, PhD, of the Yale School of Public Health, New Haven, Conn., said in a statement . She noted that the possibility that children living in close proximity to such sites are “exposed to these chemical carcinogens is a major public health concern.”
About 17 million Americans live within a half-mile of active oil and gas production, according to the Oil & Gas Threat Map, Common Dreams reports. That number includes 4 million children.
The Yale study also found that drinking water could be an important pathway of exposure to oil- and gas-related chemicals used in the UOGD methods of extraction.
Researchers used a new metric that measures exposure to contaminated drinking water and distance to a well. They were able to identify UOGD-affected wells that fell within watersheds where children and their families likely obtained their water.
“Previous health studies have found links between proximity to oil and gas drilling and various children’s health outcomes,” said Dr. Deziel. “This study is among the few to focus on drinking water specifically and the first to apply a novel metric designed to capture potential exposure through this pathway.”
A version of this article first appeared on WebMD.com.
Children born near fracking and other “unconventional” drilling sites are at two to three times greater risk of developing childhood leukemia, according to new research.
The study, published in the journal Environmental Health Perspectives, compared proximity of homes to unconventional oil and gas development (UOGD) sites and risk of the most common form of childhood leukemia, acute lymphoblastic leukemia (ALL).
Researchers looked at 405 children aged 2-7 diagnosed with ALL in Pennsylvania from 2009 to 2017. These children were compared to a control group of 2,080 without the disease matched on the year of birth.
“Unconventional oil and gas development can both use and release chemicals that have been linked to cancer,” study coauthor Nicole Deziel, PhD, of the Yale School of Public Health, New Haven, Conn., said in a statement . She noted that the possibility that children living in close proximity to such sites are “exposed to these chemical carcinogens is a major public health concern.”
About 17 million Americans live within a half-mile of active oil and gas production, according to the Oil & Gas Threat Map, Common Dreams reports. That number includes 4 million children.
The Yale study also found that drinking water could be an important pathway of exposure to oil- and gas-related chemicals used in the UOGD methods of extraction.
Researchers used a new metric that measures exposure to contaminated drinking water and distance to a well. They were able to identify UOGD-affected wells that fell within watersheds where children and their families likely obtained their water.
“Previous health studies have found links between proximity to oil and gas drilling and various children’s health outcomes,” said Dr. Deziel. “This study is among the few to focus on drinking water specifically and the first to apply a novel metric designed to capture potential exposure through this pathway.”
A version of this article first appeared on WebMD.com.
Children born near fracking and other “unconventional” drilling sites are at two to three times greater risk of developing childhood leukemia, according to new research.
The study, published in the journal Environmental Health Perspectives, compared proximity of homes to unconventional oil and gas development (UOGD) sites and risk of the most common form of childhood leukemia, acute lymphoblastic leukemia (ALL).
Researchers looked at 405 children aged 2-7 diagnosed with ALL in Pennsylvania from 2009 to 2017. These children were compared to a control group of 2,080 without the disease matched on the year of birth.
“Unconventional oil and gas development can both use and release chemicals that have been linked to cancer,” study coauthor Nicole Deziel, PhD, of the Yale School of Public Health, New Haven, Conn., said in a statement . She noted that the possibility that children living in close proximity to such sites are “exposed to these chemical carcinogens is a major public health concern.”
About 17 million Americans live within a half-mile of active oil and gas production, according to the Oil & Gas Threat Map, Common Dreams reports. That number includes 4 million children.
The Yale study also found that drinking water could be an important pathway of exposure to oil- and gas-related chemicals used in the UOGD methods of extraction.
Researchers used a new metric that measures exposure to contaminated drinking water and distance to a well. They were able to identify UOGD-affected wells that fell within watersheds where children and their families likely obtained their water.
“Previous health studies have found links between proximity to oil and gas drilling and various children’s health outcomes,” said Dr. Deziel. “This study is among the few to focus on drinking water specifically and the first to apply a novel metric designed to capture potential exposure through this pathway.”
A version of this article first appeared on WebMD.com.
Watching TV, using computer have opposite ties to dementia risk
The relationship to dementia with these activities remained strong no matter how much physical activity a person did, the authors wrote in Proceedings of the National Academy of Sciences.
Both watching TV and using a computer have been linked to increased risk of chronic disease and mortality, while exercise and physical activity (PA) have shown benefit in reducing cognitive decline, structural brain atrophy, and dementia risk in older adults, the authors wrote.
The authors said they wanted to try to understand the effects of watching TV and using computers on dementia risk, because people in the United States and Europe have been engaging in both of these activities more often.
They concluded that it’s not the sitting part of sedentary behavior (SB) that potentially has the effect on dementia but what people are doing while sitting.
Some of the results were surprising, lead author David Raichlen, PhD, professor of Human and Evolutionary Biology at University of Southern California, Los Angeles, said in an interview.
Previous literature on sedentary behaviors have documented their negative effects on a wide range of health outcomes, rather than finding positive associations, he explained.
More than 140,000 included in study
The researchers conducted their prospective cohort study using data from the United Kingdom Biobank. After excluding people younger than 60, those with prevalent dementia at the start of follow-up, and those without complete data, 146,651 participants were included.
The participants were followed from their baseline visit until they received a dementia diagnosis, died, were lost to follow-up, or were last admitted to the hospital.
TV-watching time was linked with an increased risk of incident dementia (HR [95% confidence interval] = 1.31 [1.23-1.40]), and computer use was linked with a reduced risk of incident dementia HR [95% CI] = 0.80 [0.76-0.85]).
TV’s link with higher dementia risk increased in those who had the highest use, compared with those who had the lowest use (HR [95% CI] = 1.28 [1.18-1.39].
Similarly, the link with risk reduction for dementia with computer use increased with more use.
Both medium and high computer time were associated with reduced risk of incident dementia (HR [95% CI] = 0.70 [0.64-0.76] and HR [95% CI] = 0.76 [0.70-0.83] respectively).
Dr. Raichlen pointed out that the high use of TV in this study was 4 or more hours a day and computer use – which included leisure use, not work use – had benefits on dementia risk after just half an hour.
These results remained significant after researchers adjusted for demographic, health, and lifestyle variables, including time spent on physical activity, sleeping, obesity, alcohol consumption, smoking status, diet scores, education level, body mass index, and employment type.
Physical is still better than sedentary activity
One potential reason for the different effects on dementia risk in the two activities studied, the authors write, is that sitting down to watch TV is associated with “uniquely low levels of muscle activity and energy expenditure, compared with sitting to use a computer.”
Andrew Budson, MD, chief of Cognitive & Behavioral Neurology and Associate Chief of Staff for Education for the VA Boston Healthcare System, Mass., who was not part of the study, said he thinks a more likely explanation for the study findings lies in the active versus passive tasks required in the two kinds of viewing that the authors reference.
“When we’re doing cognitive activity involving using the computer, we’re using large parts of our cortex to carry out that activity, whereas when we’re watching TV, there are probably relatively small amounts of our brain that are actually active,” Dr. Budson, author of Seven Steps to Managing Your Memory, explained in an interview.
“This is one of the first times I’ve been convinced that even when the computer activity isn’t completely new and novel, it may be beneficial,” Dr. Budson said.
It would be much better to do physical activity, but if the choice is sedentary activity, active cognitive activities, such as computer use, are better than TV watching, he continued.
The results of the current study are consistent with previous work showing that the type of sedentary behavior matters, according to the authors.
“Several studies have shown that TV time is associated with mortality and poor cardiometabolic biomarkers, whereas computer time is not,” they wrote.
A limitation of the study is that sedentary behaviors were self-reported via questionnaires, and there may be errors in recall.
“The use of objective methods for measuring both SB and PA are needed in future studies,” they write.
The authors receive support from the National Institutes of Health, the State of Arizona, the Arizona Department of Health Services, and the McKnight Brain Research Foundation. Neither the authors nor Dr. Budson declared relevant financial relationships.
The relationship to dementia with these activities remained strong no matter how much physical activity a person did, the authors wrote in Proceedings of the National Academy of Sciences.
Both watching TV and using a computer have been linked to increased risk of chronic disease and mortality, while exercise and physical activity (PA) have shown benefit in reducing cognitive decline, structural brain atrophy, and dementia risk in older adults, the authors wrote.
The authors said they wanted to try to understand the effects of watching TV and using computers on dementia risk, because people in the United States and Europe have been engaging in both of these activities more often.
They concluded that it’s not the sitting part of sedentary behavior (SB) that potentially has the effect on dementia but what people are doing while sitting.
Some of the results were surprising, lead author David Raichlen, PhD, professor of Human and Evolutionary Biology at University of Southern California, Los Angeles, said in an interview.
Previous literature on sedentary behaviors have documented their negative effects on a wide range of health outcomes, rather than finding positive associations, he explained.
More than 140,000 included in study
The researchers conducted their prospective cohort study using data from the United Kingdom Biobank. After excluding people younger than 60, those with prevalent dementia at the start of follow-up, and those without complete data, 146,651 participants were included.
The participants were followed from their baseline visit until they received a dementia diagnosis, died, were lost to follow-up, or were last admitted to the hospital.
TV-watching time was linked with an increased risk of incident dementia (HR [95% confidence interval] = 1.31 [1.23-1.40]), and computer use was linked with a reduced risk of incident dementia HR [95% CI] = 0.80 [0.76-0.85]).
TV’s link with higher dementia risk increased in those who had the highest use, compared with those who had the lowest use (HR [95% CI] = 1.28 [1.18-1.39].
Similarly, the link with risk reduction for dementia with computer use increased with more use.
Both medium and high computer time were associated with reduced risk of incident dementia (HR [95% CI] = 0.70 [0.64-0.76] and HR [95% CI] = 0.76 [0.70-0.83] respectively).
Dr. Raichlen pointed out that the high use of TV in this study was 4 or more hours a day and computer use – which included leisure use, not work use – had benefits on dementia risk after just half an hour.
These results remained significant after researchers adjusted for demographic, health, and lifestyle variables, including time spent on physical activity, sleeping, obesity, alcohol consumption, smoking status, diet scores, education level, body mass index, and employment type.
Physical is still better than sedentary activity
One potential reason for the different effects on dementia risk in the two activities studied, the authors write, is that sitting down to watch TV is associated with “uniquely low levels of muscle activity and energy expenditure, compared with sitting to use a computer.”
Andrew Budson, MD, chief of Cognitive & Behavioral Neurology and Associate Chief of Staff for Education for the VA Boston Healthcare System, Mass., who was not part of the study, said he thinks a more likely explanation for the study findings lies in the active versus passive tasks required in the two kinds of viewing that the authors reference.
“When we’re doing cognitive activity involving using the computer, we’re using large parts of our cortex to carry out that activity, whereas when we’re watching TV, there are probably relatively small amounts of our brain that are actually active,” Dr. Budson, author of Seven Steps to Managing Your Memory, explained in an interview.
“This is one of the first times I’ve been convinced that even when the computer activity isn’t completely new and novel, it may be beneficial,” Dr. Budson said.
It would be much better to do physical activity, but if the choice is sedentary activity, active cognitive activities, such as computer use, are better than TV watching, he continued.
The results of the current study are consistent with previous work showing that the type of sedentary behavior matters, according to the authors.
“Several studies have shown that TV time is associated with mortality and poor cardiometabolic biomarkers, whereas computer time is not,” they wrote.
A limitation of the study is that sedentary behaviors were self-reported via questionnaires, and there may be errors in recall.
“The use of objective methods for measuring both SB and PA are needed in future studies,” they write.
The authors receive support from the National Institutes of Health, the State of Arizona, the Arizona Department of Health Services, and the McKnight Brain Research Foundation. Neither the authors nor Dr. Budson declared relevant financial relationships.
The relationship to dementia with these activities remained strong no matter how much physical activity a person did, the authors wrote in Proceedings of the National Academy of Sciences.
Both watching TV and using a computer have been linked to increased risk of chronic disease and mortality, while exercise and physical activity (PA) have shown benefit in reducing cognitive decline, structural brain atrophy, and dementia risk in older adults, the authors wrote.
The authors said they wanted to try to understand the effects of watching TV and using computers on dementia risk, because people in the United States and Europe have been engaging in both of these activities more often.
They concluded that it’s not the sitting part of sedentary behavior (SB) that potentially has the effect on dementia but what people are doing while sitting.
Some of the results were surprising, lead author David Raichlen, PhD, professor of Human and Evolutionary Biology at University of Southern California, Los Angeles, said in an interview.
Previous literature on sedentary behaviors have documented their negative effects on a wide range of health outcomes, rather than finding positive associations, he explained.
More than 140,000 included in study
The researchers conducted their prospective cohort study using data from the United Kingdom Biobank. After excluding people younger than 60, those with prevalent dementia at the start of follow-up, and those without complete data, 146,651 participants were included.
The participants were followed from their baseline visit until they received a dementia diagnosis, died, were lost to follow-up, or were last admitted to the hospital.
TV-watching time was linked with an increased risk of incident dementia (HR [95% confidence interval] = 1.31 [1.23-1.40]), and computer use was linked with a reduced risk of incident dementia HR [95% CI] = 0.80 [0.76-0.85]).
TV’s link with higher dementia risk increased in those who had the highest use, compared with those who had the lowest use (HR [95% CI] = 1.28 [1.18-1.39].
Similarly, the link with risk reduction for dementia with computer use increased with more use.
Both medium and high computer time were associated with reduced risk of incident dementia (HR [95% CI] = 0.70 [0.64-0.76] and HR [95% CI] = 0.76 [0.70-0.83] respectively).
Dr. Raichlen pointed out that the high use of TV in this study was 4 or more hours a day and computer use – which included leisure use, not work use – had benefits on dementia risk after just half an hour.
These results remained significant after researchers adjusted for demographic, health, and lifestyle variables, including time spent on physical activity, sleeping, obesity, alcohol consumption, smoking status, diet scores, education level, body mass index, and employment type.
Physical is still better than sedentary activity
One potential reason for the different effects on dementia risk in the two activities studied, the authors write, is that sitting down to watch TV is associated with “uniquely low levels of muscle activity and energy expenditure, compared with sitting to use a computer.”
Andrew Budson, MD, chief of Cognitive & Behavioral Neurology and Associate Chief of Staff for Education for the VA Boston Healthcare System, Mass., who was not part of the study, said he thinks a more likely explanation for the study findings lies in the active versus passive tasks required in the two kinds of viewing that the authors reference.
“When we’re doing cognitive activity involving using the computer, we’re using large parts of our cortex to carry out that activity, whereas when we’re watching TV, there are probably relatively small amounts of our brain that are actually active,” Dr. Budson, author of Seven Steps to Managing Your Memory, explained in an interview.
“This is one of the first times I’ve been convinced that even when the computer activity isn’t completely new and novel, it may be beneficial,” Dr. Budson said.
It would be much better to do physical activity, but if the choice is sedentary activity, active cognitive activities, such as computer use, are better than TV watching, he continued.
The results of the current study are consistent with previous work showing that the type of sedentary behavior matters, according to the authors.
“Several studies have shown that TV time is associated with mortality and poor cardiometabolic biomarkers, whereas computer time is not,” they wrote.
A limitation of the study is that sedentary behaviors were self-reported via questionnaires, and there may be errors in recall.
“The use of objective methods for measuring both SB and PA are needed in future studies,” they write.
The authors receive support from the National Institutes of Health, the State of Arizona, the Arizona Department of Health Services, and the McKnight Brain Research Foundation. Neither the authors nor Dr. Budson declared relevant financial relationships.
FROM PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES
Higher rates of group B strep disease found in Black and Asian newborns
Health charities called for action to address racial health disparities after population-wide analysis by the UK Health Security Agency found that Black and Asian neonates had a significantly higher risk of early-onset group B streptococcal disease (GBS), compared with White infants.
One support group said more research was now needed to identify the cause of the disparity, and called for pregnant women to be better informed about the disease and what it could mean for them and their baby.
The study, published in Pediatrics, used UKHSA data on laboratory-confirmed infant group B streptococcal (iGBS) disease cases between Jan. 1, 2016, and Dec. 31, 2020, and were linked to hospital ethnicity records.
Cases of iGBS were defined as isolation of Streptococcus agalactiae from a normally sterile site at 0-6 days of life for early-onset iGBS and 7-90 days for late-onset disease.
Hospital data and parent-reported ethnicity
Researchers found 2,512 iGBS cases in England during the study period, 65.3% were early onset and 34.8% late onset, equivalent to 0.52 and 0.28 cases per 1000 live births respectively.
Researchers were able to link 85.6% of those to ethnicity. Among those 2,149 cases, Black infants had a 48% higher risk, and Asian infants a 40% higher risk of early onset iGBS, compared with White infants. Among those from an Asian background, the risk was 87% higher for Bangladeshi and 38% higher for Pakistani neonates.
Rates of early onset iGBS per 1,000 live births were 0.43 for White infants, 0.63 for Black infants, and 0.60 for those of Asian ethnicity.
In contrast, Indian infants had an early-onset rate of 0.47 per 1,000 live births, which was similar to White infants.
Black infants had 57% higher rates of late-onset iGBS (0.37) than White infants (0.24), the researchers reported.
The study authors highlighted previous research which found higher prevalence of group B streptococcal colonization in mothers from Black and some Asian ethnic groups, but lower prevalence in mothers from the Indian subcontinent. More research was needed to establish causes, the researchers said, including whether higher preterm birth rates in minority ethnic groups led to increased iGBS risk in neonates, or whether maternal group B streptococcal disease led to higher preterm birth rates and subsequent neonatal iGBS.
The researchers concluded: “Understanding the factors underpinning differences in rates of early-onset iGBS within south Asian groups in England may lead to new opportunities for prevention such as prioritized antenatal screening. Strategies to prevent neonatal iGBS must be tailored from high-quality quantitative and qualitative data to reach all women and protect all infants, irrespective of racial or ethnic background.”
‘Shocking but not surprising’
Commenting on the study, Edward Morris, president of the Royal College of Obstetricians and Gynaecologists, said: “This research is striking reading, and is yet another example of how far we have to go to tackle health inequalities within women’s health care.”
Philip Steer, professor emeritus at Imperial College London, said that the results were “consistent with previous reports of higher GBS carriage and higher maternal and neonatal mortality rates in minority groups” and “emphasize the importance of studying not just whether, but why, these differences exist.” He added: “We need to understand the reasons for the differences before we can design much-needed intervention to eliminate them.”
Jane Plumb, chief executive of Group B Strep Support, called the findings “shocking, but unfortunately not surprising” and said that they offered “another example of racial disparities in maternal and neonatal health.” She said: “We’re calling for all pregnant women and birthing people to be informed about GBS and its risks, so they can make empowered choices for themselves and their baby. It is also critical that trusts sign up to take part in the internationally significant [National Institute for Health and Care Research]–funded GBS3 clinical trial, designed to improve the prevention of GBS infection.”
Baroness Shaista Gohir, chief executive of the Muslim Women’s Network, said: “With significantly higher rates of group B Strep infection in Black and Asian babies, greater efforts must be made to improve awareness among pregnant women within these communities.”
A version of this article first appeared on Medscape UK.
Health charities called for action to address racial health disparities after population-wide analysis by the UK Health Security Agency found that Black and Asian neonates had a significantly higher risk of early-onset group B streptococcal disease (GBS), compared with White infants.
One support group said more research was now needed to identify the cause of the disparity, and called for pregnant women to be better informed about the disease and what it could mean for them and their baby.
The study, published in Pediatrics, used UKHSA data on laboratory-confirmed infant group B streptococcal (iGBS) disease cases between Jan. 1, 2016, and Dec. 31, 2020, and were linked to hospital ethnicity records.
Cases of iGBS were defined as isolation of Streptococcus agalactiae from a normally sterile site at 0-6 days of life for early-onset iGBS and 7-90 days for late-onset disease.
Hospital data and parent-reported ethnicity
Researchers found 2,512 iGBS cases in England during the study period, 65.3% were early onset and 34.8% late onset, equivalent to 0.52 and 0.28 cases per 1000 live births respectively.
Researchers were able to link 85.6% of those to ethnicity. Among those 2,149 cases, Black infants had a 48% higher risk, and Asian infants a 40% higher risk of early onset iGBS, compared with White infants. Among those from an Asian background, the risk was 87% higher for Bangladeshi and 38% higher for Pakistani neonates.
Rates of early onset iGBS per 1,000 live births were 0.43 for White infants, 0.63 for Black infants, and 0.60 for those of Asian ethnicity.
In contrast, Indian infants had an early-onset rate of 0.47 per 1,000 live births, which was similar to White infants.
Black infants had 57% higher rates of late-onset iGBS (0.37) than White infants (0.24), the researchers reported.
The study authors highlighted previous research which found higher prevalence of group B streptococcal colonization in mothers from Black and some Asian ethnic groups, but lower prevalence in mothers from the Indian subcontinent. More research was needed to establish causes, the researchers said, including whether higher preterm birth rates in minority ethnic groups led to increased iGBS risk in neonates, or whether maternal group B streptococcal disease led to higher preterm birth rates and subsequent neonatal iGBS.
The researchers concluded: “Understanding the factors underpinning differences in rates of early-onset iGBS within south Asian groups in England may lead to new opportunities for prevention such as prioritized antenatal screening. Strategies to prevent neonatal iGBS must be tailored from high-quality quantitative and qualitative data to reach all women and protect all infants, irrespective of racial or ethnic background.”
‘Shocking but not surprising’
Commenting on the study, Edward Morris, president of the Royal College of Obstetricians and Gynaecologists, said: “This research is striking reading, and is yet another example of how far we have to go to tackle health inequalities within women’s health care.”
Philip Steer, professor emeritus at Imperial College London, said that the results were “consistent with previous reports of higher GBS carriage and higher maternal and neonatal mortality rates in minority groups” and “emphasize the importance of studying not just whether, but why, these differences exist.” He added: “We need to understand the reasons for the differences before we can design much-needed intervention to eliminate them.”
Jane Plumb, chief executive of Group B Strep Support, called the findings “shocking, but unfortunately not surprising” and said that they offered “another example of racial disparities in maternal and neonatal health.” She said: “We’re calling for all pregnant women and birthing people to be informed about GBS and its risks, so they can make empowered choices for themselves and their baby. It is also critical that trusts sign up to take part in the internationally significant [National Institute for Health and Care Research]–funded GBS3 clinical trial, designed to improve the prevention of GBS infection.”
Baroness Shaista Gohir, chief executive of the Muslim Women’s Network, said: “With significantly higher rates of group B Strep infection in Black and Asian babies, greater efforts must be made to improve awareness among pregnant women within these communities.”
A version of this article first appeared on Medscape UK.
Health charities called for action to address racial health disparities after population-wide analysis by the UK Health Security Agency found that Black and Asian neonates had a significantly higher risk of early-onset group B streptococcal disease (GBS), compared with White infants.
One support group said more research was now needed to identify the cause of the disparity, and called for pregnant women to be better informed about the disease and what it could mean for them and their baby.
The study, published in Pediatrics, used UKHSA data on laboratory-confirmed infant group B streptococcal (iGBS) disease cases between Jan. 1, 2016, and Dec. 31, 2020, and were linked to hospital ethnicity records.
Cases of iGBS were defined as isolation of Streptococcus agalactiae from a normally sterile site at 0-6 days of life for early-onset iGBS and 7-90 days for late-onset disease.
Hospital data and parent-reported ethnicity
Researchers found 2,512 iGBS cases in England during the study period, 65.3% were early onset and 34.8% late onset, equivalent to 0.52 and 0.28 cases per 1000 live births respectively.
Researchers were able to link 85.6% of those to ethnicity. Among those 2,149 cases, Black infants had a 48% higher risk, and Asian infants a 40% higher risk of early onset iGBS, compared with White infants. Among those from an Asian background, the risk was 87% higher for Bangladeshi and 38% higher for Pakistani neonates.
Rates of early onset iGBS per 1,000 live births were 0.43 for White infants, 0.63 for Black infants, and 0.60 for those of Asian ethnicity.
In contrast, Indian infants had an early-onset rate of 0.47 per 1,000 live births, which was similar to White infants.
Black infants had 57% higher rates of late-onset iGBS (0.37) than White infants (0.24), the researchers reported.
The study authors highlighted previous research which found higher prevalence of group B streptococcal colonization in mothers from Black and some Asian ethnic groups, but lower prevalence in mothers from the Indian subcontinent. More research was needed to establish causes, the researchers said, including whether higher preterm birth rates in minority ethnic groups led to increased iGBS risk in neonates, or whether maternal group B streptococcal disease led to higher preterm birth rates and subsequent neonatal iGBS.
The researchers concluded: “Understanding the factors underpinning differences in rates of early-onset iGBS within south Asian groups in England may lead to new opportunities for prevention such as prioritized antenatal screening. Strategies to prevent neonatal iGBS must be tailored from high-quality quantitative and qualitative data to reach all women and protect all infants, irrespective of racial or ethnic background.”
‘Shocking but not surprising’
Commenting on the study, Edward Morris, president of the Royal College of Obstetricians and Gynaecologists, said: “This research is striking reading, and is yet another example of how far we have to go to tackle health inequalities within women’s health care.”
Philip Steer, professor emeritus at Imperial College London, said that the results were “consistent with previous reports of higher GBS carriage and higher maternal and neonatal mortality rates in minority groups” and “emphasize the importance of studying not just whether, but why, these differences exist.” He added: “We need to understand the reasons for the differences before we can design much-needed intervention to eliminate them.”
Jane Plumb, chief executive of Group B Strep Support, called the findings “shocking, but unfortunately not surprising” and said that they offered “another example of racial disparities in maternal and neonatal health.” She said: “We’re calling for all pregnant women and birthing people to be informed about GBS and its risks, so they can make empowered choices for themselves and their baby. It is also critical that trusts sign up to take part in the internationally significant [National Institute for Health and Care Research]–funded GBS3 clinical trial, designed to improve the prevention of GBS infection.”
Baroness Shaista Gohir, chief executive of the Muslim Women’s Network, said: “With significantly higher rates of group B Strep infection in Black and Asian babies, greater efforts must be made to improve awareness among pregnant women within these communities.”
A version of this article first appeared on Medscape UK.
FROM PEDIATRICS