MDedge Neurology

Drinking alcohol is linked to an increased risk of new-onset epilepsy, with greater consumption tied to greater risk, but more research is needed before any definitive conclusions can be drawn.

Results of an updated meta-analysis are consistent with those of a previous meta-analysis but contrast with some prior cohort studies.

copyright Fuse/Thinkstock

“Further large cohort studies of the general population are required to assert a definite causal relationship between alcohol consumption and epilepsy and to identify a potential threshold,” Yun Hak Kim, MD, PhD, departments of biomedical informatics and anatomy, Pusan (South Korea) National University, said in a press release.

The study was published online Jan. 11, 2022, in Drug and Alcohol Dependence.
 

Conflicting findings

Much of the research into the impact of alcohol on epilepsy risk has focused on provoked seizures related to alcohol intoxication or withdrawal, but few studies have investigated the effect of alcohol on unprovoked seizures. In addition, the research in this area has been conflicting.

A 2010 meta-analysis that included six case-control studies showed alcohol users had an increased risk of unprovoked seizure or epilepsy with a pooled relative risk of 2.19 (95% confidence interval, 1.82-2.63). This analysis also showed a dose-dependent relationship with relative risks increasing with more grams of alcohol consumed daily.

However, some recent large cohort studies showed that moderate alcohol consumption was associated with a lower risk of epilepsy.

The updated meta-analysis included eight studies – three cohort studies not included in the previous meta-analysis and five case-control studies.

The study excluded two case-control studies included in the previous meta-analysis. One of these studies used duplicated data, and the other included epilepsy patients and did not present results of subgroup analysis for patients experiencing their first seizure.

Results of the new analysis showed the pooled odds ratio for newly diagnosed epilepsy was 1.70 (95% CI, 1.16-2.49) in alcohol users versus nondrinkers.

A dose-response analysis of case-control studies carried out using the cubic spline analysis showed a significant positive dose-response relationship. A dose-response graph showed a steep increase in risk above about 150 g/day and 250 g/day of alcohol consumption.

However, a subgroup analysis showed that epilepsy risk was only found in the case-control studies. In fact, two of the three cohort studies showed that alcohol consumption was associated with a lower risk of epilepsy, although this was not significant.

Cohort studies often include more control subjects and longer follow-up periods and are less prone to bias, such as selection and recall biases, the investigators noted.

“Therefore, cohort studies usually provide a stronger association between exposure and disease than case-control studies, despite having limitations for diseases with low incidence levels,” they wrote.
 

More research needed

The researchers added that most case-control studies included in the new meta-analysis assessed alcohol consumption only in the 6 months prior to the onset of seizures. Research shows it usually takes heavy drinkers 5 or more years to develop repetitive unprovoked seizures.

“Considering these temporal relationships and differences in study design, alcohol may not actually increase the risk of epilepsy, as seen in our subgroup analysis for cohort studies,” the investigators wrote.

They noted that the cohort studies in the meta-analysis were variously limited to young women, elderly patients, and post–subdural hematoma patients. “This limitation makes it difficult to confirm or generalize the results of the subgroup analysis.”

To resolve this “discrepancy,” further large cohort studies of the general population over a longer period are needed, the investigators wrote.

Examining the risk of bias within studies, the authors evaluated three cohort studies as “good” quality. Of the case-control studies, they rated two as “good,” one as “fair,” and two as “poor.”

For primary prevention, an assessment of the risk of alcohol consumption in various clinical situations, such as the time relation of alcohol consumption with seizures, will be important, lead author Kyoung Nam Woo, department of neurology, Pusan National University, said in the release.

“To increase the applicability to the general population, future studies should be conducted in which the potential confounders such as age, sex, and smoking have been adjusted.”

Commenting on the study, Jacqueline French, MD, professor, New York University Comprehensive Epilepsy Center, echoed the authors in noting a number of weaknesses in the study.

The analysis was unable to exclude alcohol withdrawal seizures. Also, while some studies suggested a positive relationship, others suggested a negative relationship, she said. “The authors suggest further work is needed before a definitive determination is made, and I agree.”

The study received funding from the Medical Research Center Program, the Basic Science Research Program, and the Collaborative Genome Program for Fostering New Post-Genome Industry through a National Research Foundation of Korea grant funded by the Korean government. The authors disclosed no relevant financial relationships.

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

Drinking alcohol is linked to an increased risk of new-onset epilepsy, with greater consumption tied to greater risk, but more research is needed before any definitive conclusions can be drawn.

Results of an updated meta-analysis are consistent with those of a previous meta-analysis but contrast with some prior cohort studies.

copyright Fuse/Thinkstock

“Further large cohort studies of the general population are required to assert a definite causal relationship between alcohol consumption and epilepsy and to identify a potential threshold,” Yun Hak Kim, MD, PhD, departments of biomedical informatics and anatomy, Pusan (South Korea) National University, said in a press release.

The study was published online Jan. 11, 2022, in Drug and Alcohol Dependence.
 

Conflicting findings

Much of the research into the impact of alcohol on epilepsy risk has focused on provoked seizures related to alcohol intoxication or withdrawal, but few studies have investigated the effect of alcohol on unprovoked seizures. In addition, the research in this area has been conflicting.

A 2010 meta-analysis that included six case-control studies showed alcohol users had an increased risk of unprovoked seizure or epilepsy with a pooled relative risk of 2.19 (95% confidence interval, 1.82-2.63). This analysis also showed a dose-dependent relationship with relative risks increasing with more grams of alcohol consumed daily.

However, some recent large cohort studies showed that moderate alcohol consumption was associated with a lower risk of epilepsy.

The updated meta-analysis included eight studies – three cohort studies not included in the previous meta-analysis and five case-control studies.

The study excluded two case-control studies included in the previous meta-analysis. One of these studies used duplicated data, and the other included epilepsy patients and did not present results of subgroup analysis for patients experiencing their first seizure.

Results of the new analysis showed the pooled odds ratio for newly diagnosed epilepsy was 1.70 (95% CI, 1.16-2.49) in alcohol users versus nondrinkers.

A dose-response analysis of case-control studies carried out using the cubic spline analysis showed a significant positive dose-response relationship. A dose-response graph showed a steep increase in risk above about 150 g/day and 250 g/day of alcohol consumption.

However, a subgroup analysis showed that epilepsy risk was only found in the case-control studies. In fact, two of the three cohort studies showed that alcohol consumption was associated with a lower risk of epilepsy, although this was not significant.

Cohort studies often include more control subjects and longer follow-up periods and are less prone to bias, such as selection and recall biases, the investigators noted.

“Therefore, cohort studies usually provide a stronger association between exposure and disease than case-control studies, despite having limitations for diseases with low incidence levels,” they wrote.
 

More research needed

The researchers added that most case-control studies included in the new meta-analysis assessed alcohol consumption only in the 6 months prior to the onset of seizures. Research shows it usually takes heavy drinkers 5 or more years to develop repetitive unprovoked seizures.

“Considering these temporal relationships and differences in study design, alcohol may not actually increase the risk of epilepsy, as seen in our subgroup analysis for cohort studies,” the investigators wrote.

They noted that the cohort studies in the meta-analysis were variously limited to young women, elderly patients, and post–subdural hematoma patients. “This limitation makes it difficult to confirm or generalize the results of the subgroup analysis.”

To resolve this “discrepancy,” further large cohort studies of the general population over a longer period are needed, the investigators wrote.

Examining the risk of bias within studies, the authors evaluated three cohort studies as “good” quality. Of the case-control studies, they rated two as “good,” one as “fair,” and two as “poor.”

For primary prevention, an assessment of the risk of alcohol consumption in various clinical situations, such as the time relation of alcohol consumption with seizures, will be important, lead author Kyoung Nam Woo, department of neurology, Pusan National University, said in the release.

“To increase the applicability to the general population, future studies should be conducted in which the potential confounders such as age, sex, and smoking have been adjusted.”

Commenting on the study, Jacqueline French, MD, professor, New York University Comprehensive Epilepsy Center, echoed the authors in noting a number of weaknesses in the study.

The analysis was unable to exclude alcohol withdrawal seizures. Also, while some studies suggested a positive relationship, others suggested a negative relationship, she said. “The authors suggest further work is needed before a definitive determination is made, and I agree.”

The study received funding from the Medical Research Center Program, the Basic Science Research Program, and the Collaborative Genome Program for Fostering New Post-Genome Industry through a National Research Foundation of Korea grant funded by the Korean government. The authors disclosed no relevant financial relationships.

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

Drinking alcohol is linked to an increased risk of new-onset epilepsy, with greater consumption tied to greater risk, but more research is needed before any definitive conclusions can be drawn.

Results of an updated meta-analysis are consistent with those of a previous meta-analysis but contrast with some prior cohort studies.

copyright Fuse/Thinkstock

“Further large cohort studies of the general population are required to assert a definite causal relationship between alcohol consumption and epilepsy and to identify a potential threshold,” Yun Hak Kim, MD, PhD, departments of biomedical informatics and anatomy, Pusan (South Korea) National University, said in a press release.

The study was published online Jan. 11, 2022, in Drug and Alcohol Dependence.
 

Conflicting findings

Much of the research into the impact of alcohol on epilepsy risk has focused on provoked seizures related to alcohol intoxication or withdrawal, but few studies have investigated the effect of alcohol on unprovoked seizures. In addition, the research in this area has been conflicting.

A 2010 meta-analysis that included six case-control studies showed alcohol users had an increased risk of unprovoked seizure or epilepsy with a pooled relative risk of 2.19 (95% confidence interval, 1.82-2.63). This analysis also showed a dose-dependent relationship with relative risks increasing with more grams of alcohol consumed daily.

However, some recent large cohort studies showed that moderate alcohol consumption was associated with a lower risk of epilepsy.

The updated meta-analysis included eight studies – three cohort studies not included in the previous meta-analysis and five case-control studies.

The study excluded two case-control studies included in the previous meta-analysis. One of these studies used duplicated data, and the other included epilepsy patients and did not present results of subgroup analysis for patients experiencing their first seizure.

Results of the new analysis showed the pooled odds ratio for newly diagnosed epilepsy was 1.70 (95% CI, 1.16-2.49) in alcohol users versus nondrinkers.

A dose-response analysis of case-control studies carried out using the cubic spline analysis showed a significant positive dose-response relationship. A dose-response graph showed a steep increase in risk above about 150 g/day and 250 g/day of alcohol consumption.

However, a subgroup analysis showed that epilepsy risk was only found in the case-control studies. In fact, two of the three cohort studies showed that alcohol consumption was associated with a lower risk of epilepsy, although this was not significant.

Cohort studies often include more control subjects and longer follow-up periods and are less prone to bias, such as selection and recall biases, the investigators noted.

“Therefore, cohort studies usually provide a stronger association between exposure and disease than case-control studies, despite having limitations for diseases with low incidence levels,” they wrote.
 

More research needed

The researchers added that most case-control studies included in the new meta-analysis assessed alcohol consumption only in the 6 months prior to the onset of seizures. Research shows it usually takes heavy drinkers 5 or more years to develop repetitive unprovoked seizures.

“Considering these temporal relationships and differences in study design, alcohol may not actually increase the risk of epilepsy, as seen in our subgroup analysis for cohort studies,” the investigators wrote.

They noted that the cohort studies in the meta-analysis were variously limited to young women, elderly patients, and post–subdural hematoma patients. “This limitation makes it difficult to confirm or generalize the results of the subgroup analysis.”

To resolve this “discrepancy,” further large cohort studies of the general population over a longer period are needed, the investigators wrote.

Examining the risk of bias within studies, the authors evaluated three cohort studies as “good” quality. Of the case-control studies, they rated two as “good,” one as “fair,” and two as “poor.”

For primary prevention, an assessment of the risk of alcohol consumption in various clinical situations, such as the time relation of alcohol consumption with seizures, will be important, lead author Kyoung Nam Woo, department of neurology, Pusan National University, said in the release.

“To increase the applicability to the general population, future studies should be conducted in which the potential confounders such as age, sex, and smoking have been adjusted.”

Commenting on the study, Jacqueline French, MD, professor, New York University Comprehensive Epilepsy Center, echoed the authors in noting a number of weaknesses in the study.

The analysis was unable to exclude alcohol withdrawal seizures. Also, while some studies suggested a positive relationship, others suggested a negative relationship, she said. “The authors suggest further work is needed before a definitive determination is made, and I agree.”

The study received funding from the Medical Research Center Program, the Basic Science Research Program, and the Collaborative Genome Program for Fostering New Post-Genome Industry through a National Research Foundation of Korea grant funded by the Korean government. The authors disclosed no relevant financial relationships.

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

Dietary intake of polyunsaturated fatty acids (PUFA), particularly omega 6, is associated with improved cognitive function in older adults, new research suggests.

The study provides important “pieces of the puzzle” of the diet and cognition connection, but the results aren’t “ready for prime time,” study investigator Roger S. McIntyre, MD, professor of psychiatry and pharmacology, University of Toronto, said in an interview.

“I don’t think we’re there yet when it comes to recommending supplementation to the general public,” said Dr. McIntyre, adding a larger “more compelling study” is needed.

The study was published online Jan. 14 in The American Journal of Geriatric Psychiatry.
 

Clinically meaningful?

Research shows that 25%-50% of community-dwelling adults aged 65-85 years have some cognitive impairment. Other evidence indicates cognition is affected by dietary fat intake.

Many lines of research show that alterations in lipid homeostasis can cause brain dysfunction, said Dr. McIntyre. “This shouldn’t surprise us because our brain is made up of protein, water, and fat.”

This new analysis used combined data from the 2011-2012 and 2013-2014 cycles of the National Health and Nutrition Examination Survey (NHANES), a series of ongoing cross-sectional surveys conducted by the Centers for Disease Control and Prevention. The data are collected in two phases, an in-home face-to-face interview and a physical examination.

Researchers obtained dietary intake information through two 24-hour dietary recall interviews. Dietary information included total energy (kcal/d), intakes in grams per day (g/d) of total fat, saturated fatty acid (SFAT), monounsaturated fatty acid (MUFA), PUFA, total omega-3 and total omega-6 fatty acids, and milligrams per day (mg/d) of cholesterol.

For cognitive function, the researchers used total and delayed recall scores of the Consortium to Establish a Registry for Alzheimer’s Disease (CERAD), the animal fluency test, and the digit symbol substitution test (DSST).

The study included 2,253 adults aged 60 years and older (mean age, 69.4 years) and 51% were non-Hispanic White individuals.

After adjustment for age, sex, race/ethnicity, educational attainment, smoking status, alcohol consumption, income, and total energy, dietary intake of PUFA and omega-6 fatty acid was positively associated with DSST.

The DSST score increased about 0.06 standard deviation (SD) (about 1 score) with each SD increase in these fatty acids (8.8 g/d for PUFA and 7.9 g/d for omega-6) (P values were .02 for PUFA and .01 for omega-6).

However, it’s unclear what an improvement of 1 DSST score means clinically, said Dr. McIntyre. “The P value is significant, but how does that translate? Does this mean a person can now think more clearly or function better?”
 

‘Million dollar question’ remains unanswered

The fact that omega-6, considered neuroinflammatory, was associated with improved DSST score illustrates the complexity of this field, said Dr. McIntyre.

“We’re learning that when it comes to inflammation, many of the molecules in our brain that are implicated as anti-inflammatory can also be pro-inflammatory, so bad guys can be good guys and good guys can be bad guys.”

It speaks to the notion of homeostasis, he added. “Just like a seesaw; when you push this part down, that part goes up.”

The analysis showed the animal fluency score increased about 0.05 SD (around 0.3 score) with each SD (1.1 g/d) increase in dietary intake of omega-3.

There were no significant associations between other dietary fat intake and cognitive performance.

The researchers investigated the role of oxidative stress and antioxidant biomarkers (gamma glutamyl transpeptidase [GGT], bilirubin, uric acid, and vitamin D).

Cells produce oxidative radicals that are normally “mopped up” by our “innate antioxidant capability,” said Dr. McIntyre. “But in states of cognitive impairment, these oxidative stress markers accumulate and they exceed what the normal innate response is able to manage.”

The study showed GGT levels decreased with increased PUFA and omega-6 fatty acid intakes; levels of bilirubin decreased with increase in most dietary fat intakes; uric acid levels decreased with MUFA intake and omega-6/omega-3 ratio; and vitamin D levels increased with omega-3 fatty acid intake but decreased with SFAT intake.

Causal mediation analysis showed the association between dietary intake of fatty acids and DSST performance was partially mediated by GGT levels. However, Dr. McIntyre emphasized that this does not prove causality.

“The million dollar question is, is this the sole explanation for the association? In other words, is it the oxidative stress that caused the cognitive impairment and therefore correcting it improved it, or is it the case that oxidative stress is a proxy of other activities that are also taking place?”
 

A ‘plausible’ link

In an editorial, Candida Rebello, PhD, of the department of integrated physiology and molecular medicine at Pennington Biomedical Research Center, Baton Rouge, La., said the finding that omega-3 and omega-6 fatty acids are positively associated with cognition in older adults makes some sense.

She noted that aging is associated with an overt inflammatory phenotype, and evidence shows these fatty acids are precursors for bioactive molecules that play a role in self-limiting the acute inflammatory response.

Dr. Rebello said the positive association of omega-6 fatty acid with cognition shown in this study contrasts with the “common belief” that increasing dietary intake of these fatty acids enhances inflammation, but agreed the association is “plausible.”

She said it’s “essential” to determine “the underlying mechanisms that regulate the diverse features of inflammation and sort out the processes that protect from neuronal damage and those that contribute towards it.”

She noted the ratio of omega-6 to omega-3 is about 15:1 in the present day Western diet, as opposed to a 1:1 ratio in diets of the past. Omega-3 fatty acids are found in fish oil supplements and fatty fish like mackerel and salmon, while cereal, grains, and vegetable oil are sources of omega-6.

Attaining a measure of balance of fatty acids in the diet may be a “prudent approach,” said Dr. Rebello. “Substituting some meat entrées with fatty fish and polyunsaturated vegetable oils with monounsaturated fats such as olive oil are small changes that are likely to garner adherence.”

Dr. Rebello noted that the study used NHANES food intake data, which rely on participant self-report and so may not be accurate.

The study received funding from the MOE (Ministry of Education in China) Project of Humanities and Social Sciences and the Research Startup Fund of Southwest University. Dr. McIntyre has received research grant support from CIHR/GACD/Chinese National Natural Research Foundation and speaker/consultation fees from Lundbeck, Janssen, Purdue, Pfizer, Otsuka, Takeda, Neurocrine, Sunovion, Bausch Health, Novo Nordisk, Kris, Sanofi, Eisai, Intra-Cellular, NewBridge Pharmaceuticals, and AbbVie. He is a CEO of Braxia Scientific Corp.

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

Dietary intake of polyunsaturated fatty acids (PUFA), particularly omega 6, is associated with improved cognitive function in older adults, new research suggests.

The study provides important “pieces of the puzzle” of the diet and cognition connection, but the results aren’t “ready for prime time,” study investigator Roger S. McIntyre, MD, professor of psychiatry and pharmacology, University of Toronto, said in an interview.

“I don’t think we’re there yet when it comes to recommending supplementation to the general public,” said Dr. McIntyre, adding a larger “more compelling study” is needed.

The study was published online Jan. 14 in The American Journal of Geriatric Psychiatry.
 

Clinically meaningful?

Research shows that 25%-50% of community-dwelling adults aged 65-85 years have some cognitive impairment. Other evidence indicates cognition is affected by dietary fat intake.

Many lines of research show that alterations in lipid homeostasis can cause brain dysfunction, said Dr. McIntyre. “This shouldn’t surprise us because our brain is made up of protein, water, and fat.”

This new analysis used combined data from the 2011-2012 and 2013-2014 cycles of the National Health and Nutrition Examination Survey (NHANES), a series of ongoing cross-sectional surveys conducted by the Centers for Disease Control and Prevention. The data are collected in two phases, an in-home face-to-face interview and a physical examination.

Researchers obtained dietary intake information through two 24-hour dietary recall interviews. Dietary information included total energy (kcal/d), intakes in grams per day (g/d) of total fat, saturated fatty acid (SFAT), monounsaturated fatty acid (MUFA), PUFA, total omega-3 and total omega-6 fatty acids, and milligrams per day (mg/d) of cholesterol.

For cognitive function, the researchers used total and delayed recall scores of the Consortium to Establish a Registry for Alzheimer’s Disease (CERAD), the animal fluency test, and the digit symbol substitution test (DSST).

The study included 2,253 adults aged 60 years and older (mean age, 69.4 years) and 51% were non-Hispanic White individuals.

After adjustment for age, sex, race/ethnicity, educational attainment, smoking status, alcohol consumption, income, and total energy, dietary intake of PUFA and omega-6 fatty acid was positively associated with DSST.

The DSST score increased about 0.06 standard deviation (SD) (about 1 score) with each SD increase in these fatty acids (8.8 g/d for PUFA and 7.9 g/d for omega-6) (P values were .02 for PUFA and .01 for omega-6).

However, it’s unclear what an improvement of 1 DSST score means clinically, said Dr. McIntyre. “The P value is significant, but how does that translate? Does this mean a person can now think more clearly or function better?”
 

‘Million dollar question’ remains unanswered

The fact that omega-6, considered neuroinflammatory, was associated with improved DSST score illustrates the complexity of this field, said Dr. McIntyre.

“We’re learning that when it comes to inflammation, many of the molecules in our brain that are implicated as anti-inflammatory can also be pro-inflammatory, so bad guys can be good guys and good guys can be bad guys.”

It speaks to the notion of homeostasis, he added. “Just like a seesaw; when you push this part down, that part goes up.”

The analysis showed the animal fluency score increased about 0.05 SD (around 0.3 score) with each SD (1.1 g/d) increase in dietary intake of omega-3.

There were no significant associations between other dietary fat intake and cognitive performance.

The researchers investigated the role of oxidative stress and antioxidant biomarkers (gamma glutamyl transpeptidase [GGT], bilirubin, uric acid, and vitamin D).

Cells produce oxidative radicals that are normally “mopped up” by our “innate antioxidant capability,” said Dr. McIntyre. “But in states of cognitive impairment, these oxidative stress markers accumulate and they exceed what the normal innate response is able to manage.”

The study showed GGT levels decreased with increased PUFA and omega-6 fatty acid intakes; levels of bilirubin decreased with increase in most dietary fat intakes; uric acid levels decreased with MUFA intake and omega-6/omega-3 ratio; and vitamin D levels increased with omega-3 fatty acid intake but decreased with SFAT intake.

Causal mediation analysis showed the association between dietary intake of fatty acids and DSST performance was partially mediated by GGT levels. However, Dr. McIntyre emphasized that this does not prove causality.

“The million dollar question is, is this the sole explanation for the association? In other words, is it the oxidative stress that caused the cognitive impairment and therefore correcting it improved it, or is it the case that oxidative stress is a proxy of other activities that are also taking place?”
 

A ‘plausible’ link

In an editorial, Candida Rebello, PhD, of the department of integrated physiology and molecular medicine at Pennington Biomedical Research Center, Baton Rouge, La., said the finding that omega-3 and omega-6 fatty acids are positively associated with cognition in older adults makes some sense.

She noted that aging is associated with an overt inflammatory phenotype, and evidence shows these fatty acids are precursors for bioactive molecules that play a role in self-limiting the acute inflammatory response.

Dr. Rebello said the positive association of omega-6 fatty acid with cognition shown in this study contrasts with the “common belief” that increasing dietary intake of these fatty acids enhances inflammation, but agreed the association is “plausible.”

She said it’s “essential” to determine “the underlying mechanisms that regulate the diverse features of inflammation and sort out the processes that protect from neuronal damage and those that contribute towards it.”

She noted the ratio of omega-6 to omega-3 is about 15:1 in the present day Western diet, as opposed to a 1:1 ratio in diets of the past. Omega-3 fatty acids are found in fish oil supplements and fatty fish like mackerel and salmon, while cereal, grains, and vegetable oil are sources of omega-6.

Attaining a measure of balance of fatty acids in the diet may be a “prudent approach,” said Dr. Rebello. “Substituting some meat entrées with fatty fish and polyunsaturated vegetable oils with monounsaturated fats such as olive oil are small changes that are likely to garner adherence.”

Dr. Rebello noted that the study used NHANES food intake data, which rely on participant self-report and so may not be accurate.

The study received funding from the MOE (Ministry of Education in China) Project of Humanities and Social Sciences and the Research Startup Fund of Southwest University. Dr. McIntyre has received research grant support from CIHR/GACD/Chinese National Natural Research Foundation and speaker/consultation fees from Lundbeck, Janssen, Purdue, Pfizer, Otsuka, Takeda, Neurocrine, Sunovion, Bausch Health, Novo Nordisk, Kris, Sanofi, Eisai, Intra-Cellular, NewBridge Pharmaceuticals, and AbbVie. He is a CEO of Braxia Scientific Corp.

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

Dietary intake of polyunsaturated fatty acids (PUFA), particularly omega 6, is associated with improved cognitive function in older adults, new research suggests.

The study provides important “pieces of the puzzle” of the diet and cognition connection, but the results aren’t “ready for prime time,” study investigator Roger S. McIntyre, MD, professor of psychiatry and pharmacology, University of Toronto, said in an interview.

“I don’t think we’re there yet when it comes to recommending supplementation to the general public,” said Dr. McIntyre, adding a larger “more compelling study” is needed.

The study was published online Jan. 14 in The American Journal of Geriatric Psychiatry.
 

Clinically meaningful?

Research shows that 25%-50% of community-dwelling adults aged 65-85 years have some cognitive impairment. Other evidence indicates cognition is affected by dietary fat intake.

Many lines of research show that alterations in lipid homeostasis can cause brain dysfunction, said Dr. McIntyre. “This shouldn’t surprise us because our brain is made up of protein, water, and fat.”

This new analysis used combined data from the 2011-2012 and 2013-2014 cycles of the National Health and Nutrition Examination Survey (NHANES), a series of ongoing cross-sectional surveys conducted by the Centers for Disease Control and Prevention. The data are collected in two phases, an in-home face-to-face interview and a physical examination.

Researchers obtained dietary intake information through two 24-hour dietary recall interviews. Dietary information included total energy (kcal/d), intakes in grams per day (g/d) of total fat, saturated fatty acid (SFAT), monounsaturated fatty acid (MUFA), PUFA, total omega-3 and total omega-6 fatty acids, and milligrams per day (mg/d) of cholesterol.

For cognitive function, the researchers used total and delayed recall scores of the Consortium to Establish a Registry for Alzheimer’s Disease (CERAD), the animal fluency test, and the digit symbol substitution test (DSST).

The study included 2,253 adults aged 60 years and older (mean age, 69.4 years) and 51% were non-Hispanic White individuals.

After adjustment for age, sex, race/ethnicity, educational attainment, smoking status, alcohol consumption, income, and total energy, dietary intake of PUFA and omega-6 fatty acid was positively associated with DSST.

The DSST score increased about 0.06 standard deviation (SD) (about 1 score) with each SD increase in these fatty acids (8.8 g/d for PUFA and 7.9 g/d for omega-6) (P values were .02 for PUFA and .01 for omega-6).

However, it’s unclear what an improvement of 1 DSST score means clinically, said Dr. McIntyre. “The P value is significant, but how does that translate? Does this mean a person can now think more clearly or function better?”
 

‘Million dollar question’ remains unanswered

The fact that omega-6, considered neuroinflammatory, was associated with improved DSST score illustrates the complexity of this field, said Dr. McIntyre.

“We’re learning that when it comes to inflammation, many of the molecules in our brain that are implicated as anti-inflammatory can also be pro-inflammatory, so bad guys can be good guys and good guys can be bad guys.”

It speaks to the notion of homeostasis, he added. “Just like a seesaw; when you push this part down, that part goes up.”

The analysis showed the animal fluency score increased about 0.05 SD (around 0.3 score) with each SD (1.1 g/d) increase in dietary intake of omega-3.

There were no significant associations between other dietary fat intake and cognitive performance.

The researchers investigated the role of oxidative stress and antioxidant biomarkers (gamma glutamyl transpeptidase [GGT], bilirubin, uric acid, and vitamin D).

Cells produce oxidative radicals that are normally “mopped up” by our “innate antioxidant capability,” said Dr. McIntyre. “But in states of cognitive impairment, these oxidative stress markers accumulate and they exceed what the normal innate response is able to manage.”

The study showed GGT levels decreased with increased PUFA and omega-6 fatty acid intakes; levels of bilirubin decreased with increase in most dietary fat intakes; uric acid levels decreased with MUFA intake and omega-6/omega-3 ratio; and vitamin D levels increased with omega-3 fatty acid intake but decreased with SFAT intake.

Causal mediation analysis showed the association between dietary intake of fatty acids and DSST performance was partially mediated by GGT levels. However, Dr. McIntyre emphasized that this does not prove causality.

“The million dollar question is, is this the sole explanation for the association? In other words, is it the oxidative stress that caused the cognitive impairment and therefore correcting it improved it, or is it the case that oxidative stress is a proxy of other activities that are also taking place?”
 

A ‘plausible’ link

In an editorial, Candida Rebello, PhD, of the department of integrated physiology and molecular medicine at Pennington Biomedical Research Center, Baton Rouge, La., said the finding that omega-3 and omega-6 fatty acids are positively associated with cognition in older adults makes some sense.

She noted that aging is associated with an overt inflammatory phenotype, and evidence shows these fatty acids are precursors for bioactive molecules that play a role in self-limiting the acute inflammatory response.

Dr. Rebello said the positive association of omega-6 fatty acid with cognition shown in this study contrasts with the “common belief” that increasing dietary intake of these fatty acids enhances inflammation, but agreed the association is “plausible.”

She said it’s “essential” to determine “the underlying mechanisms that regulate the diverse features of inflammation and sort out the processes that protect from neuronal damage and those that contribute towards it.”

She noted the ratio of omega-6 to omega-3 is about 15:1 in the present day Western diet, as opposed to a 1:1 ratio in diets of the past. Omega-3 fatty acids are found in fish oil supplements and fatty fish like mackerel and salmon, while cereal, grains, and vegetable oil are sources of omega-6.

Attaining a measure of balance of fatty acids in the diet may be a “prudent approach,” said Dr. Rebello. “Substituting some meat entrées with fatty fish and polyunsaturated vegetable oils with monounsaturated fats such as olive oil are small changes that are likely to garner adherence.”

Dr. Rebello noted that the study used NHANES food intake data, which rely on participant self-report and so may not be accurate.

The study received funding from the MOE (Ministry of Education in China) Project of Humanities and Social Sciences and the Research Startup Fund of Southwest University. Dr. McIntyre has received research grant support from CIHR/GACD/Chinese National Natural Research Foundation and speaker/consultation fees from Lundbeck, Janssen, Purdue, Pfizer, Otsuka, Takeda, Neurocrine, Sunovion, Bausch Health, Novo Nordisk, Kris, Sanofi, Eisai, Intra-Cellular, NewBridge Pharmaceuticals, and AbbVie. He is a CEO of Braxia Scientific Corp.

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

Heart disease. Cancer. Diabetes. Dementia.

Researchers spend billions of dollars every year trying to eradicate these medical scourges.

Yet even if we discover cures to these and all other chronic conditions, it won’t change our ultimate prognosis: death.

“That’s because you haven’t stopped aging,” says Jay Olshansky, PhD, a professor of epidemiology and biostatistics at the University of Illinois at Chicago School of Public Health.

But what if we could? What if we are trying to extend longevity in the wrong way? Instead of focusing on diseases, should we take aim at aging itself?

Some scientists think so. Fueled in part by a billion dollars of investor money, they are attempting to reverse-engineer your molecular biological clock. Their goal? To eliminate not merely diseases that kill people, but to prevent death itself. 
 

Hacking the code for immortality

Aubrey de Grey, PhD, a biomedical gerontologist, has drawn wide attention for his belief that the first person who will live to be 1,000 years old is already among us. 

He believes there’s no cap on how long we can live, depending on what medicines we develop in the future.

“The whole idea is that there would not be a limit on how long we can keep people healthy,” Dr. de Grey says. He’s the chief science officer and co-founder of the SENS Research Foundation, which funds research on how to put the brakes on aging.

Dr. De Grey’s view, in theory, isn’t so far-fetched.

Scientists have studied the immortal jellyfish, Turritopsis dohrnii. It’s the only animal that can cheat death by reverting from adulthood back to its polyp stage when threatened with danger or starvation.

Other clues to possible eternal life also may exist underwater. Certain marine clams can live more than 500 years. And lobsters stock a seemingly limitless supply of a youthful enzyme that has some scientists wondering if the crustacean, under the best conditions, just might live forever.

Among humans, researchers have been studying “super-agers” – people who not only live exceptionally long, but also do so without many of the chronic diseases that plague their peers. That’s even though they share some of the same bad habits as everyone else.

“They are making it past the age of 80 with their minds completely intact. That’s what’s so unusual,” Dr. Olshansky says. The rest of their bodies are doing better than those of average 80-year-olds, too.

People who reached ages 95 to 112 got cancer, heart disease, diabetes, osteoporosis, and stroke up to 24 years later than those with average lifespans, data show. Figuring out why might pave the way for targeted gene therapy to mimic the DNA of these nonagenarians and centenarians.

“There’s likely to be secrets contained within their genome that are eventually discovered that will help us develop therapeutic interventions to mimic the effects of decelerated aging,” Dr. Olshansky says.

Treating aging this way may offer a bigger payoff than targeting individual diseases. That’s because even if you manage to dodge any illnesses, there’s ultimately no escaping old age.

“Longevity is a side effect of health,” Dr. de Grey says. “If we can keep people healthy, then their likelihood of dying is reduced.”
 

Aging as a preventable condition

In 2015, Michael Cantor was prescribed metformin for prediabetes. Once that was under control, his doctor said Mr. Cantor could quit the drug. But Mr. Cantor had heard about studies testing it as an anti-aging drug. The 62-year-old Connecticut-based attorney asked if he could stay on it. A year ago Cantor’s wife, Shari, who is mayor of West Hartford, Conn., started to take metformin, too.

“I read the articles, they made a lot of sense to me, and with the number of people that have been taking this drug worldwide for decades, I felt like there was nothing to lose,” he says.

The couple can’t say if their daily doses have led to any changes in how they look or feel. After all, they’re taking the pills not to treat current ailments but to prevent ones in the future.

They may have answers soon. Nir Barzilai, MD, director of the National Institutes of Health’s Nathan Shock Centers of Excellence in the Basic Biology of Aging, is leading a study that hopes to prove aging is a preventable health condition. The TAME (Targeting Aging with Metformin) study is designed to do this by demonstrating that metformin, a cheap and widely prescribed pill for diabetes, may also be an anti-aging elixir.

The TAME trial is currently in phase III – typically the final step of research into any treatment before drugmakers can apply for FDA approval.

Earlier studies found that people with type 2 diabetes who take metformin have lower death rates from any cause, compared to peers who don’t take the drug. Metformin also seems to help curb the incidence of age-related diseases, including heart disease, dementia, and Alzheimer›s. It also may lower the risk of many types of cancer as well as raise the chances of survival. Observations made since the beginning of the COVID-19 pandemic suggest that people who get the virus while taking metformin are less likely to land in the hospital or die from it.

It’s not clear exactly how metformin works to do all that. The compound was originally derived from Galega officinalis, also known as goat’s rue, a perennial plant used as medicine since medieval times.

Dr. Barzilai says he hopes to prove that aging is a preventable condition.

“If the results are what they think they will be, the whole world could go on metformin and extend life for everybody – extend your good quality of life,” Dr. Barzilai says. “That’s what we all want. Every extra year that we could get where we’re still vigorous and vital would be amazing.”

Long life versus healthy life

Some researchers argue that only the “healthspan” – the period of life free of illness – is worth extending. Of course, a healthy lifestyle can add years to most people’s lives and actually improve cellular aging. Some of the biggest payoffs come from quitting or never smoking, logging more than 5½ hours of physical activity per week, and keeping a normal weight.

Drugs may be able to do that as well by interrupting common markers of aging, including telomere length, inflammation, oxidative stress, and slower cell metabolism.

“You don’t have to target all of these hallmarks to get improvement” in healthspans, says Dr. Barzilai, who also is director of the Institute for Aging Research at the Albert Einstein College of Medicine in the Bronx and scientific director of the American Federation for Aging Research.

“If you target one, you show benefit in the others.”

The medical term for growing old is senescence. Buffeted by DNA damage and stresses, your cells deteriorate and eventually stop multiplying, but don’t die.

That slowdown may have big consequences for your health. Your genes become more likely to get mutations, which can pave the way for cancer. Mitochondria, which produce energy in the cell, struggle to fuel your body. That can damage cells and cause chronic inflammation, which plays a part in diabetes, arthritis, ulcerative colitis, and many other diseases.

One major hallmark of aging is the growing stockpile of these senescent cells. Damaged cells become deactivated as a way to protect your body from harmful or uncontrolled cell division. But like the rotten apple that spoils the whole bunch, senescent cells encourage their neighbors to turn dysfunctional, too. They also emit proteins that trigger inflammation. Your body naturally removes these dormant cells. But older immune systems have a harder time cleaning up, so the senescent cells are more likely to hang around.

Flushing out this accumulated debris may be one way to avert aging, some experts say.

Dr. De Grey also believes that could be done with drugs.

“These therapies would actually repair [cellular] damage,” he says. “They’ll eliminate damage from the body by resetting or turning back the clock.”

James Kirkland, MD, PhD, of the Mayo Clinic, is one researcher exploring this theory. He gave a mixture of the cancer drug dasatinib and a plant pigment called quercetin to people with diabetic kidney disease. Quercetin is an antioxidant that gives grapes, tomatoes, and other fruits and vegetables their flavor.

A small phase I clinical trial showed that the dasatinib-quercetin combination got rid of senescent cells in the tissues of people with the disease.

The researchers don’t know yet if the results will translate into prolonged youth. They also don’t know how high a dosage is needed and what long-term problems the treatment might cause. People with chronic leukemia take dasatinib for years with few serious ill effects.

In another recent study, scientists used oxygen therapy to tackle senescent cells. Thirty-five adults ages 64 and older received oxygen therapy in a pressurized chamber. After 60 daily sessions, they showed a decrease in senescent cells and improvement in the length of DNA segments called telomeres. Shortened segments of telomeres are thought to be another marker of aging.

Researchers are also looking to the gene-editing technology CRISPR for anti-aging treatments, but the testing is only in mice so far.

Dr. Barzilai hopes that if the metformin trial succeeds, it will open the floodgates to a wave of new drugs that can stop or reverse human aging. Some of the major players in this field include Juvenescence, AgeX Therapeutics, LyGenesis, and Life Biosciences, which Dr. Barzilai founded.

“Until aging is seen as preventable, health plans won’t have to pay for this type of treatment,” he says. And if health plans won’t cover aging, pharmaceutical companies have little incentive to invest in drug development.

That may be the only thing standing between humans and unprecedented lifespans. The Census Bureau projects that Americans born in 2060 should live an average of 85.6 years, up from 78.7 years in 2018. Dr. De Grey’s prediction tops that mark by a factor of about 50. He believes that the life expectancy for someone born in 2100 may well be 5,000 years.

Dr. Barzilai, for his part, has a prediction that’s seemingly more modest.

“We die at 80. Getting an additional 35 years is relatively low-hanging fruit,” he says. “But I don’t believe that is a fixed limit.”

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

Heart disease. Cancer. Diabetes. Dementia.

Researchers spend billions of dollars every year trying to eradicate these medical scourges.

Yet even if we discover cures to these and all other chronic conditions, it won’t change our ultimate prognosis: death.

“That’s because you haven’t stopped aging,” says Jay Olshansky, PhD, a professor of epidemiology and biostatistics at the University of Illinois at Chicago School of Public Health.

But what if we could? What if we are trying to extend longevity in the wrong way? Instead of focusing on diseases, should we take aim at aging itself?

Some scientists think so. Fueled in part by a billion dollars of investor money, they are attempting to reverse-engineer your molecular biological clock. Their goal? To eliminate not merely diseases that kill people, but to prevent death itself. 
 

Hacking the code for immortality

Aubrey de Grey, PhD, a biomedical gerontologist, has drawn wide attention for his belief that the first person who will live to be 1,000 years old is already among us. 

He believes there’s no cap on how long we can live, depending on what medicines we develop in the future.

“The whole idea is that there would not be a limit on how long we can keep people healthy,” Dr. de Grey says. He’s the chief science officer and co-founder of the SENS Research Foundation, which funds research on how to put the brakes on aging.

Dr. De Grey’s view, in theory, isn’t so far-fetched.

Scientists have studied the immortal jellyfish, Turritopsis dohrnii. It’s the only animal that can cheat death by reverting from adulthood back to its polyp stage when threatened with danger or starvation.

Other clues to possible eternal life also may exist underwater. Certain marine clams can live more than 500 years. And lobsters stock a seemingly limitless supply of a youthful enzyme that has some scientists wondering if the crustacean, under the best conditions, just might live forever.

Among humans, researchers have been studying “super-agers” – people who not only live exceptionally long, but also do so without many of the chronic diseases that plague their peers. That’s even though they share some of the same bad habits as everyone else.

“They are making it past the age of 80 with their minds completely intact. That’s what’s so unusual,” Dr. Olshansky says. The rest of their bodies are doing better than those of average 80-year-olds, too.

People who reached ages 95 to 112 got cancer, heart disease, diabetes, osteoporosis, and stroke up to 24 years later than those with average lifespans, data show. Figuring out why might pave the way for targeted gene therapy to mimic the DNA of these nonagenarians and centenarians.

“There’s likely to be secrets contained within their genome that are eventually discovered that will help us develop therapeutic interventions to mimic the effects of decelerated aging,” Dr. Olshansky says.

Treating aging this way may offer a bigger payoff than targeting individual diseases. That’s because even if you manage to dodge any illnesses, there’s ultimately no escaping old age.

“Longevity is a side effect of health,” Dr. de Grey says. “If we can keep people healthy, then their likelihood of dying is reduced.”
 

Aging as a preventable condition

In 2015, Michael Cantor was prescribed metformin for prediabetes. Once that was under control, his doctor said Mr. Cantor could quit the drug. But Mr. Cantor had heard about studies testing it as an anti-aging drug. The 62-year-old Connecticut-based attorney asked if he could stay on it. A year ago Cantor’s wife, Shari, who is mayor of West Hartford, Conn., started to take metformin, too.

“I read the articles, they made a lot of sense to me, and with the number of people that have been taking this drug worldwide for decades, I felt like there was nothing to lose,” he says.

The couple can’t say if their daily doses have led to any changes in how they look or feel. After all, they’re taking the pills not to treat current ailments but to prevent ones in the future.

They may have answers soon. Nir Barzilai, MD, director of the National Institutes of Health’s Nathan Shock Centers of Excellence in the Basic Biology of Aging, is leading a study that hopes to prove aging is a preventable health condition. The TAME (Targeting Aging with Metformin) study is designed to do this by demonstrating that metformin, a cheap and widely prescribed pill for diabetes, may also be an anti-aging elixir.

The TAME trial is currently in phase III – typically the final step of research into any treatment before drugmakers can apply for FDA approval.

Earlier studies found that people with type 2 diabetes who take metformin have lower death rates from any cause, compared to peers who don’t take the drug. Metformin also seems to help curb the incidence of age-related diseases, including heart disease, dementia, and Alzheimer›s. It also may lower the risk of many types of cancer as well as raise the chances of survival. Observations made since the beginning of the COVID-19 pandemic suggest that people who get the virus while taking metformin are less likely to land in the hospital or die from it.

It’s not clear exactly how metformin works to do all that. The compound was originally derived from Galega officinalis, also known as goat’s rue, a perennial plant used as medicine since medieval times.

Dr. Barzilai says he hopes to prove that aging is a preventable condition.

“If the results are what they think they will be, the whole world could go on metformin and extend life for everybody – extend your good quality of life,” Dr. Barzilai says. “That’s what we all want. Every extra year that we could get where we’re still vigorous and vital would be amazing.”

Long life versus healthy life

Some researchers argue that only the “healthspan” – the period of life free of illness – is worth extending. Of course, a healthy lifestyle can add years to most people’s lives and actually improve cellular aging. Some of the biggest payoffs come from quitting or never smoking, logging more than 5½ hours of physical activity per week, and keeping a normal weight.

Drugs may be able to do that as well by interrupting common markers of aging, including telomere length, inflammation, oxidative stress, and slower cell metabolism.

“You don’t have to target all of these hallmarks to get improvement” in healthspans, says Dr. Barzilai, who also is director of the Institute for Aging Research at the Albert Einstein College of Medicine in the Bronx and scientific director of the American Federation for Aging Research.

“If you target one, you show benefit in the others.”

The medical term for growing old is senescence. Buffeted by DNA damage and stresses, your cells deteriorate and eventually stop multiplying, but don’t die.

That slowdown may have big consequences for your health. Your genes become more likely to get mutations, which can pave the way for cancer. Mitochondria, which produce energy in the cell, struggle to fuel your body. That can damage cells and cause chronic inflammation, which plays a part in diabetes, arthritis, ulcerative colitis, and many other diseases.

One major hallmark of aging is the growing stockpile of these senescent cells. Damaged cells become deactivated as a way to protect your body from harmful or uncontrolled cell division. But like the rotten apple that spoils the whole bunch, senescent cells encourage their neighbors to turn dysfunctional, too. They also emit proteins that trigger inflammation. Your body naturally removes these dormant cells. But older immune systems have a harder time cleaning up, so the senescent cells are more likely to hang around.

Flushing out this accumulated debris may be one way to avert aging, some experts say.

Dr. De Grey also believes that could be done with drugs.

“These therapies would actually repair [cellular] damage,” he says. “They’ll eliminate damage from the body by resetting or turning back the clock.”

James Kirkland, MD, PhD, of the Mayo Clinic, is one researcher exploring this theory. He gave a mixture of the cancer drug dasatinib and a plant pigment called quercetin to people with diabetic kidney disease. Quercetin is an antioxidant that gives grapes, tomatoes, and other fruits and vegetables their flavor.

A small phase I clinical trial showed that the dasatinib-quercetin combination got rid of senescent cells in the tissues of people with the disease.

The researchers don’t know yet if the results will translate into prolonged youth. They also don’t know how high a dosage is needed and what long-term problems the treatment might cause. People with chronic leukemia take dasatinib for years with few serious ill effects.

In another recent study, scientists used oxygen therapy to tackle senescent cells. Thirty-five adults ages 64 and older received oxygen therapy in a pressurized chamber. After 60 daily sessions, they showed a decrease in senescent cells and improvement in the length of DNA segments called telomeres. Shortened segments of telomeres are thought to be another marker of aging.

Researchers are also looking to the gene-editing technology CRISPR for anti-aging treatments, but the testing is only in mice so far.

Dr. Barzilai hopes that if the metformin trial succeeds, it will open the floodgates to a wave of new drugs that can stop or reverse human aging. Some of the major players in this field include Juvenescence, AgeX Therapeutics, LyGenesis, and Life Biosciences, which Dr. Barzilai founded.

“Until aging is seen as preventable, health plans won’t have to pay for this type of treatment,” he says. And if health plans won’t cover aging, pharmaceutical companies have little incentive to invest in drug development.

That may be the only thing standing between humans and unprecedented lifespans. The Census Bureau projects that Americans born in 2060 should live an average of 85.6 years, up from 78.7 years in 2018. Dr. De Grey’s prediction tops that mark by a factor of about 50. He believes that the life expectancy for someone born in 2100 may well be 5,000 years.

Dr. Barzilai, for his part, has a prediction that’s seemingly more modest.

“We die at 80. Getting an additional 35 years is relatively low-hanging fruit,” he says. “But I don’t believe that is a fixed limit.”

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

Heart disease. Cancer. Diabetes. Dementia.

Researchers spend billions of dollars every year trying to eradicate these medical scourges.

Yet even if we discover cures to these and all other chronic conditions, it won’t change our ultimate prognosis: death.

“That’s because you haven’t stopped aging,” says Jay Olshansky, PhD, a professor of epidemiology and biostatistics at the University of Illinois at Chicago School of Public Health.

But what if we could? What if we are trying to extend longevity in the wrong way? Instead of focusing on diseases, should we take aim at aging itself?

Some scientists think so. Fueled in part by a billion dollars of investor money, they are attempting to reverse-engineer your molecular biological clock. Their goal? To eliminate not merely diseases that kill people, but to prevent death itself. 
 

Hacking the code for immortality

Aubrey de Grey, PhD, a biomedical gerontologist, has drawn wide attention for his belief that the first person who will live to be 1,000 years old is already among us. 

He believes there’s no cap on how long we can live, depending on what medicines we develop in the future.

“The whole idea is that there would not be a limit on how long we can keep people healthy,” Dr. de Grey says. He’s the chief science officer and co-founder of the SENS Research Foundation, which funds research on how to put the brakes on aging.

Dr. De Grey’s view, in theory, isn’t so far-fetched.

Scientists have studied the immortal jellyfish, Turritopsis dohrnii. It’s the only animal that can cheat death by reverting from adulthood back to its polyp stage when threatened with danger or starvation.

Other clues to possible eternal life also may exist underwater. Certain marine clams can live more than 500 years. And lobsters stock a seemingly limitless supply of a youthful enzyme that has some scientists wondering if the crustacean, under the best conditions, just might live forever.

Among humans, researchers have been studying “super-agers” – people who not only live exceptionally long, but also do so without many of the chronic diseases that plague their peers. That’s even though they share some of the same bad habits as everyone else.

“They are making it past the age of 80 with their minds completely intact. That’s what’s so unusual,” Dr. Olshansky says. The rest of their bodies are doing better than those of average 80-year-olds, too.

People who reached ages 95 to 112 got cancer, heart disease, diabetes, osteoporosis, and stroke up to 24 years later than those with average lifespans, data show. Figuring out why might pave the way for targeted gene therapy to mimic the DNA of these nonagenarians and centenarians.

“There’s likely to be secrets contained within their genome that are eventually discovered that will help us develop therapeutic interventions to mimic the effects of decelerated aging,” Dr. Olshansky says.

Treating aging this way may offer a bigger payoff than targeting individual diseases. That’s because even if you manage to dodge any illnesses, there’s ultimately no escaping old age.

“Longevity is a side effect of health,” Dr. de Grey says. “If we can keep people healthy, then their likelihood of dying is reduced.”
 

Aging as a preventable condition

In 2015, Michael Cantor was prescribed metformin for prediabetes. Once that was under control, his doctor said Mr. Cantor could quit the drug. But Mr. Cantor had heard about studies testing it as an anti-aging drug. The 62-year-old Connecticut-based attorney asked if he could stay on it. A year ago Cantor’s wife, Shari, who is mayor of West Hartford, Conn., started to take metformin, too.

“I read the articles, they made a lot of sense to me, and with the number of people that have been taking this drug worldwide for decades, I felt like there was nothing to lose,” he says.

The couple can’t say if their daily doses have led to any changes in how they look or feel. After all, they’re taking the pills not to treat current ailments but to prevent ones in the future.

They may have answers soon. Nir Barzilai, MD, director of the National Institutes of Health’s Nathan Shock Centers of Excellence in the Basic Biology of Aging, is leading a study that hopes to prove aging is a preventable health condition. The TAME (Targeting Aging with Metformin) study is designed to do this by demonstrating that metformin, a cheap and widely prescribed pill for diabetes, may also be an anti-aging elixir.

The TAME trial is currently in phase III – typically the final step of research into any treatment before drugmakers can apply for FDA approval.

Earlier studies found that people with type 2 diabetes who take metformin have lower death rates from any cause, compared to peers who don’t take the drug. Metformin also seems to help curb the incidence of age-related diseases, including heart disease, dementia, and Alzheimer›s. It also may lower the risk of many types of cancer as well as raise the chances of survival. Observations made since the beginning of the COVID-19 pandemic suggest that people who get the virus while taking metformin are less likely to land in the hospital or die from it.

It’s not clear exactly how metformin works to do all that. The compound was originally derived from Galega officinalis, also known as goat’s rue, a perennial plant used as medicine since medieval times.

Dr. Barzilai says he hopes to prove that aging is a preventable condition.

“If the results are what they think they will be, the whole world could go on metformin and extend life for everybody – extend your good quality of life,” Dr. Barzilai says. “That’s what we all want. Every extra year that we could get where we’re still vigorous and vital would be amazing.”

Long life versus healthy life

Some researchers argue that only the “healthspan” – the period of life free of illness – is worth extending. Of course, a healthy lifestyle can add years to most people’s lives and actually improve cellular aging. Some of the biggest payoffs come from quitting or never smoking, logging more than 5½ hours of physical activity per week, and keeping a normal weight.

Drugs may be able to do that as well by interrupting common markers of aging, including telomere length, inflammation, oxidative stress, and slower cell metabolism.

“You don’t have to target all of these hallmarks to get improvement” in healthspans, says Dr. Barzilai, who also is director of the Institute for Aging Research at the Albert Einstein College of Medicine in the Bronx and scientific director of the American Federation for Aging Research.

“If you target one, you show benefit in the others.”

The medical term for growing old is senescence. Buffeted by DNA damage and stresses, your cells deteriorate and eventually stop multiplying, but don’t die.

That slowdown may have big consequences for your health. Your genes become more likely to get mutations, which can pave the way for cancer. Mitochondria, which produce energy in the cell, struggle to fuel your body. That can damage cells and cause chronic inflammation, which plays a part in diabetes, arthritis, ulcerative colitis, and many other diseases.

One major hallmark of aging is the growing stockpile of these senescent cells. Damaged cells become deactivated as a way to protect your body from harmful or uncontrolled cell division. But like the rotten apple that spoils the whole bunch, senescent cells encourage their neighbors to turn dysfunctional, too. They also emit proteins that trigger inflammation. Your body naturally removes these dormant cells. But older immune systems have a harder time cleaning up, so the senescent cells are more likely to hang around.

Flushing out this accumulated debris may be one way to avert aging, some experts say.

Dr. De Grey also believes that could be done with drugs.

“These therapies would actually repair [cellular] damage,” he says. “They’ll eliminate damage from the body by resetting or turning back the clock.”

James Kirkland, MD, PhD, of the Mayo Clinic, is one researcher exploring this theory. He gave a mixture of the cancer drug dasatinib and a plant pigment called quercetin to people with diabetic kidney disease. Quercetin is an antioxidant that gives grapes, tomatoes, and other fruits and vegetables their flavor.

A small phase I clinical trial showed that the dasatinib-quercetin combination got rid of senescent cells in the tissues of people with the disease.

The researchers don’t know yet if the results will translate into prolonged youth. They also don’t know how high a dosage is needed and what long-term problems the treatment might cause. People with chronic leukemia take dasatinib for years with few serious ill effects.

In another recent study, scientists used oxygen therapy to tackle senescent cells. Thirty-five adults ages 64 and older received oxygen therapy in a pressurized chamber. After 60 daily sessions, they showed a decrease in senescent cells and improvement in the length of DNA segments called telomeres. Shortened segments of telomeres are thought to be another marker of aging.

Researchers are also looking to the gene-editing technology CRISPR for anti-aging treatments, but the testing is only in mice so far.

Dr. Barzilai hopes that if the metformin trial succeeds, it will open the floodgates to a wave of new drugs that can stop or reverse human aging. Some of the major players in this field include Juvenescence, AgeX Therapeutics, LyGenesis, and Life Biosciences, which Dr. Barzilai founded.

“Until aging is seen as preventable, health plans won’t have to pay for this type of treatment,” he says. And if health plans won’t cover aging, pharmaceutical companies have little incentive to invest in drug development.

That may be the only thing standing between humans and unprecedented lifespans. The Census Bureau projects that Americans born in 2060 should live an average of 85.6 years, up from 78.7 years in 2018. Dr. De Grey’s prediction tops that mark by a factor of about 50. He believes that the life expectancy for someone born in 2100 may well be 5,000 years.

Dr. Barzilai, for his part, has a prediction that’s seemingly more modest.

“We die at 80. Getting an additional 35 years is relatively low-hanging fruit,” he says. “But I don’t believe that is a fixed limit.”

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

Americans who have received a COVID-19 booster shot are 97 times less likely to die from the coronavirus than those who aren’t vaccinated, according to a new update from the CDC.

In addition, fully vaccinated Americans — meaning those with up to two doses, but no booster — are 14 times less likely to die from COVID-19 than unvaccinated people.

“These data confirm that vaccination and boosting continues to protect against severe illness and hospitalization, even during the Omicron surge,” Rochelle Walensky, MD, director of the CDC, said during a briefing by the White House COVID-19 Response Team.

“If you are not up to date on your COVID-19 vaccinations, you have not optimized your protection against severe disease and death, and you should get vaccinated and boosted if you are eligible,” she said.

Dr. Walensky presented the latest numbers on Feb. 2 based on reports from 25 jurisdictions in early December. The number of average weekly deaths for those who were unvaccinated was 9.7 per 100,000 people, as compared with 0.7 of those who were vaccinated and 0.1 of those who had received a booster.

“The data are really stunningly obvious why a booster is really very important,” Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, said during the briefing.

Dr. Fauci also encouraged vaccination for those who are pregnant and couples who may want to conceive in the near feature. He highlighted two recent studies that found vaccination in either partner didn’t affect fertility, including in vitro fertilization.

Meanwhile, fertility fell temporarily among men who were infected with the coronavirus. Couples were 18% less likely to conceive if the male partner had contracted the coronavirus within 60 days before a menstrual cycle.

“New data adds to previous studies that indicate that COVID-19 vaccination does not negatively impact fertility,” Dr. Fauci said. “Vaccination is recommended for people who are trying to get pregnant now or might become pregnant in the future, as well as their partners.”

About 80% of eligible Americans have received at least one vaccine dose, and 68% are fully vaccinated, according to the latest CDC data. About 51% of those who are eligible for a booster dose have received one.

The FDA could authorize the Pfizer vaccine for children under age 5 later this month. When that happens, about 18 million children will qualify for a shot, Jeff Zients, coordinator of the White House COVID-19 Response Team, said during the briefing. The Biden administration is already working on distribution plans for the shot for young kids, he added.

“We’ll be ready to start getting shots in arms soon after FDA and CDC make their decisions,” he said.

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

Americans who have received a COVID-19 booster shot are 97 times less likely to die from the coronavirus than those who aren’t vaccinated, according to a new update from the CDC.

In addition, fully vaccinated Americans — meaning those with up to two doses, but no booster — are 14 times less likely to die from COVID-19 than unvaccinated people.

“These data confirm that vaccination and boosting continues to protect against severe illness and hospitalization, even during the Omicron surge,” Rochelle Walensky, MD, director of the CDC, said during a briefing by the White House COVID-19 Response Team.

“If you are not up to date on your COVID-19 vaccinations, you have not optimized your protection against severe disease and death, and you should get vaccinated and boosted if you are eligible,” she said.

Dr. Walensky presented the latest numbers on Feb. 2 based on reports from 25 jurisdictions in early December. The number of average weekly deaths for those who were unvaccinated was 9.7 per 100,000 people, as compared with 0.7 of those who were vaccinated and 0.1 of those who had received a booster.

“The data are really stunningly obvious why a booster is really very important,” Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, said during the briefing.

Dr. Fauci also encouraged vaccination for those who are pregnant and couples who may want to conceive in the near feature. He highlighted two recent studies that found vaccination in either partner didn’t affect fertility, including in vitro fertilization.

Meanwhile, fertility fell temporarily among men who were infected with the coronavirus. Couples were 18% less likely to conceive if the male partner had contracted the coronavirus within 60 days before a menstrual cycle.

“New data adds to previous studies that indicate that COVID-19 vaccination does not negatively impact fertility,” Dr. Fauci said. “Vaccination is recommended for people who are trying to get pregnant now or might become pregnant in the future, as well as their partners.”

About 80% of eligible Americans have received at least one vaccine dose, and 68% are fully vaccinated, according to the latest CDC data. About 51% of those who are eligible for a booster dose have received one.

The FDA could authorize the Pfizer vaccine for children under age 5 later this month. When that happens, about 18 million children will qualify for a shot, Jeff Zients, coordinator of the White House COVID-19 Response Team, said during the briefing. The Biden administration is already working on distribution plans for the shot for young kids, he added.

“We’ll be ready to start getting shots in arms soon after FDA and CDC make their decisions,” he said.

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

Americans who have received a COVID-19 booster shot are 97 times less likely to die from the coronavirus than those who aren’t vaccinated, according to a new update from the CDC.

In addition, fully vaccinated Americans — meaning those with up to two doses, but no booster — are 14 times less likely to die from COVID-19 than unvaccinated people.

“These data confirm that vaccination and boosting continues to protect against severe illness and hospitalization, even during the Omicron surge,” Rochelle Walensky, MD, director of the CDC, said during a briefing by the White House COVID-19 Response Team.

“If you are not up to date on your COVID-19 vaccinations, you have not optimized your protection against severe disease and death, and you should get vaccinated and boosted if you are eligible,” she said.

Dr. Walensky presented the latest numbers on Feb. 2 based on reports from 25 jurisdictions in early December. The number of average weekly deaths for those who were unvaccinated was 9.7 per 100,000 people, as compared with 0.7 of those who were vaccinated and 0.1 of those who had received a booster.

“The data are really stunningly obvious why a booster is really very important,” Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, said during the briefing.

Dr. Fauci also encouraged vaccination for those who are pregnant and couples who may want to conceive in the near feature. He highlighted two recent studies that found vaccination in either partner didn’t affect fertility, including in vitro fertilization.

Meanwhile, fertility fell temporarily among men who were infected with the coronavirus. Couples were 18% less likely to conceive if the male partner had contracted the coronavirus within 60 days before a menstrual cycle.

“New data adds to previous studies that indicate that COVID-19 vaccination does not negatively impact fertility,” Dr. Fauci said. “Vaccination is recommended for people who are trying to get pregnant now or might become pregnant in the future, as well as their partners.”

About 80% of eligible Americans have received at least one vaccine dose, and 68% are fully vaccinated, according to the latest CDC data. About 51% of those who are eligible for a booster dose have received one.

The FDA could authorize the Pfizer vaccine for children under age 5 later this month. When that happens, about 18 million children will qualify for a shot, Jeff Zients, coordinator of the White House COVID-19 Response Team, said during the briefing. The Biden administration is already working on distribution plans for the shot for young kids, he added.

“We’ll be ready to start getting shots in arms soon after FDA and CDC make their decisions,” he said.

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

Boys exposed to at least 2 hours a day of screen time by 1 year of age were significantly more likely to have an autism spectrum disorder (ASD) diagnosis at 3 years, based on data from more than 80,000 children.

The World Health Organization and the American Academy of Pediatrics recommend against any screen time for infants up to 1 year of age and 18 months of age, respectively, wrote Megumi Kushima, MA, of the University of Yamanashi (Japan), and colleagues on behalf of the Japan Environment and Children’s Study Group.

The extent to which screen time duration in infancy is associated with subsequent ASD diagnosis remains unclear, the researchers said. The ongoing COVID-19 pandemic has increased screen time among children worldwide, which makes an examination of the impact of screen time on children’s health an important public health issue.

In a study published in JAMA Pediatrics, the researchers recruited pregnant women between 2011 and 2014; data were analyzed in December 2020. The final study population included 84,030 mother-child pairs. The primary exposure of screen time at 1 year of age was assessed by questionnaire, in which mothers were asked to report their number of hours they let their child watch TV or DVDs daily. Responses were none (no screen time), less than 1 hour, 1 hour or more but less than 2 hours, 2 hours or more but less than 4 hours, and 4 hours or more.

The primary outcome was ASD diagnosis at 3 years of age, and mothers were asked via questionnaire whether their 3-year-old had been diagnosed with ASD from age 2.

The study was conducted by the Japan Environment and Children’s Study Group at 15 regional centers across Japan.

Overall, 330 children had received an ASD diagnosis at age 3 years, a prevalence of 0.4%. Of these, 251 (76%) were boys, and 79 (24%) were girls. Independent of ASD, the most common response for screen time was less than 1 hour, which was reported by 27,707 mothers. The proportion of children with ASD at age 3 increased as screen time at age 1 increased, the percentages were 5.8%, 22.3%, 30.2%, and 31.7% for children with no screen time, less than 1 hour, 1 to less than 2 hours, and 2 to less than 4 hours, respectively. The percentage of children with ASD diagnoses who had 4 hours or more of daily screen time was 10%.

Logistic regression analysis showed that longer screen time at age 1 year was significantly associated with higher odds of ASD at 3 years in boys, but not in girls. The researchers controlled for variables including maternal maltreatment and children’s predisposition to ASD. Among boys, the adjusted odds ratios for screen times of less than 1 hour, 1 hour to less than 2 hours, 2 hours to less than 4 hours, and more than 4 hours were 1.38, 2.16, 3.48, and 3.02, respectively.

Screen time at age 3 years was not associated with ASD diagnosis at age 3 years, potentially “because the association with environmental factors on brain development varies with age,” the researchers noted.

The study findings were limited by several factors including the reliance on parental reports of screen time and potential for reporting bias, the researchers noted. Other limitations included the possible missed diagnoses of mild ASD cases at 3 years, and the inability to consider variables such as childcare environment, living conditions, diseases, genetics, and disabilities.

However, the results were strengthened by the large study population and examination of screen time in early childhood, they said. More research is needed to examine other factors that contribute to the association between ASD and screen time, but given the rapid increase in device use in children, “it is necessary to review its health effects on infants and control excessive screen time.”
 

Strong study, but some gaps appear

The study is strong in many respects, Karalyn Kinsella, MD, a pediatrician in private practice in Cheshire, Conn., said in an interview.

However, “what I am not sure they addressed is that children on the spectrum are often not entertained by basic toys and may be hard to manage behaviorally,” Dr. Kinsella said. Consequently, parents may be more inclined to offer screen time as a way to pacify children with behavioral difficulties. “Parents also may see that their children are happier interacting with devices, so they may be more apt to let them continue with screen time.We know screen time is not good for the developing brain, however; I worry that the message from this study is that screen time causes autism in boys.

“What I would have liked to know from the parents who allowed more screen time was why they were offering it,” Dr. Kinsella said. “Was it because their child was difficult behaviorally or because that is the one place that they seemed to have satisfaction? To me, that would indicate the reverse hypothesis.” That said, the study findings “remind us to counsel families about screen time, especially in the age of COVID-19. Kids are home much longer than usual, which ultimately leads to more screen time.”

The study was funded by the Japanese Ministry of Environment. The researchers had no financial conflicts to disclose. Dr. Kinsella had no financial conflicts to disclose, but serves as a member of the Pediatric News editorial advisory board.

Boys exposed to at least 2 hours a day of screen time by 1 year of age were significantly more likely to have an autism spectrum disorder (ASD) diagnosis at 3 years, based on data from more than 80,000 children.

The World Health Organization and the American Academy of Pediatrics recommend against any screen time for infants up to 1 year of age and 18 months of age, respectively, wrote Megumi Kushima, MA, of the University of Yamanashi (Japan), and colleagues on behalf of the Japan Environment and Children’s Study Group.

The extent to which screen time duration in infancy is associated with subsequent ASD diagnosis remains unclear, the researchers said. The ongoing COVID-19 pandemic has increased screen time among children worldwide, which makes an examination of the impact of screen time on children’s health an important public health issue.

In a study published in JAMA Pediatrics, the researchers recruited pregnant women between 2011 and 2014; data were analyzed in December 2020. The final study population included 84,030 mother-child pairs. The primary exposure of screen time at 1 year of age was assessed by questionnaire, in which mothers were asked to report their number of hours they let their child watch TV or DVDs daily. Responses were none (no screen time), less than 1 hour, 1 hour or more but less than 2 hours, 2 hours or more but less than 4 hours, and 4 hours or more.

The primary outcome was ASD diagnosis at 3 years of age, and mothers were asked via questionnaire whether their 3-year-old had been diagnosed with ASD from age 2.

The study was conducted by the Japan Environment and Children’s Study Group at 15 regional centers across Japan.

Overall, 330 children had received an ASD diagnosis at age 3 years, a prevalence of 0.4%. Of these, 251 (76%) were boys, and 79 (24%) were girls. Independent of ASD, the most common response for screen time was less than 1 hour, which was reported by 27,707 mothers. The proportion of children with ASD at age 3 increased as screen time at age 1 increased, the percentages were 5.8%, 22.3%, 30.2%, and 31.7% for children with no screen time, less than 1 hour, 1 to less than 2 hours, and 2 to less than 4 hours, respectively. The percentage of children with ASD diagnoses who had 4 hours or more of daily screen time was 10%.

Logistic regression analysis showed that longer screen time at age 1 year was significantly associated with higher odds of ASD at 3 years in boys, but not in girls. The researchers controlled for variables including maternal maltreatment and children’s predisposition to ASD. Among boys, the adjusted odds ratios for screen times of less than 1 hour, 1 hour to less than 2 hours, 2 hours to less than 4 hours, and more than 4 hours were 1.38, 2.16, 3.48, and 3.02, respectively.

Screen time at age 3 years was not associated with ASD diagnosis at age 3 years, potentially “because the association with environmental factors on brain development varies with age,” the researchers noted.

The study findings were limited by several factors including the reliance on parental reports of screen time and potential for reporting bias, the researchers noted. Other limitations included the possible missed diagnoses of mild ASD cases at 3 years, and the inability to consider variables such as childcare environment, living conditions, diseases, genetics, and disabilities.

However, the results were strengthened by the large study population and examination of screen time in early childhood, they said. More research is needed to examine other factors that contribute to the association between ASD and screen time, but given the rapid increase in device use in children, “it is necessary to review its health effects on infants and control excessive screen time.”
 

Strong study, but some gaps appear

The study is strong in many respects, Karalyn Kinsella, MD, a pediatrician in private practice in Cheshire, Conn., said in an interview.

However, “what I am not sure they addressed is that children on the spectrum are often not entertained by basic toys and may be hard to manage behaviorally,” Dr. Kinsella said. Consequently, parents may be more inclined to offer screen time as a way to pacify children with behavioral difficulties. “Parents also may see that their children are happier interacting with devices, so they may be more apt to let them continue with screen time.We know screen time is not good for the developing brain, however; I worry that the message from this study is that screen time causes autism in boys.

“What I would have liked to know from the parents who allowed more screen time was why they were offering it,” Dr. Kinsella said. “Was it because their child was difficult behaviorally or because that is the one place that they seemed to have satisfaction? To me, that would indicate the reverse hypothesis.” That said, the study findings “remind us to counsel families about screen time, especially in the age of COVID-19. Kids are home much longer than usual, which ultimately leads to more screen time.”

The study was funded by the Japanese Ministry of Environment. The researchers had no financial conflicts to disclose. Dr. Kinsella had no financial conflicts to disclose, but serves as a member of the Pediatric News editorial advisory board.

Boys exposed to at least 2 hours a day of screen time by 1 year of age were significantly more likely to have an autism spectrum disorder (ASD) diagnosis at 3 years, based on data from more than 80,000 children.

The World Health Organization and the American Academy of Pediatrics recommend against any screen time for infants up to 1 year of age and 18 months of age, respectively, wrote Megumi Kushima, MA, of the University of Yamanashi (Japan), and colleagues on behalf of the Japan Environment and Children’s Study Group.

The extent to which screen time duration in infancy is associated with subsequent ASD diagnosis remains unclear, the researchers said. The ongoing COVID-19 pandemic has increased screen time among children worldwide, which makes an examination of the impact of screen time on children’s health an important public health issue.

In a study published in JAMA Pediatrics, the researchers recruited pregnant women between 2011 and 2014; data were analyzed in December 2020. The final study population included 84,030 mother-child pairs. The primary exposure of screen time at 1 year of age was assessed by questionnaire, in which mothers were asked to report their number of hours they let their child watch TV or DVDs daily. Responses were none (no screen time), less than 1 hour, 1 hour or more but less than 2 hours, 2 hours or more but less than 4 hours, and 4 hours or more.

The primary outcome was ASD diagnosis at 3 years of age, and mothers were asked via questionnaire whether their 3-year-old had been diagnosed with ASD from age 2.

The study was conducted by the Japan Environment and Children’s Study Group at 15 regional centers across Japan.

Overall, 330 children had received an ASD diagnosis at age 3 years, a prevalence of 0.4%. Of these, 251 (76%) were boys, and 79 (24%) were girls. Independent of ASD, the most common response for screen time was less than 1 hour, which was reported by 27,707 mothers. The proportion of children with ASD at age 3 increased as screen time at age 1 increased, the percentages were 5.8%, 22.3%, 30.2%, and 31.7% for children with no screen time, less than 1 hour, 1 to less than 2 hours, and 2 to less than 4 hours, respectively. The percentage of children with ASD diagnoses who had 4 hours or more of daily screen time was 10%.

Logistic regression analysis showed that longer screen time at age 1 year was significantly associated with higher odds of ASD at 3 years in boys, but not in girls. The researchers controlled for variables including maternal maltreatment and children’s predisposition to ASD. Among boys, the adjusted odds ratios for screen times of less than 1 hour, 1 hour to less than 2 hours, 2 hours to less than 4 hours, and more than 4 hours were 1.38, 2.16, 3.48, and 3.02, respectively.

Screen time at age 3 years was not associated with ASD diagnosis at age 3 years, potentially “because the association with environmental factors on brain development varies with age,” the researchers noted.

The study findings were limited by several factors including the reliance on parental reports of screen time and potential for reporting bias, the researchers noted. Other limitations included the possible missed diagnoses of mild ASD cases at 3 years, and the inability to consider variables such as childcare environment, living conditions, diseases, genetics, and disabilities.

However, the results were strengthened by the large study population and examination of screen time in early childhood, they said. More research is needed to examine other factors that contribute to the association between ASD and screen time, but given the rapid increase in device use in children, “it is necessary to review its health effects on infants and control excessive screen time.”
 

Strong study, but some gaps appear

The study is strong in many respects, Karalyn Kinsella, MD, a pediatrician in private practice in Cheshire, Conn., said in an interview.

However, “what I am not sure they addressed is that children on the spectrum are often not entertained by basic toys and may be hard to manage behaviorally,” Dr. Kinsella said. Consequently, parents may be more inclined to offer screen time as a way to pacify children with behavioral difficulties. “Parents also may see that their children are happier interacting with devices, so they may be more apt to let them continue with screen time.We know screen time is not good for the developing brain, however; I worry that the message from this study is that screen time causes autism in boys.

“What I would have liked to know from the parents who allowed more screen time was why they were offering it,” Dr. Kinsella said. “Was it because their child was difficult behaviorally or because that is the one place that they seemed to have satisfaction? To me, that would indicate the reverse hypothesis.” That said, the study findings “remind us to counsel families about screen time, especially in the age of COVID-19. Kids are home much longer than usual, which ultimately leads to more screen time.”

The study was funded by the Japanese Ministry of Environment. The researchers had no financial conflicts to disclose. Dr. Kinsella had no financial conflicts to disclose, but serves as a member of the Pediatric News editorial advisory board.

A subcutaneous antibody combination of casirivimab and imdevimab given to asymptomatic people who tested positive for SARS-CoV-2 significantly lowered the incidence of symptomatic COVID-19 over 28 days, new research shows.

Results of the study by Meagan P. O’Brien, MD, from Regeneron Pharmaceuticals and one of the study’s funders, and coauthors were published online Jan. 14, 2022, in an original investigation in JAMA.

The results suggest new potential for monoclonal antibodies currently used for postexposure prophylaxis and treatment of symptomatic SARS-CoV-2. It has not been clear whether monoclonal antibodies can benefit people with asymptomatic SARS-CoV-2 infection.

The trial included 314 participants (mean age, 41 years; 51.6% women). Of the participants, 310 (99.7%) completed the efficacy assessment period, and 204 were asymptomatic and tested negative at baseline and were included in the primary efficacy analysis.

The subcutaneous combination of casirivimab and imdevimab, 1,200 mg (600 mg each), significantly prevented progression to symptomatic disease (29/100 [29.0%] vs. 44/104 [42.3%] with placebo; odds ratio, 0.54 [95% confidence interval, 0.30-0.97]; P = .04; absolute risk difference, −13.3% [95% CI, −26.3% to −0.3%]).

These results were part of a randomized, double-blind, placebo-controlled, phase 3 trial of close household contacts of a SARS-CoV-2–infected person at 112 sites in the United States, Romania, and Moldova. They were enrolled between July 13, 2020, and Jan. 28, 2021; follow-up ended March 11, 2021.

Asymptomatic people at least 12 years old were eligible if identified within 96 hours of index case positive test collection and were randomly assigned 1:1 to receive one dose of subcutaneous casirivimab and imdevimab (n = 158), or placebo (n = 156).

COVID-19 vaccination was prohibited before enrollment but was allowed after completing the 28-day efficacy assessment period.
 

Caution warranted

In an accompanying editorial, however, Jonathan Z. Li, MD, Brigham and Women’s Hospital and Harvard Medical School, both in Boston, and Rajesh T. Gandhi, MD, Massachusetts General Hospital, Boston, and Harvard Medical School, urged caution in interpreting the results.

They wrote that, although monoclonal antibodies are generally used in individuals at high risk for severe COVID-19, this study population was less vulnerable, with an average age of 41, and 30% had no risk for the disease.

“Of the remainder, the most common risk factor was being overweight (which confers less risk than other factors),” the editorialists wrote.

They pointed out, as did the study authors, that enrollment came before the emergence of the Delta and Omicron variants, and that both casirivimab and imdevimab maintain their activity against Delta but not against Omicron.

“While prevention of symptomatic infection has benefits,” they wrote, “the primary goal of monoclonal antibody therapy is to prevent progression to severe disease; however, this trial was unable to assess this outcome because there were only three hospitalizations (all in the placebo group). Also, this study was conducted prior to widespread COVID-19 vaccination; whether monoclonal antibodies have the same benefit in people who have breakthrough infection after vaccination is not known.”

The editorialists highlighted the subcutaneous delivery in this study.

They wrote that Dr. O’Brien and coauthors provide evidence that subcutaneous administration is effective in infected individuals. “However, high serum monoclonal antibody levels are achieved more quickly after intravenous administration than following subcutaneous injection; it is unknown whether intravenous administration might have led to even greater efficacy for individuals with asymptomatic SARS-CoV-2 infection.”

The authors of the study also add that, despite efforts to recruit non-White participants, relatively few non-White people were enrolled. Additionally, few adolescents were enrolled.

The sample size was also relatively small, they acknowledge, because of a study design in which the infection status of asymptomatic participants was not confirmed at inclusion.

Several of the authors are employees/stockholders of Regeneron, and have a patent pending, which has been licensed and is receiving royalties. The study was supported by Regeneron and F. Hoffmann–La Roche. This trial was conducted jointly with the National Institute of Allergy and Infectious Diseases and the National Institutes of Health. The CoVPN (COVID-19 Prevention Network) is supported by cooperative agreement awards from the NIAID and NIH.

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

A subcutaneous antibody combination of casirivimab and imdevimab given to asymptomatic people who tested positive for SARS-CoV-2 significantly lowered the incidence of symptomatic COVID-19 over 28 days, new research shows.

Results of the study by Meagan P. O’Brien, MD, from Regeneron Pharmaceuticals and one of the study’s funders, and coauthors were published online Jan. 14, 2022, in an original investigation in JAMA.

The results suggest new potential for monoclonal antibodies currently used for postexposure prophylaxis and treatment of symptomatic SARS-CoV-2. It has not been clear whether monoclonal antibodies can benefit people with asymptomatic SARS-CoV-2 infection.

The trial included 314 participants (mean age, 41 years; 51.6% women). Of the participants, 310 (99.7%) completed the efficacy assessment period, and 204 were asymptomatic and tested negative at baseline and were included in the primary efficacy analysis.

The subcutaneous combination of casirivimab and imdevimab, 1,200 mg (600 mg each), significantly prevented progression to symptomatic disease (29/100 [29.0%] vs. 44/104 [42.3%] with placebo; odds ratio, 0.54 [95% confidence interval, 0.30-0.97]; P = .04; absolute risk difference, −13.3% [95% CI, −26.3% to −0.3%]).

These results were part of a randomized, double-blind, placebo-controlled, phase 3 trial of close household contacts of a SARS-CoV-2–infected person at 112 sites in the United States, Romania, and Moldova. They were enrolled between July 13, 2020, and Jan. 28, 2021; follow-up ended March 11, 2021.

Asymptomatic people at least 12 years old were eligible if identified within 96 hours of index case positive test collection and were randomly assigned 1:1 to receive one dose of subcutaneous casirivimab and imdevimab (n = 158), or placebo (n = 156).

COVID-19 vaccination was prohibited before enrollment but was allowed after completing the 28-day efficacy assessment period.
 

Caution warranted

In an accompanying editorial, however, Jonathan Z. Li, MD, Brigham and Women’s Hospital and Harvard Medical School, both in Boston, and Rajesh T. Gandhi, MD, Massachusetts General Hospital, Boston, and Harvard Medical School, urged caution in interpreting the results.

They wrote that, although monoclonal antibodies are generally used in individuals at high risk for severe COVID-19, this study population was less vulnerable, with an average age of 41, and 30% had no risk for the disease.

“Of the remainder, the most common risk factor was being overweight (which confers less risk than other factors),” the editorialists wrote.

They pointed out, as did the study authors, that enrollment came before the emergence of the Delta and Omicron variants, and that both casirivimab and imdevimab maintain their activity against Delta but not against Omicron.

“While prevention of symptomatic infection has benefits,” they wrote, “the primary goal of monoclonal antibody therapy is to prevent progression to severe disease; however, this trial was unable to assess this outcome because there were only three hospitalizations (all in the placebo group). Also, this study was conducted prior to widespread COVID-19 vaccination; whether monoclonal antibodies have the same benefit in people who have breakthrough infection after vaccination is not known.”

The editorialists highlighted the subcutaneous delivery in this study.

They wrote that Dr. O’Brien and coauthors provide evidence that subcutaneous administration is effective in infected individuals. “However, high serum monoclonal antibody levels are achieved more quickly after intravenous administration than following subcutaneous injection; it is unknown whether intravenous administration might have led to even greater efficacy for individuals with asymptomatic SARS-CoV-2 infection.”

The authors of the study also add that, despite efforts to recruit non-White participants, relatively few non-White people were enrolled. Additionally, few adolescents were enrolled.

The sample size was also relatively small, they acknowledge, because of a study design in which the infection status of asymptomatic participants was not confirmed at inclusion.

Several of the authors are employees/stockholders of Regeneron, and have a patent pending, which has been licensed and is receiving royalties. The study was supported by Regeneron and F. Hoffmann–La Roche. This trial was conducted jointly with the National Institute of Allergy and Infectious Diseases and the National Institutes of Health. The CoVPN (COVID-19 Prevention Network) is supported by cooperative agreement awards from the NIAID and NIH.

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

A subcutaneous antibody combination of casirivimab and imdevimab given to asymptomatic people who tested positive for SARS-CoV-2 significantly lowered the incidence of symptomatic COVID-19 over 28 days, new research shows.

Results of the study by Meagan P. O’Brien, MD, from Regeneron Pharmaceuticals and one of the study’s funders, and coauthors were published online Jan. 14, 2022, in an original investigation in JAMA.

The results suggest new potential for monoclonal antibodies currently used for postexposure prophylaxis and treatment of symptomatic SARS-CoV-2. It has not been clear whether monoclonal antibodies can benefit people with asymptomatic SARS-CoV-2 infection.

The trial included 314 participants (mean age, 41 years; 51.6% women). Of the participants, 310 (99.7%) completed the efficacy assessment period, and 204 were asymptomatic and tested negative at baseline and were included in the primary efficacy analysis.

The subcutaneous combination of casirivimab and imdevimab, 1,200 mg (600 mg each), significantly prevented progression to symptomatic disease (29/100 [29.0%] vs. 44/104 [42.3%] with placebo; odds ratio, 0.54 [95% confidence interval, 0.30-0.97]; P = .04; absolute risk difference, −13.3% [95% CI, −26.3% to −0.3%]).

These results were part of a randomized, double-blind, placebo-controlled, phase 3 trial of close household contacts of a SARS-CoV-2–infected person at 112 sites in the United States, Romania, and Moldova. They were enrolled between July 13, 2020, and Jan. 28, 2021; follow-up ended March 11, 2021.

Asymptomatic people at least 12 years old were eligible if identified within 96 hours of index case positive test collection and were randomly assigned 1:1 to receive one dose of subcutaneous casirivimab and imdevimab (n = 158), or placebo (n = 156).

COVID-19 vaccination was prohibited before enrollment but was allowed after completing the 28-day efficacy assessment period.
 

Caution warranted

In an accompanying editorial, however, Jonathan Z. Li, MD, Brigham and Women’s Hospital and Harvard Medical School, both in Boston, and Rajesh T. Gandhi, MD, Massachusetts General Hospital, Boston, and Harvard Medical School, urged caution in interpreting the results.

They wrote that, although monoclonal antibodies are generally used in individuals at high risk for severe COVID-19, this study population was less vulnerable, with an average age of 41, and 30% had no risk for the disease.

“Of the remainder, the most common risk factor was being overweight (which confers less risk than other factors),” the editorialists wrote.

They pointed out, as did the study authors, that enrollment came before the emergence of the Delta and Omicron variants, and that both casirivimab and imdevimab maintain their activity against Delta but not against Omicron.

“While prevention of symptomatic infection has benefits,” they wrote, “the primary goal of monoclonal antibody therapy is to prevent progression to severe disease; however, this trial was unable to assess this outcome because there were only three hospitalizations (all in the placebo group). Also, this study was conducted prior to widespread COVID-19 vaccination; whether monoclonal antibodies have the same benefit in people who have breakthrough infection after vaccination is not known.”

The editorialists highlighted the subcutaneous delivery in this study.

They wrote that Dr. O’Brien and coauthors provide evidence that subcutaneous administration is effective in infected individuals. “However, high serum monoclonal antibody levels are achieved more quickly after intravenous administration than following subcutaneous injection; it is unknown whether intravenous administration might have led to even greater efficacy for individuals with asymptomatic SARS-CoV-2 infection.”

The authors of the study also add that, despite efforts to recruit non-White participants, relatively few non-White people were enrolled. Additionally, few adolescents were enrolled.

The sample size was also relatively small, they acknowledge, because of a study design in which the infection status of asymptomatic participants was not confirmed at inclusion.

Several of the authors are employees/stockholders of Regeneron, and have a patent pending, which has been licensed and is receiving royalties. The study was supported by Regeneron and F. Hoffmann–La Roche. This trial was conducted jointly with the National Institute of Allergy and Infectious Diseases and the National Institutes of Health. The CoVPN (COVID-19 Prevention Network) is supported by cooperative agreement awards from the NIAID and NIH.

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

The world’s most valuable mouse

You’ve heard of Mighty Mouse. Now say hello to the world’s newest mouse superhero, Crypto-Mouse! After being bitten by a radioactive cryptocurrency investor, Crypto-Mouse can tap directly into the power of the blockchain itself, allowing it to perform incredible, death-defying feats of strength!

We’re going to stop right there before Crypto-Mouse gains entry into the Marvel cinematic universe. Let’s rewind to the beginning, because that’s precisely where this crazy scheme is at. In late January, a new decentralized autonomous organization, BitMouseDAO, launched to enormous … -ly little fanfare, according to Vice. Two investors as of Jan. 31. But what they lack in money they make up for in sheer ambition.

Clker-Free-Vector-Images/Pixabay

BitMouseDAO’s $100 million dollar idea is to genetically engineer mice to carry bitcoin, the first cryptocurrency and one of the most valuable. This isn’t as crazy an idea as it sounds since DNA can be modified to store information, potentially even bitcoin information. Their plan is to create a private bitcoin wallet, which will be stored in the mouse DNA, and purchase online bitcoin to store in this wallet.

BitMouseDAO, being a “collection of artists,” plans to partner with a lab to translate its private key into a specific DNA sequence to be encoded into the mice during fertilization; or, if that doesn’t work, inject them with a harmless virus that carries the key.

Since these are artists, their ultimate plan is to use their bitcoin mice to make NFTs (scratch that off your cryptocurrency bingo card) and auction them off to people. Or, as Vice put it, BitMouseDAO essentially plans to send preserved dead mice to people. Artistic dead mice! Artistic dead mice worth millions! Maybe. Even BitMouseDAO admits bitcoin could be worthless by the time the project gets off the ground.

If this all sounds completely insane, that’s because it is. But it also sounds crazy enough to work. Now, if you’ll excuse us, we’re off to write a screenplay about a scrappy group of high-tech thieves who steal a group of genetically altered bitcoin mice to sell for millions, only to keep them as their adorable pets. Trust us Hollywood, it’ll make millions!
 

Alcoholic monkeys vs. the future of feces

Which is more important, the journey or the destination? Science is all about the destination, yes? Solving the problem, saving a life, expanding horizons. That’s science. Or is it? The scientific method is a process, so does that make it a journey?

Amandad/Pixabay

For us, today’s journey begins at the University of Iowa, where investigators are trying to reduce alcohol consumption. A worthy goal, and they seem to have made some progress by targeting a liver hormone called fibroblast growth factor 21 (FGF21). But we’re more interested in the process right now, so bring on the alcoholic monkeys. And no, that’s not a death metal/reggae fusion band. Should be, though.

“The vervet monkey population is [composed] of alcohol avoiders, moderate alcohol drinkers, and a group of heavy drinkers,” Matthew Potthoff, PhD, and associates wrote in Cell Metabolism. When this particular bunch of heavy-drinking vervets were given FGF21, they consumed 50% less alcohol than did vehicle-treated controls, so mission accomplished.

Maybe it could be a breakfast cereal. Who wouldn’t enjoy a bowl of alcoholic monkeys in the morning?

And after breakfast, you might be ready for a digitized bowel movement, courtesy of researchers at University of California, San Diego. They’re studying ulcerative colitis (UC) by examining the gut microbiome, and their “most useful biological sample is patient stool,” according to a written statement from the university.

“Once we had all the technology to digitize the stool, the question was, is this going to tell us what’s happening in these patients? The answer turned out to be yes,” co-senior author Rob Knight, PhD, said in the statement. “Digitizing fecal material is the future.” The road to UC treatment, in other words, is paved with digital stool.

About 40% of the UC patients had elevated protease levels, and their high-protease feces were then transplanted into germ-free mice, which subsequently developed colitis and were successfully treated with protease inhibitors. And that is our final destination.

As our revered founder and mentor, Josephine Lotmevich, used to say, an alcoholic monkey in the hand is worth a number 2 in the bush.
 

Raise a glass to delinquency

You wouldn’t think that a glass of water could lead to a life of crime, but a recent study suggests just that.

PxHere

Children exposed to lead in their drinking water during their early years had a 21% higher risk of delinquency after the age of 14 years and a 38% higher risk of having a record for a serious complaint, Jackie MacDonald Gibson and associates said in a statement on Eurekalert.

Data for the study came from Wake County, N.C., which includes rural areas, wealthy exurban developments, and predominantly Black communities. The investigators compared the blood lead levels for children tested between 1998 and 2011 with juvenile delinquency reports of the same children from the N.C. Department of Public Safety.

The main culprit, they found, was well water. Blood lead levels were 11% higher in the children whose water came from private wells, compared with children using community water. About 13% of U.S. households rely on private wells, which are not regulated under the Safe Drinking Water Act, for their water supply.

The researchers said there is an urgent need for better drinking-water solutions in communities that rely on well water, whether it be through subsidized home filtration or infrastructure redevelopment.

An earlier study had estimated that preventing just one child from entering the adult criminal justice system would save $1.3 to $1.5 million in 1997 dollars. That’s about $2.2 to $2.5 million dollars today!

If you do the math, it’s not hard to see what’s cheaper (and healthier) in the long run.
 

A ‘dirty’ scam

Another one? This is just getting sad. You’ve probably heard of muds and clays being good for the skin and maybe you’ve gone to a spa and sat in a mud bath, but would you believe it if someone told you that mud can cure all your ailments? No? Neither would we. Senatorial candidate Beto O’Rourke was definitely someone who brought this strange treatment to light, but it seems like this is something that has been going on for years, even before the pandemic.

Nandan/Pixahive

A company called Black Oxygen Organics (BOO) was selling “magic dirt” for $110 per 4-ounce package. It claimed the dirt was high in fulvic acid and humic acid, which are good for many things. They were, however, literally getting this mud from bogs with landfills nearby, Mel magazine reported.

That doesn’t sound appealing at all, but wait, there’s more. People were eating, drinking, bathing, and feeding their families this sludge in hopes that they would be cured of their ailments. A lot of people jumped aboard the magic dirt train when the pandemic arose, but it quickly became clear that this mud was not as helpful as BOO claimed it to be.

“We began to receive inquiries and calls on our website with people having problems and issues. Ultimately, we sent the products out for independent testing, and then when that came back and showed that there were toxic heavy metals [lead, arsenic, and cadmium among them] at an unsafe level, that’s when we knew we had to act,” Atlanta-based attorney Matt Wetherington, who filed a federal lawsuit against BOO, told Mel.

After a very complicated series of events involving an expose by NBC, product recalls, extortion claims, and grassroots activism, BOO was shut down by both the Canadian and U.S. governments.

As always, please listen only to health care professionals when you wish to use natural remedies for illnesses and ailments.

The world’s most valuable mouse

You’ve heard of Mighty Mouse. Now say hello to the world’s newest mouse superhero, Crypto-Mouse! After being bitten by a radioactive cryptocurrency investor, Crypto-Mouse can tap directly into the power of the blockchain itself, allowing it to perform incredible, death-defying feats of strength!

We’re going to stop right there before Crypto-Mouse gains entry into the Marvel cinematic universe. Let’s rewind to the beginning, because that’s precisely where this crazy scheme is at. In late January, a new decentralized autonomous organization, BitMouseDAO, launched to enormous … -ly little fanfare, according to Vice. Two investors as of Jan. 31. But what they lack in money they make up for in sheer ambition.

Clker-Free-Vector-Images/Pixabay

BitMouseDAO’s $100 million dollar idea is to genetically engineer mice to carry bitcoin, the first cryptocurrency and one of the most valuable. This isn’t as crazy an idea as it sounds since DNA can be modified to store information, potentially even bitcoin information. Their plan is to create a private bitcoin wallet, which will be stored in the mouse DNA, and purchase online bitcoin to store in this wallet.

BitMouseDAO, being a “collection of artists,” plans to partner with a lab to translate its private key into a specific DNA sequence to be encoded into the mice during fertilization; or, if that doesn’t work, inject them with a harmless virus that carries the key.

Since these are artists, their ultimate plan is to use their bitcoin mice to make NFTs (scratch that off your cryptocurrency bingo card) and auction them off to people. Or, as Vice put it, BitMouseDAO essentially plans to send preserved dead mice to people. Artistic dead mice! Artistic dead mice worth millions! Maybe. Even BitMouseDAO admits bitcoin could be worthless by the time the project gets off the ground.

If this all sounds completely insane, that’s because it is. But it also sounds crazy enough to work. Now, if you’ll excuse us, we’re off to write a screenplay about a scrappy group of high-tech thieves who steal a group of genetically altered bitcoin mice to sell for millions, only to keep them as their adorable pets. Trust us Hollywood, it’ll make millions!
 

Alcoholic monkeys vs. the future of feces

Which is more important, the journey or the destination? Science is all about the destination, yes? Solving the problem, saving a life, expanding horizons. That’s science. Or is it? The scientific method is a process, so does that make it a journey?

Amandad/Pixabay

For us, today’s journey begins at the University of Iowa, where investigators are trying to reduce alcohol consumption. A worthy goal, and they seem to have made some progress by targeting a liver hormone called fibroblast growth factor 21 (FGF21). But we’re more interested in the process right now, so bring on the alcoholic monkeys. And no, that’s not a death metal/reggae fusion band. Should be, though.

“The vervet monkey population is [composed] of alcohol avoiders, moderate alcohol drinkers, and a group of heavy drinkers,” Matthew Potthoff, PhD, and associates wrote in Cell Metabolism. When this particular bunch of heavy-drinking vervets were given FGF21, they consumed 50% less alcohol than did vehicle-treated controls, so mission accomplished.

Maybe it could be a breakfast cereal. Who wouldn’t enjoy a bowl of alcoholic monkeys in the morning?

And after breakfast, you might be ready for a digitized bowel movement, courtesy of researchers at University of California, San Diego. They’re studying ulcerative colitis (UC) by examining the gut microbiome, and their “most useful biological sample is patient stool,” according to a written statement from the university.

“Once we had all the technology to digitize the stool, the question was, is this going to tell us what’s happening in these patients? The answer turned out to be yes,” co-senior author Rob Knight, PhD, said in the statement. “Digitizing fecal material is the future.” The road to UC treatment, in other words, is paved with digital stool.

About 40% of the UC patients had elevated protease levels, and their high-protease feces were then transplanted into germ-free mice, which subsequently developed colitis and were successfully treated with protease inhibitors. And that is our final destination.

As our revered founder and mentor, Josephine Lotmevich, used to say, an alcoholic monkey in the hand is worth a number 2 in the bush.
 

Raise a glass to delinquency

You wouldn’t think that a glass of water could lead to a life of crime, but a recent study suggests just that.

PxHere

Children exposed to lead in their drinking water during their early years had a 21% higher risk of delinquency after the age of 14 years and a 38% higher risk of having a record for a serious complaint, Jackie MacDonald Gibson and associates said in a statement on Eurekalert.

Data for the study came from Wake County, N.C., which includes rural areas, wealthy exurban developments, and predominantly Black communities. The investigators compared the blood lead levels for children tested between 1998 and 2011 with juvenile delinquency reports of the same children from the N.C. Department of Public Safety.

The main culprit, they found, was well water. Blood lead levels were 11% higher in the children whose water came from private wells, compared with children using community water. About 13% of U.S. households rely on private wells, which are not regulated under the Safe Drinking Water Act, for their water supply.

The researchers said there is an urgent need for better drinking-water solutions in communities that rely on well water, whether it be through subsidized home filtration or infrastructure redevelopment.

An earlier study had estimated that preventing just one child from entering the adult criminal justice system would save $1.3 to $1.5 million in 1997 dollars. That’s about $2.2 to $2.5 million dollars today!

If you do the math, it’s not hard to see what’s cheaper (and healthier) in the long run.
 

A ‘dirty’ scam

Another one? This is just getting sad. You’ve probably heard of muds and clays being good for the skin and maybe you’ve gone to a spa and sat in a mud bath, but would you believe it if someone told you that mud can cure all your ailments? No? Neither would we. Senatorial candidate Beto O’Rourke was definitely someone who brought this strange treatment to light, but it seems like this is something that has been going on for years, even before the pandemic.

Nandan/Pixahive

A company called Black Oxygen Organics (BOO) was selling “magic dirt” for $110 per 4-ounce package. It claimed the dirt was high in fulvic acid and humic acid, which are good for many things. They were, however, literally getting this mud from bogs with landfills nearby, Mel magazine reported.

That doesn’t sound appealing at all, but wait, there’s more. People were eating, drinking, bathing, and feeding their families this sludge in hopes that they would be cured of their ailments. A lot of people jumped aboard the magic dirt train when the pandemic arose, but it quickly became clear that this mud was not as helpful as BOO claimed it to be.

“We began to receive inquiries and calls on our website with people having problems and issues. Ultimately, we sent the products out for independent testing, and then when that came back and showed that there were toxic heavy metals [lead, arsenic, and cadmium among them] at an unsafe level, that’s when we knew we had to act,” Atlanta-based attorney Matt Wetherington, who filed a federal lawsuit against BOO, told Mel.

After a very complicated series of events involving an expose by NBC, product recalls, extortion claims, and grassroots activism, BOO was shut down by both the Canadian and U.S. governments.

As always, please listen only to health care professionals when you wish to use natural remedies for illnesses and ailments.

The world’s most valuable mouse

You’ve heard of Mighty Mouse. Now say hello to the world’s newest mouse superhero, Crypto-Mouse! After being bitten by a radioactive cryptocurrency investor, Crypto-Mouse can tap directly into the power of the blockchain itself, allowing it to perform incredible, death-defying feats of strength!

We’re going to stop right there before Crypto-Mouse gains entry into the Marvel cinematic universe. Let’s rewind to the beginning, because that’s precisely where this crazy scheme is at. In late January, a new decentralized autonomous organization, BitMouseDAO, launched to enormous … -ly little fanfare, according to Vice. Two investors as of Jan. 31. But what they lack in money they make up for in sheer ambition.

Clker-Free-Vector-Images/Pixabay

BitMouseDAO’s $100 million dollar idea is to genetically engineer mice to carry bitcoin, the first cryptocurrency and one of the most valuable. This isn’t as crazy an idea as it sounds since DNA can be modified to store information, potentially even bitcoin information. Their plan is to create a private bitcoin wallet, which will be stored in the mouse DNA, and purchase online bitcoin to store in this wallet.

BitMouseDAO, being a “collection of artists,” plans to partner with a lab to translate its private key into a specific DNA sequence to be encoded into the mice during fertilization; or, if that doesn’t work, inject them with a harmless virus that carries the key.

Since these are artists, their ultimate plan is to use their bitcoin mice to make NFTs (scratch that off your cryptocurrency bingo card) and auction them off to people. Or, as Vice put it, BitMouseDAO essentially plans to send preserved dead mice to people. Artistic dead mice! Artistic dead mice worth millions! Maybe. Even BitMouseDAO admits bitcoin could be worthless by the time the project gets off the ground.

If this all sounds completely insane, that’s because it is. But it also sounds crazy enough to work. Now, if you’ll excuse us, we’re off to write a screenplay about a scrappy group of high-tech thieves who steal a group of genetically altered bitcoin mice to sell for millions, only to keep them as their adorable pets. Trust us Hollywood, it’ll make millions!
 

Alcoholic monkeys vs. the future of feces

Which is more important, the journey or the destination? Science is all about the destination, yes? Solving the problem, saving a life, expanding horizons. That’s science. Or is it? The scientific method is a process, so does that make it a journey?

Amandad/Pixabay

For us, today’s journey begins at the University of Iowa, where investigators are trying to reduce alcohol consumption. A worthy goal, and they seem to have made some progress by targeting a liver hormone called fibroblast growth factor 21 (FGF21). But we’re more interested in the process right now, so bring on the alcoholic monkeys. And no, that’s not a death metal/reggae fusion band. Should be, though.

“The vervet monkey population is [composed] of alcohol avoiders, moderate alcohol drinkers, and a group of heavy drinkers,” Matthew Potthoff, PhD, and associates wrote in Cell Metabolism. When this particular bunch of heavy-drinking vervets were given FGF21, they consumed 50% less alcohol than did vehicle-treated controls, so mission accomplished.

Maybe it could be a breakfast cereal. Who wouldn’t enjoy a bowl of alcoholic monkeys in the morning?

And after breakfast, you might be ready for a digitized bowel movement, courtesy of researchers at University of California, San Diego. They’re studying ulcerative colitis (UC) by examining the gut microbiome, and their “most useful biological sample is patient stool,” according to a written statement from the university.

“Once we had all the technology to digitize the stool, the question was, is this going to tell us what’s happening in these patients? The answer turned out to be yes,” co-senior author Rob Knight, PhD, said in the statement. “Digitizing fecal material is the future.” The road to UC treatment, in other words, is paved with digital stool.

About 40% of the UC patients had elevated protease levels, and their high-protease feces were then transplanted into germ-free mice, which subsequently developed colitis and were successfully treated with protease inhibitors. And that is our final destination.

As our revered founder and mentor, Josephine Lotmevich, used to say, an alcoholic monkey in the hand is worth a number 2 in the bush.
 

Raise a glass to delinquency

You wouldn’t think that a glass of water could lead to a life of crime, but a recent study suggests just that.

PxHere

Children exposed to lead in their drinking water during their early years had a 21% higher risk of delinquency after the age of 14 years and a 38% higher risk of having a record for a serious complaint, Jackie MacDonald Gibson and associates said in a statement on Eurekalert.

Data for the study came from Wake County, N.C., which includes rural areas, wealthy exurban developments, and predominantly Black communities. The investigators compared the blood lead levels for children tested between 1998 and 2011 with juvenile delinquency reports of the same children from the N.C. Department of Public Safety.

The main culprit, they found, was well water. Blood lead levels were 11% higher in the children whose water came from private wells, compared with children using community water. About 13% of U.S. households rely on private wells, which are not regulated under the Safe Drinking Water Act, for their water supply.

The researchers said there is an urgent need for better drinking-water solutions in communities that rely on well water, whether it be through subsidized home filtration or infrastructure redevelopment.

An earlier study had estimated that preventing just one child from entering the adult criminal justice system would save $1.3 to $1.5 million in 1997 dollars. That’s about $2.2 to $2.5 million dollars today!

If you do the math, it’s not hard to see what’s cheaper (and healthier) in the long run.
 

A ‘dirty’ scam

Another one? This is just getting sad. You’ve probably heard of muds and clays being good for the skin and maybe you’ve gone to a spa and sat in a mud bath, but would you believe it if someone told you that mud can cure all your ailments? No? Neither would we. Senatorial candidate Beto O’Rourke was definitely someone who brought this strange treatment to light, but it seems like this is something that has been going on for years, even before the pandemic.

Nandan/Pixahive

A company called Black Oxygen Organics (BOO) was selling “magic dirt” for $110 per 4-ounce package. It claimed the dirt was high in fulvic acid and humic acid, which are good for many things. They were, however, literally getting this mud from bogs with landfills nearby, Mel magazine reported.

That doesn’t sound appealing at all, but wait, there’s more. People were eating, drinking, bathing, and feeding their families this sludge in hopes that they would be cured of their ailments. A lot of people jumped aboard the magic dirt train when the pandemic arose, but it quickly became clear that this mud was not as helpful as BOO claimed it to be.

“We began to receive inquiries and calls on our website with people having problems and issues. Ultimately, we sent the products out for independent testing, and then when that came back and showed that there were toxic heavy metals [lead, arsenic, and cadmium among them] at an unsafe level, that’s when we knew we had to act,” Atlanta-based attorney Matt Wetherington, who filed a federal lawsuit against BOO, told Mel.

After a very complicated series of events involving an expose by NBC, product recalls, extortion claims, and grassroots activism, BOO was shut down by both the Canadian and U.S. governments.

As always, please listen only to health care professionals when you wish to use natural remedies for illnesses and ailments.

A Florida doctor told his patient her test result would be available in 3-4 days. When the patient didn’t hear back, she called the practice several times, but she didn’t receive a return call. So she filed a complaint against the doctor with the medical board.

When the board investigator interviewed the doctor, the physician said he wasn’t aware the patient had called. But his staff said otherwise. Because the doctor had not been truthful, the board sent him a letter of guidance and required him to attend a training program in ethics.

Miami attorney William J. Spratt Jr., who supplied this anecdote about a former client, said that most complaints are dismissed with no action taken, but some complaints don’t go away because doctors mishandle them.

The following are some common mistakes that physicians make when dealing with a board complaint.
 

1. Not responding to the complaint

The complaint you get from the board – which often comes with a subpoena and a response deadline – usually asks for medical records pertinent to the case.

You can’t disregard the board’s letter, said Doug Brocker, an attorney handling board actions in Raleigh, N.C. “It’s amazing to me that some people just ignore a board complaint. Sometimes it’s because the doctor is just burnt out, which may have gotten the doctor into trouble in the first place.”

If you do not respond to a subpoena, “the board can file a court order holding you in contempt and start taking action on your license,” said Jeff Segal, MD, a neurosurgeon and attorney in Greensboro, N.C. Dr. Segal is CEO of Medical Justice Services, which protects physicians’ reputations associated with malpractice suits and board actions. “Not responding is not much different from agreeing to all of the charges.”
 

2. Not recognizing the seriousness of the complaint

“The biggest mistake is not taking a complaint seriously,” said Linda Stimmel, an attorney at Wilson Elser in Dallas. “Physicians who get a complaint often fire off a brief response stating that the complaint has no merit, without offering any evidence.”

According to Ms. Stimmel, “it’s really important to back up your assertions, such as using excerpts from the medical record, citations of peer-reviewed articles, or a letter of support from a colleague.”

“Weigh your answers carefully, because lack of accuracy will complicate your case,” Mr. Brocker said. “Consult the medical record rather than rely on your memory.”

“Present your version of events, in your own words, because that’s almost always better than the board’s version,” said Dr. Segal.

Even if there was a bad clinical outcome, Dr. Segal said you might point out that the patient was at high risk, or you could show that your clinical outcomes are better than the national average.
 

3. Thinking the board is on your side

You may be lulled into a false sense of security because the physicians on the medical board are your peers, but they can be as tough as any medical malpractice judge, said William P. Sullivan, DO, an emergency physician and attorney in Frankfort, Ill.

As per the National Practitioner Data Bank, physicians are three to four times more likely to incur an adverse board action than make a malpractice payout, Dr. Sullivan said.

Also, although a malpractice lawsuit rarely involves more than a monetary payment, a board action, like a monitoring plan, can restrict your ability to practice medicine. In fact, any kind of board action against you can make it harder to find employment.
 

4. Not being honest or forthcoming

“Lying to the board is the fastest way to turn what would have been a minor infraction into putting your license at risk,” Mr. Brocker said. This can happen when doctors update a medical record to support their version of events.

As per Dr. Sullivan, another way to put your license at risk is to withhold adverse information, which the board can detect by obtaining your application for hospital privileges or for licensure to another state, in which you revealed the adverse information.

Dr. Sullivan also advised against claiming you “always” take a certain precautionary measure. “In reality, we doctors don’t always do what we would like to have done. By saying you always do it when you didn’t, you appear less than truthful to the board, and boards have a hard time with that.”

Similarly, “when doctors don’t want to recognize that they could have handled things better, they tend to dance around the issue,” Mr. Brocker said. “This does not sit well with the board.” Insisting that you did everything right when it’s obvious that you didn’t can lead to harsher sanctions. “The board wants to make sure doctors recognize their mistakes and are willing to learn from them.”
 

5. Providing too much information

You may think that providing a great deal of information strengthens your case, but it can actually weaken it, Mr. Brocker said. Irrelevant information makes your response hard to follow, and it may contain evidence that could prompt another line of inquiry.

“Less is more,” Dr. Segal advised. “Present a coherent argument and keep to the most salient points.” Being concise is also good advice if your complaint proceeds to the board and you have to present your case.

Dr. Segal said the board will stop paying attention to long-winded presentations. He tells his clients to imagine the board is watching a movie. “If your presentation is tedious or hard to follow, you will lose them.”
 

6. Trying to contact the complainant

Complaints are kept anonymous, but in many cases, the doctor has an idea who the complainant was and may try to contact that person. “It’s natural to wonder why a patient would file a complaint against you,” Mr. Brocker said, but if you reach out to the patient to ask why, “it could look like you’re trying to persuade the patient to drop the complaint.”

Doctors who are involved in a practice breakup or a divorce can be victims of false and malicious complaints, but Beth Y. Collis, a partner at the law firm of Dinsmore & Shohl in Columbus, said boards are onto this tactic and usually reject these complaints.

The doctor may be tempted to sue the complainant, but Mr. Brocker said this won’t stop the complaint and could strengthen it. “Most statements to the medical board are protected from defamation lawsuits, and any lawsuit could appear to be intimidation.”
 

7. Simply signing a consent agreement

A small minority of complaints may result in the board taking action against the doctor. Typically, this involves getting the doctor to sign a consent agreement stating that he or she agrees with the board’s decision and its remedy, such as continuing education, a fine, or being placed under another doctor’s supervision.

“When the board sends you a consent agreement, it’s usually about something fairly minor,” Ms. Collis said. “You can make a counteroffer and see if they accept that. But once you enter into the agreement, you waive any right to appeal the board’s decision.”
 

8. Not hiring an attorney

Although some doctors manage to deal with a board complaint on their own, many will need to get an attorney, Mr. Brocker said. “An experienced attorney can help you navigate the board’s process.”

Clients often look for attorneys at the end of the process, when formal charges have already been filed, Mr. Brocker said. At that point, “it’s harder to get things moving in the right direction. You can’t unring the bell.”

Even if you don’t think you need an attorney throughout the case, “it helps to get advice from an attorney at the beginning,” Dr. Segal said. Doctors may think they can’t afford an attorney, but many malpractice carriers pay attorneys’ fees in medical board investigations.

Mr. Brocker advised finding an attorney who is familiar with licensing boards. “Malpractice attorneys may think they can deal with medical boards, but boards are quite different.” For example, “malpractice cases involve an adversarial approach, but licensing boards normally require working collaboratively.”
 

9. Not requesting a hearing

When the board takes action against you, it can be tempting to just accept the allegations and move on with your life, but it may be possible to undo the action, Dr. Sullivan said. “The board still has to prove its allegations, and it may not have a strong case against you.”

In some states, the medical board has to meet a very high standard of proof, Dr. Sullivan said. In Illinois, for example, the board must show “clear and convincing evidence,” while a malpractice plaintiff must only prove that it’s “more likely than not” that a physician violated the standard of care.

A hearing can especially help doctors facing harsh sanctions for minor offenses. For example, in a case handled by the law firm of Ray & Bishop in Newport Beach, Calif., a doctor who was stopped by police while driving home after having wine at a family gathering was found to have a blood alcohol level of 0.11%. Noting that the physician was on call at the time, the Medical Board of California decided to give him 5 years of probation.

Ray & Bishop asked for a judicial hearing to contest the decision. At the hearing, the physician noted that other physicians were also available to take call that night, and an expert stated that the doctor was not an alcohol abuser. The judge ruled that the board’s action was unduly harsh, and the physician received a public reprimand with no further penalties.
 

10. Getting upset with board officials

A board investigator may show up at your office uninvited and ask you to answer some questions, but you aren’t required to answer then and there, said Ms. Collis.

In fact, she noted, it’s never a good idea to let investigators into your office. “They can walk around, look through your records, and find more things to investigate.” For this reason, Ms. Collis makes it a point to schedule meetings with investigators at her office.

When you have to interact with board officials, such as during hearings, expressing anger is a mistake. “Some board members may raise their voices and make untrue assertions about your medical care,” Dr. Sullivan said. “You may wish you could respond in kind, but that will not help you.” Instead, calmly provide studies or guidelines supporting the care you provided.

Taking board investigators to task is also a mistake, Mr. Brocker pointed out. In his words, “investigators have to follow the rules. Getting mad at them will only make your case more difficult. Even if you believe the complaint against you is totally without merit, the process needs to run its course.”

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

A Florida doctor told his patient her test result would be available in 3-4 days. When the patient didn’t hear back, she called the practice several times, but she didn’t receive a return call. So she filed a complaint against the doctor with the medical board.

When the board investigator interviewed the doctor, the physician said he wasn’t aware the patient had called. But his staff said otherwise. Because the doctor had not been truthful, the board sent him a letter of guidance and required him to attend a training program in ethics.

Miami attorney William J. Spratt Jr., who supplied this anecdote about a former client, said that most complaints are dismissed with no action taken, but some complaints don’t go away because doctors mishandle them.

The following are some common mistakes that physicians make when dealing with a board complaint.
 

1. Not responding to the complaint

The complaint you get from the board – which often comes with a subpoena and a response deadline – usually asks for medical records pertinent to the case.

You can’t disregard the board’s letter, said Doug Brocker, an attorney handling board actions in Raleigh, N.C. “It’s amazing to me that some people just ignore a board complaint. Sometimes it’s because the doctor is just burnt out, which may have gotten the doctor into trouble in the first place.”

If you do not respond to a subpoena, “the board can file a court order holding you in contempt and start taking action on your license,” said Jeff Segal, MD, a neurosurgeon and attorney in Greensboro, N.C. Dr. Segal is CEO of Medical Justice Services, which protects physicians’ reputations associated with malpractice suits and board actions. “Not responding is not much different from agreeing to all of the charges.”
 

2. Not recognizing the seriousness of the complaint

“The biggest mistake is not taking a complaint seriously,” said Linda Stimmel, an attorney at Wilson Elser in Dallas. “Physicians who get a complaint often fire off a brief response stating that the complaint has no merit, without offering any evidence.”

According to Ms. Stimmel, “it’s really important to back up your assertions, such as using excerpts from the medical record, citations of peer-reviewed articles, or a letter of support from a colleague.”

“Weigh your answers carefully, because lack of accuracy will complicate your case,” Mr. Brocker said. “Consult the medical record rather than rely on your memory.”

“Present your version of events, in your own words, because that’s almost always better than the board’s version,” said Dr. Segal.

Even if there was a bad clinical outcome, Dr. Segal said you might point out that the patient was at high risk, or you could show that your clinical outcomes are better than the national average.
 

3. Thinking the board is on your side

You may be lulled into a false sense of security because the physicians on the medical board are your peers, but they can be as tough as any medical malpractice judge, said William P. Sullivan, DO, an emergency physician and attorney in Frankfort, Ill.

As per the National Practitioner Data Bank, physicians are three to four times more likely to incur an adverse board action than make a malpractice payout, Dr. Sullivan said.

Also, although a malpractice lawsuit rarely involves more than a monetary payment, a board action, like a monitoring plan, can restrict your ability to practice medicine. In fact, any kind of board action against you can make it harder to find employment.
 

4. Not being honest or forthcoming

“Lying to the board is the fastest way to turn what would have been a minor infraction into putting your license at risk,” Mr. Brocker said. This can happen when doctors update a medical record to support their version of events.

As per Dr. Sullivan, another way to put your license at risk is to withhold adverse information, which the board can detect by obtaining your application for hospital privileges or for licensure to another state, in which you revealed the adverse information.

Dr. Sullivan also advised against claiming you “always” take a certain precautionary measure. “In reality, we doctors don’t always do what we would like to have done. By saying you always do it when you didn’t, you appear less than truthful to the board, and boards have a hard time with that.”

Similarly, “when doctors don’t want to recognize that they could have handled things better, they tend to dance around the issue,” Mr. Brocker said. “This does not sit well with the board.” Insisting that you did everything right when it’s obvious that you didn’t can lead to harsher sanctions. “The board wants to make sure doctors recognize their mistakes and are willing to learn from them.”
 

5. Providing too much information

You may think that providing a great deal of information strengthens your case, but it can actually weaken it, Mr. Brocker said. Irrelevant information makes your response hard to follow, and it may contain evidence that could prompt another line of inquiry.

“Less is more,” Dr. Segal advised. “Present a coherent argument and keep to the most salient points.” Being concise is also good advice if your complaint proceeds to the board and you have to present your case.

Dr. Segal said the board will stop paying attention to long-winded presentations. He tells his clients to imagine the board is watching a movie. “If your presentation is tedious or hard to follow, you will lose them.”
 

6. Trying to contact the complainant

Complaints are kept anonymous, but in many cases, the doctor has an idea who the complainant was and may try to contact that person. “It’s natural to wonder why a patient would file a complaint against you,” Mr. Brocker said, but if you reach out to the patient to ask why, “it could look like you’re trying to persuade the patient to drop the complaint.”

Doctors who are involved in a practice breakup or a divorce can be victims of false and malicious complaints, but Beth Y. Collis, a partner at the law firm of Dinsmore & Shohl in Columbus, said boards are onto this tactic and usually reject these complaints.

The doctor may be tempted to sue the complainant, but Mr. Brocker said this won’t stop the complaint and could strengthen it. “Most statements to the medical board are protected from defamation lawsuits, and any lawsuit could appear to be intimidation.”
 

7. Simply signing a consent agreement

A small minority of complaints may result in the board taking action against the doctor. Typically, this involves getting the doctor to sign a consent agreement stating that he or she agrees with the board’s decision and its remedy, such as continuing education, a fine, or being placed under another doctor’s supervision.

“When the board sends you a consent agreement, it’s usually about something fairly minor,” Ms. Collis said. “You can make a counteroffer and see if they accept that. But once you enter into the agreement, you waive any right to appeal the board’s decision.”
 

8. Not hiring an attorney

Although some doctors manage to deal with a board complaint on their own, many will need to get an attorney, Mr. Brocker said. “An experienced attorney can help you navigate the board’s process.”

Clients often look for attorneys at the end of the process, when formal charges have already been filed, Mr. Brocker said. At that point, “it’s harder to get things moving in the right direction. You can’t unring the bell.”

Even if you don’t think you need an attorney throughout the case, “it helps to get advice from an attorney at the beginning,” Dr. Segal said. Doctors may think they can’t afford an attorney, but many malpractice carriers pay attorneys’ fees in medical board investigations.

Mr. Brocker advised finding an attorney who is familiar with licensing boards. “Malpractice attorneys may think they can deal with medical boards, but boards are quite different.” For example, “malpractice cases involve an adversarial approach, but licensing boards normally require working collaboratively.”
 

9. Not requesting a hearing

When the board takes action against you, it can be tempting to just accept the allegations and move on with your life, but it may be possible to undo the action, Dr. Sullivan said. “The board still has to prove its allegations, and it may not have a strong case against you.”

In some states, the medical board has to meet a very high standard of proof, Dr. Sullivan said. In Illinois, for example, the board must show “clear and convincing evidence,” while a malpractice plaintiff must only prove that it’s “more likely than not” that a physician violated the standard of care.

A hearing can especially help doctors facing harsh sanctions for minor offenses. For example, in a case handled by the law firm of Ray & Bishop in Newport Beach, Calif., a doctor who was stopped by police while driving home after having wine at a family gathering was found to have a blood alcohol level of 0.11%. Noting that the physician was on call at the time, the Medical Board of California decided to give him 5 years of probation.

Ray & Bishop asked for a judicial hearing to contest the decision. At the hearing, the physician noted that other physicians were also available to take call that night, and an expert stated that the doctor was not an alcohol abuser. The judge ruled that the board’s action was unduly harsh, and the physician received a public reprimand with no further penalties.
 

10. Getting upset with board officials

A board investigator may show up at your office uninvited and ask you to answer some questions, but you aren’t required to answer then and there, said Ms. Collis.

In fact, she noted, it’s never a good idea to let investigators into your office. “They can walk around, look through your records, and find more things to investigate.” For this reason, Ms. Collis makes it a point to schedule meetings with investigators at her office.

When you have to interact with board officials, such as during hearings, expressing anger is a mistake. “Some board members may raise their voices and make untrue assertions about your medical care,” Dr. Sullivan said. “You may wish you could respond in kind, but that will not help you.” Instead, calmly provide studies or guidelines supporting the care you provided.

Taking board investigators to task is also a mistake, Mr. Brocker pointed out. In his words, “investigators have to follow the rules. Getting mad at them will only make your case more difficult. Even if you believe the complaint against you is totally without merit, the process needs to run its course.”

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

A Florida doctor told his patient her test result would be available in 3-4 days. When the patient didn’t hear back, she called the practice several times, but she didn’t receive a return call. So she filed a complaint against the doctor with the medical board.

When the board investigator interviewed the doctor, the physician said he wasn’t aware the patient had called. But his staff said otherwise. Because the doctor had not been truthful, the board sent him a letter of guidance and required him to attend a training program in ethics.

Miami attorney William J. Spratt Jr., who supplied this anecdote about a former client, said that most complaints are dismissed with no action taken, but some complaints don’t go away because doctors mishandle them.

The following are some common mistakes that physicians make when dealing with a board complaint.
 

1. Not responding to the complaint

The complaint you get from the board – which often comes with a subpoena and a response deadline – usually asks for medical records pertinent to the case.

You can’t disregard the board’s letter, said Doug Brocker, an attorney handling board actions in Raleigh, N.C. “It’s amazing to me that some people just ignore a board complaint. Sometimes it’s because the doctor is just burnt out, which may have gotten the doctor into trouble in the first place.”

If you do not respond to a subpoena, “the board can file a court order holding you in contempt and start taking action on your license,” said Jeff Segal, MD, a neurosurgeon and attorney in Greensboro, N.C. Dr. Segal is CEO of Medical Justice Services, which protects physicians’ reputations associated with malpractice suits and board actions. “Not responding is not much different from agreeing to all of the charges.”
 

2. Not recognizing the seriousness of the complaint

“The biggest mistake is not taking a complaint seriously,” said Linda Stimmel, an attorney at Wilson Elser in Dallas. “Physicians who get a complaint often fire off a brief response stating that the complaint has no merit, without offering any evidence.”

According to Ms. Stimmel, “it’s really important to back up your assertions, such as using excerpts from the medical record, citations of peer-reviewed articles, or a letter of support from a colleague.”

“Weigh your answers carefully, because lack of accuracy will complicate your case,” Mr. Brocker said. “Consult the medical record rather than rely on your memory.”

“Present your version of events, in your own words, because that’s almost always better than the board’s version,” said Dr. Segal.

Even if there was a bad clinical outcome, Dr. Segal said you might point out that the patient was at high risk, or you could show that your clinical outcomes are better than the national average.
 

3. Thinking the board is on your side

You may be lulled into a false sense of security because the physicians on the medical board are your peers, but they can be as tough as any medical malpractice judge, said William P. Sullivan, DO, an emergency physician and attorney in Frankfort, Ill.

As per the National Practitioner Data Bank, physicians are three to four times more likely to incur an adverse board action than make a malpractice payout, Dr. Sullivan said.

Also, although a malpractice lawsuit rarely involves more than a monetary payment, a board action, like a monitoring plan, can restrict your ability to practice medicine. In fact, any kind of board action against you can make it harder to find employment.
 

4. Not being honest or forthcoming

“Lying to the board is the fastest way to turn what would have been a minor infraction into putting your license at risk,” Mr. Brocker said. This can happen when doctors update a medical record to support their version of events.

As per Dr. Sullivan, another way to put your license at risk is to withhold adverse information, which the board can detect by obtaining your application for hospital privileges or for licensure to another state, in which you revealed the adverse information.

Dr. Sullivan also advised against claiming you “always” take a certain precautionary measure. “In reality, we doctors don’t always do what we would like to have done. By saying you always do it when you didn’t, you appear less than truthful to the board, and boards have a hard time with that.”

Similarly, “when doctors don’t want to recognize that they could have handled things better, they tend to dance around the issue,” Mr. Brocker said. “This does not sit well with the board.” Insisting that you did everything right when it’s obvious that you didn’t can lead to harsher sanctions. “The board wants to make sure doctors recognize their mistakes and are willing to learn from them.”
 

5. Providing too much information

You may think that providing a great deal of information strengthens your case, but it can actually weaken it, Mr. Brocker said. Irrelevant information makes your response hard to follow, and it may contain evidence that could prompt another line of inquiry.

“Less is more,” Dr. Segal advised. “Present a coherent argument and keep to the most salient points.” Being concise is also good advice if your complaint proceeds to the board and you have to present your case.

Dr. Segal said the board will stop paying attention to long-winded presentations. He tells his clients to imagine the board is watching a movie. “If your presentation is tedious or hard to follow, you will lose them.”
 

6. Trying to contact the complainant

Complaints are kept anonymous, but in many cases, the doctor has an idea who the complainant was and may try to contact that person. “It’s natural to wonder why a patient would file a complaint against you,” Mr. Brocker said, but if you reach out to the patient to ask why, “it could look like you’re trying to persuade the patient to drop the complaint.”

Doctors who are involved in a practice breakup or a divorce can be victims of false and malicious complaints, but Beth Y. Collis, a partner at the law firm of Dinsmore & Shohl in Columbus, said boards are onto this tactic and usually reject these complaints.

The doctor may be tempted to sue the complainant, but Mr. Brocker said this won’t stop the complaint and could strengthen it. “Most statements to the medical board are protected from defamation lawsuits, and any lawsuit could appear to be intimidation.”
 

7. Simply signing a consent agreement

A small minority of complaints may result in the board taking action against the doctor. Typically, this involves getting the doctor to sign a consent agreement stating that he or she agrees with the board’s decision and its remedy, such as continuing education, a fine, or being placed under another doctor’s supervision.

“When the board sends you a consent agreement, it’s usually about something fairly minor,” Ms. Collis said. “You can make a counteroffer and see if they accept that. But once you enter into the agreement, you waive any right to appeal the board’s decision.”
 

8. Not hiring an attorney

Although some doctors manage to deal with a board complaint on their own, many will need to get an attorney, Mr. Brocker said. “An experienced attorney can help you navigate the board’s process.”

Clients often look for attorneys at the end of the process, when formal charges have already been filed, Mr. Brocker said. At that point, “it’s harder to get things moving in the right direction. You can’t unring the bell.”

Even if you don’t think you need an attorney throughout the case, “it helps to get advice from an attorney at the beginning,” Dr. Segal said. Doctors may think they can’t afford an attorney, but many malpractice carriers pay attorneys’ fees in medical board investigations.

Mr. Brocker advised finding an attorney who is familiar with licensing boards. “Malpractice attorneys may think they can deal with medical boards, but boards are quite different.” For example, “malpractice cases involve an adversarial approach, but licensing boards normally require working collaboratively.”
 

9. Not requesting a hearing

When the board takes action against you, it can be tempting to just accept the allegations and move on with your life, but it may be possible to undo the action, Dr. Sullivan said. “The board still has to prove its allegations, and it may not have a strong case against you.”

In some states, the medical board has to meet a very high standard of proof, Dr. Sullivan said. In Illinois, for example, the board must show “clear and convincing evidence,” while a malpractice plaintiff must only prove that it’s “more likely than not” that a physician violated the standard of care.

A hearing can especially help doctors facing harsh sanctions for minor offenses. For example, in a case handled by the law firm of Ray & Bishop in Newport Beach, Calif., a doctor who was stopped by police while driving home after having wine at a family gathering was found to have a blood alcohol level of 0.11%. Noting that the physician was on call at the time, the Medical Board of California decided to give him 5 years of probation.

Ray & Bishop asked for a judicial hearing to contest the decision. At the hearing, the physician noted that other physicians were also available to take call that night, and an expert stated that the doctor was not an alcohol abuser. The judge ruled that the board’s action was unduly harsh, and the physician received a public reprimand with no further penalties.
 

10. Getting upset with board officials

A board investigator may show up at your office uninvited and ask you to answer some questions, but you aren’t required to answer then and there, said Ms. Collis.

In fact, she noted, it’s never a good idea to let investigators into your office. “They can walk around, look through your records, and find more things to investigate.” For this reason, Ms. Collis makes it a point to schedule meetings with investigators at her office.

When you have to interact with board officials, such as during hearings, expressing anger is a mistake. “Some board members may raise their voices and make untrue assertions about your medical care,” Dr. Sullivan said. “You may wish you could respond in kind, but that will not help you.” Instead, calmly provide studies or guidelines supporting the care you provided.

Taking board investigators to task is also a mistake, Mr. Brocker pointed out. In his words, “investigators have to follow the rules. Getting mad at them will only make your case more difficult. Even if you believe the complaint against you is totally without merit, the process needs to run its course.”

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

Men with hypersexual disorder showed higher levels of oxytocin in their blood than did healthy control men without the disorder, in a study with 102 participants.

Hypersexual disorder (HD) is characterized by “excessive and persistent sexual behaviors in relation to various mood states, with an impulsivity component and experienced loss of control,” John Flanagan, MD, of the Karolinska Institutet in Stockholm and colleagues wrote. Although HD is not included as a separate diagnosis in the current DSM, the similar disorder of compulsive sexual behavior is included in the ICD.

Data on the pathophysiology of HD are limited, although a previous study by corresponding author Andreas Chatzittofis, MD, and colleagues showed evidence of neuroendocrine dysregulation in men with HD, and prompted the current study to explore the possible involvement of the oxytocinergic system in HD.

In the current study, published in the Journal of Clinical Endocrinology & Metabolism, the researchers identified 64 men with HD and 38 healthy male controls. The patients were help-seeking men older than 18 years diagnosed with HD who presented to a single center in Sweden during 2013-2014. The men were included in a randomized clinical trial of cognitive-behavioral therapy for HD, and 30 of them participated in a 7-week CBT program.

Oxytocin, secreted by the pituitary gland, is known to play a role in sexual behavior, but has not been examined in HD men, the researchers said. At baseline, the mean plasma oxytocin was 31.0 pM in the HD patients, which was significantly higher than the mean 16.9 pM in healthy controls (P < .001). However, the 30 HD men who underwent CBT showed significant improvement in oxytocin levels, from a mean pretreatment level of 30.5 to a mean posttreatment level of 20.2 pM (P = .0000019).

The study findings were limited by several factors, including the lack of data on oxytocin for a wait list or control group, as well as the inability to control for confounding factors such as diet, physical activity, ethnicity, and stress, and a lack of data on sexual activity prior to oxytocin measurements, the researchers noted.

However, “although there is no clear consensus at this point, previous studies support the use of oxytocin plasma levels as a surrogate variable for [cerebrospinal fluid] oxytocin activity,” the researchers wrote in their discussion. The current study findings support the potential of oxytocin as a biomarker for HD diagnostics and also as a measure of disease severity. Larger studies to confirm the findings, especially those that exclude potential confounders, would be valuable.

Oxytocin may be treatment target

The study is important because of the lack of knowledge regarding the pathophysiology underlying hypersexual disorder, Dr. Chatzittofis of the University of Cyprus, Nicosia, said in an interview. “This is the first study to indicate a role for oxytocin’s involvement” in hypersexual disorder in men. Dr. Chatzittofis led a team in a previous study that showed an association between HD in men and dysregulation of the hypothalamic pituitary adrenal axis.

In the current study, “we discovered that men with compulsive sexual behavior disorder had higher oxytocin levels, compared with healthy men,” said Dr. Chatzittofis, adding that the take-home message for clinicians is the potential of CBT for treatment. “Cognitive-behavior therapy led to a reduction in both hypersexual behavior and oxytocin levels.” The results suggest that oxytocin plays an important role in sex addiction.

Consequently, oxytocin may be a potential drug target for future pharmacologic treatment of hypersexual disorder, he added.

The study was supported by the Swedish Research Council, the Stockholm County Council, and by a partnership between Umeå University and Västerbotten County Council. The researchers had no financial conflicts to disclose.

Men with hypersexual disorder showed higher levels of oxytocin in their blood than did healthy control men without the disorder, in a study with 102 participants.

Hypersexual disorder (HD) is characterized by “excessive and persistent sexual behaviors in relation to various mood states, with an impulsivity component and experienced loss of control,” John Flanagan, MD, of the Karolinska Institutet in Stockholm and colleagues wrote. Although HD is not included as a separate diagnosis in the current DSM, the similar disorder of compulsive sexual behavior is included in the ICD.

Data on the pathophysiology of HD are limited, although a previous study by corresponding author Andreas Chatzittofis, MD, and colleagues showed evidence of neuroendocrine dysregulation in men with HD, and prompted the current study to explore the possible involvement of the oxytocinergic system in HD.

In the current study, published in the Journal of Clinical Endocrinology & Metabolism, the researchers identified 64 men with HD and 38 healthy male controls. The patients were help-seeking men older than 18 years diagnosed with HD who presented to a single center in Sweden during 2013-2014. The men were included in a randomized clinical trial of cognitive-behavioral therapy for HD, and 30 of them participated in a 7-week CBT program.

Oxytocin, secreted by the pituitary gland, is known to play a role in sexual behavior, but has not been examined in HD men, the researchers said. At baseline, the mean plasma oxytocin was 31.0 pM in the HD patients, which was significantly higher than the mean 16.9 pM in healthy controls (P < .001). However, the 30 HD men who underwent CBT showed significant improvement in oxytocin levels, from a mean pretreatment level of 30.5 to a mean posttreatment level of 20.2 pM (P = .0000019).

The study findings were limited by several factors, including the lack of data on oxytocin for a wait list or control group, as well as the inability to control for confounding factors such as diet, physical activity, ethnicity, and stress, and a lack of data on sexual activity prior to oxytocin measurements, the researchers noted.

However, “although there is no clear consensus at this point, previous studies support the use of oxytocin plasma levels as a surrogate variable for [cerebrospinal fluid] oxytocin activity,” the researchers wrote in their discussion. The current study findings support the potential of oxytocin as a biomarker for HD diagnostics and also as a measure of disease severity. Larger studies to confirm the findings, especially those that exclude potential confounders, would be valuable.

Oxytocin may be treatment target

The study is important because of the lack of knowledge regarding the pathophysiology underlying hypersexual disorder, Dr. Chatzittofis of the University of Cyprus, Nicosia, said in an interview. “This is the first study to indicate a role for oxytocin’s involvement” in hypersexual disorder in men. Dr. Chatzittofis led a team in a previous study that showed an association between HD in men and dysregulation of the hypothalamic pituitary adrenal axis.

In the current study, “we discovered that men with compulsive sexual behavior disorder had higher oxytocin levels, compared with healthy men,” said Dr. Chatzittofis, adding that the take-home message for clinicians is the potential of CBT for treatment. “Cognitive-behavior therapy led to a reduction in both hypersexual behavior and oxytocin levels.” The results suggest that oxytocin plays an important role in sex addiction.

Consequently, oxytocin may be a potential drug target for future pharmacologic treatment of hypersexual disorder, he added.

The study was supported by the Swedish Research Council, the Stockholm County Council, and by a partnership between Umeå University and Västerbotten County Council. The researchers had no financial conflicts to disclose.

Men with hypersexual disorder showed higher levels of oxytocin in their blood than did healthy control men without the disorder, in a study with 102 participants.

Hypersexual disorder (HD) is characterized by “excessive and persistent sexual behaviors in relation to various mood states, with an impulsivity component and experienced loss of control,” John Flanagan, MD, of the Karolinska Institutet in Stockholm and colleagues wrote. Although HD is not included as a separate diagnosis in the current DSM, the similar disorder of compulsive sexual behavior is included in the ICD.

Data on the pathophysiology of HD are limited, although a previous study by corresponding author Andreas Chatzittofis, MD, and colleagues showed evidence of neuroendocrine dysregulation in men with HD, and prompted the current study to explore the possible involvement of the oxytocinergic system in HD.

In the current study, published in the Journal of Clinical Endocrinology & Metabolism, the researchers identified 64 men with HD and 38 healthy male controls. The patients were help-seeking men older than 18 years diagnosed with HD who presented to a single center in Sweden during 2013-2014. The men were included in a randomized clinical trial of cognitive-behavioral therapy for HD, and 30 of them participated in a 7-week CBT program.

Oxytocin, secreted by the pituitary gland, is known to play a role in sexual behavior, but has not been examined in HD men, the researchers said. At baseline, the mean plasma oxytocin was 31.0 pM in the HD patients, which was significantly higher than the mean 16.9 pM in healthy controls (P < .001). However, the 30 HD men who underwent CBT showed significant improvement in oxytocin levels, from a mean pretreatment level of 30.5 to a mean posttreatment level of 20.2 pM (P = .0000019).

The study findings were limited by several factors, including the lack of data on oxytocin for a wait list or control group, as well as the inability to control for confounding factors such as diet, physical activity, ethnicity, and stress, and a lack of data on sexual activity prior to oxytocin measurements, the researchers noted.

However, “although there is no clear consensus at this point, previous studies support the use of oxytocin plasma levels as a surrogate variable for [cerebrospinal fluid] oxytocin activity,” the researchers wrote in their discussion. The current study findings support the potential of oxytocin as a biomarker for HD diagnostics and also as a measure of disease severity. Larger studies to confirm the findings, especially those that exclude potential confounders, would be valuable.

Oxytocin may be treatment target

The study is important because of the lack of knowledge regarding the pathophysiology underlying hypersexual disorder, Dr. Chatzittofis of the University of Cyprus, Nicosia, said in an interview. “This is the first study to indicate a role for oxytocin’s involvement” in hypersexual disorder in men. Dr. Chatzittofis led a team in a previous study that showed an association between HD in men and dysregulation of the hypothalamic pituitary adrenal axis.

In the current study, “we discovered that men with compulsive sexual behavior disorder had higher oxytocin levels, compared with healthy men,” said Dr. Chatzittofis, adding that the take-home message for clinicians is the potential of CBT for treatment. “Cognitive-behavior therapy led to a reduction in both hypersexual behavior and oxytocin levels.” The results suggest that oxytocin plays an important role in sex addiction.

Consequently, oxytocin may be a potential drug target for future pharmacologic treatment of hypersexual disorder, he added.

The study was supported by the Swedish Research Council, the Stockholm County Council, and by a partnership between Umeå University and Västerbotten County Council. The researchers had no financial conflicts to disclose.

The use of over-the-counter melatonin supplements grew by fivefold over the past 2 decades in the United States, a new study finds, although only 2% of a recent group of survey respondents said they had taken the sleep aid within the past month.

The findings, reported Feb. 1 in a research letter in the Journal of the American Medical Association, suggest that “millions of U.S. individuals are using melatonin,” study coauthor Naima Covassin, PhD, an associate consultant at Mayo Clinic in Rochester, Minn., told this news organization. “It is important to ask patients who report sleep problems whether they consume melatonin supplements, and these findings should certainly prompt more research in this area.”

The supplements boost the levels of melatonin, a hormone that is linked to the sleep-wake cycle. “Melatonin facilitates our ability to fall asleep at our bedtime by decreasing the natural early evening circadian arousal that helps keep us alert despite our having been awake since the morning,” said David N. Neubauer, MD, a sleep specialist at Johns Hopkins University, Baltimore. “It isn’t so much that melatonin is sedating, but rather that it turns off arousal.”

For the new study, researchers tracked data from the National Health and Nutrition Examination Survey from 1999-2000 to 2017-2018 and focused on respondents aged 20 and older (n = 55,021, mean age, 47.5, 52% women). As the researchers noted, response rates dipped mightily from a high of 84% in 2001-2002 to just 51.9% in 2017-2018.

The study found that the overall reported weighted prevalence of melatonin use grew from 0.4% (95% confidence interval, 0.2%-1.0%) in 1999-2000 to 2.1% (95% CI, 1.5%-2.9%) in 2017-2018 (linear P = .004). In 93.9% of cases of reported melatonin use, the surveyors confirmed it by checking for supplement bottles.

“These trends were similar in men and women and across age groups,” Dr. Covassin said. “We also found that use of more than 5 mg/day melatonin was not reported till 2005-2006, and it has been increasing since.”

Melatonin supplements are now available in tablets, capsules, gummies, powders, liquids, sprays, and other formulations. Users can even buy CBD-melatonin combos.

The survey doesn’t explore why the respondents used melatonin nor whether they thought it actually helped them. “The study was designed to evaluate the breadth of use of melatonin, rather than its effectiveness as a sleep aid,” Dr. Covassin said.

Dr. Neubauer, who wasn’t associated with the study, said the research seems valid. According to him, melatonin use has likely grown because of marketing and a higher number of products. He added that melatonin products are being manufactured at higher doses, although melatonin has a flat dose-response curve. “Higher doses typically do not have a greater effect,” he said.

According to Dr. Covassin, melatonin is generally considered to be safe, although side effects such as fatigue, dizziness, and headaches have been reported in clinical trials. “This is especially evident when high doses are administered,” Dr. Covassin said. “Other potentially more harmful consequences have also been noted. For instance, it has been found that acute administration of melatonin may decrease glucose tolerance, which may be especially problematic in patients with preexisting vulnerabilities such in those with diabetes. There are also very limited data on whether sustained use is safe in the long run.”

Moving forward, Dr. Covassin said, “we are interested in better understanding consumption of melatonin supplements across different populations as well as the impact of chronic use.”

The study authors are supported by grants from the National Natural Science Foundation of China, National Institutes of Health, Sleep Number Corporation (to Mayo Clinic), the Alice Sheets Marriott Professorship, and the Mayo Clinic Marie Ingalls Research Career Development Award.

Dr. Covassin and Dr. Neubauer have disclosed no relevant financial relationships. Study coauthor Virend K. Somers, MD, PhD, reports having served as a consultant for Respicardia, Baker Tilly, Bayer, and Jazz Pharmaceuticals and serving on the Sleep Number Research Advisory Board.

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

The use of over-the-counter melatonin supplements grew by fivefold over the past 2 decades in the United States, a new study finds, although only 2% of a recent group of survey respondents said they had taken the sleep aid within the past month.

The findings, reported Feb. 1 in a research letter in the Journal of the American Medical Association, suggest that “millions of U.S. individuals are using melatonin,” study coauthor Naima Covassin, PhD, an associate consultant at Mayo Clinic in Rochester, Minn., told this news organization. “It is important to ask patients who report sleep problems whether they consume melatonin supplements, and these findings should certainly prompt more research in this area.”

The supplements boost the levels of melatonin, a hormone that is linked to the sleep-wake cycle. “Melatonin facilitates our ability to fall asleep at our bedtime by decreasing the natural early evening circadian arousal that helps keep us alert despite our having been awake since the morning,” said David N. Neubauer, MD, a sleep specialist at Johns Hopkins University, Baltimore. “It isn’t so much that melatonin is sedating, but rather that it turns off arousal.”

For the new study, researchers tracked data from the National Health and Nutrition Examination Survey from 1999-2000 to 2017-2018 and focused on respondents aged 20 and older (n = 55,021, mean age, 47.5, 52% women). As the researchers noted, response rates dipped mightily from a high of 84% in 2001-2002 to just 51.9% in 2017-2018.

The study found that the overall reported weighted prevalence of melatonin use grew from 0.4% (95% confidence interval, 0.2%-1.0%) in 1999-2000 to 2.1% (95% CI, 1.5%-2.9%) in 2017-2018 (linear P = .004). In 93.9% of cases of reported melatonin use, the surveyors confirmed it by checking for supplement bottles.

“These trends were similar in men and women and across age groups,” Dr. Covassin said. “We also found that use of more than 5 mg/day melatonin was not reported till 2005-2006, and it has been increasing since.”

Melatonin supplements are now available in tablets, capsules, gummies, powders, liquids, sprays, and other formulations. Users can even buy CBD-melatonin combos.

The survey doesn’t explore why the respondents used melatonin nor whether they thought it actually helped them. “The study was designed to evaluate the breadth of use of melatonin, rather than its effectiveness as a sleep aid,” Dr. Covassin said.

Dr. Neubauer, who wasn’t associated with the study, said the research seems valid. According to him, melatonin use has likely grown because of marketing and a higher number of products. He added that melatonin products are being manufactured at higher doses, although melatonin has a flat dose-response curve. “Higher doses typically do not have a greater effect,” he said.

According to Dr. Covassin, melatonin is generally considered to be safe, although side effects such as fatigue, dizziness, and headaches have been reported in clinical trials. “This is especially evident when high doses are administered,” Dr. Covassin said. “Other potentially more harmful consequences have also been noted. For instance, it has been found that acute administration of melatonin may decrease glucose tolerance, which may be especially problematic in patients with preexisting vulnerabilities such in those with diabetes. There are also very limited data on whether sustained use is safe in the long run.”

Moving forward, Dr. Covassin said, “we are interested in better understanding consumption of melatonin supplements across different populations as well as the impact of chronic use.”

The study authors are supported by grants from the National Natural Science Foundation of China, National Institutes of Health, Sleep Number Corporation (to Mayo Clinic), the Alice Sheets Marriott Professorship, and the Mayo Clinic Marie Ingalls Research Career Development Award.

Dr. Covassin and Dr. Neubauer have disclosed no relevant financial relationships. Study coauthor Virend K. Somers, MD, PhD, reports having served as a consultant for Respicardia, Baker Tilly, Bayer, and Jazz Pharmaceuticals and serving on the Sleep Number Research Advisory Board.

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

The use of over-the-counter melatonin supplements grew by fivefold over the past 2 decades in the United States, a new study finds, although only 2% of a recent group of survey respondents said they had taken the sleep aid within the past month.

The findings, reported Feb. 1 in a research letter in the Journal of the American Medical Association, suggest that “millions of U.S. individuals are using melatonin,” study coauthor Naima Covassin, PhD, an associate consultant at Mayo Clinic in Rochester, Minn., told this news organization. “It is important to ask patients who report sleep problems whether they consume melatonin supplements, and these findings should certainly prompt more research in this area.”

The supplements boost the levels of melatonin, a hormone that is linked to the sleep-wake cycle. “Melatonin facilitates our ability to fall asleep at our bedtime by decreasing the natural early evening circadian arousal that helps keep us alert despite our having been awake since the morning,” said David N. Neubauer, MD, a sleep specialist at Johns Hopkins University, Baltimore. “It isn’t so much that melatonin is sedating, but rather that it turns off arousal.”

For the new study, researchers tracked data from the National Health and Nutrition Examination Survey from 1999-2000 to 2017-2018 and focused on respondents aged 20 and older (n = 55,021, mean age, 47.5, 52% women). As the researchers noted, response rates dipped mightily from a high of 84% in 2001-2002 to just 51.9% in 2017-2018.

The study found that the overall reported weighted prevalence of melatonin use grew from 0.4% (95% confidence interval, 0.2%-1.0%) in 1999-2000 to 2.1% (95% CI, 1.5%-2.9%) in 2017-2018 (linear P = .004). In 93.9% of cases of reported melatonin use, the surveyors confirmed it by checking for supplement bottles.

“These trends were similar in men and women and across age groups,” Dr. Covassin said. “We also found that use of more than 5 mg/day melatonin was not reported till 2005-2006, and it has been increasing since.”

Melatonin supplements are now available in tablets, capsules, gummies, powders, liquids, sprays, and other formulations. Users can even buy CBD-melatonin combos.

The survey doesn’t explore why the respondents used melatonin nor whether they thought it actually helped them. “The study was designed to evaluate the breadth of use of melatonin, rather than its effectiveness as a sleep aid,” Dr. Covassin said.

Dr. Neubauer, who wasn’t associated with the study, said the research seems valid. According to him, melatonin use has likely grown because of marketing and a higher number of products. He added that melatonin products are being manufactured at higher doses, although melatonin has a flat dose-response curve. “Higher doses typically do not have a greater effect,” he said.

According to Dr. Covassin, melatonin is generally considered to be safe, although side effects such as fatigue, dizziness, and headaches have been reported in clinical trials. “This is especially evident when high doses are administered,” Dr. Covassin said. “Other potentially more harmful consequences have also been noted. For instance, it has been found that acute administration of melatonin may decrease glucose tolerance, which may be especially problematic in patients with preexisting vulnerabilities such in those with diabetes. There are also very limited data on whether sustained use is safe in the long run.”

Moving forward, Dr. Covassin said, “we are interested in better understanding consumption of melatonin supplements across different populations as well as the impact of chronic use.”

The study authors are supported by grants from the National Natural Science Foundation of China, National Institutes of Health, Sleep Number Corporation (to Mayo Clinic), the Alice Sheets Marriott Professorship, and the Mayo Clinic Marie Ingalls Research Career Development Award.

Dr. Covassin and Dr. Neubauer have disclosed no relevant financial relationships. Study coauthor Virend K. Somers, MD, PhD, reports having served as a consultant for Respicardia, Baker Tilly, Bayer, and Jazz Pharmaceuticals and serving on the Sleep Number Research Advisory Board.

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