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Risky drinking common in cancer survivors
An analysis of more than 15,000 adults with a cancer diagnosis revealed that nearly 80% were current drinkers. Among current drinkers, 13% consumed a moderate amount of alcohol in a typical day, while close to 40% engaged in hazardous drinking.
The numbers are “staggering,” Yin Cao, ScD, MPH, of Washington University in St. Louis, said in an interview. “Most concerning is that those on cancer treatment are engaged in a similar level of risky drinking.”
The study was published online in JAMA Network Open.
Drinking alcohol can increase a person’s risk for a variety of cancers, including oral and pharyngeal cancer as well as esophageal, colorectal, liver, and female breast cancers.
Consuming alcohol is also associated with numerous risks among people diagnosed with cancer. In the short term, alcohol consumption can worsen postsurgical outcomes as well as impair cognition and amplify cardiotoxicity in patients undergoing chemotherapy. In the long term, drinking alcohol can elevate a person’s risk of recurrence, secondary tumors, and mortality.
The American Society of Clinical Oncology recently issued a statement reinforcing the need to prioritize alcohol consumption as a key modifiable behavioral factor in the cancer control research agenda.
The current American Cancer Society guidelines indicate that it’s best to avoid or, at least, minimize alcohol consumption. Men should limit their intake to no more than two drinks per day and women should have no more than one drink per day.
Despite this data and guidelines, alcohol drinking patterns among cancer survivors in the United States remain poorly understood.
To explore further, the researchers identified 15,199 adult cancer survivors enrolled in the National Institutes of Health’s All of Us Research Program.
Overall, 78% of the cohort – more than 11,800 individuals – were current drinkers. In a typical day, 24% engaged in binge drinking – consuming six or more drinks on a single occasion – and 38% engaged in hazardous drinking. Using the Alcohol Use Disorders Identification Test–Consumption, the researchers classified hazardous drinking as scores of 4 or higher in men and 3 or higher in women.
Drinking patterns looked similar in the subset of 1,839 patients undergoing cancer treatment. In this group, 76% were current drinkers. Among current drinkers, 12% exceeded moderate drinking levels, 23% reported binge drinking, and 38% engaged in hazardous drinking. In this group, men, Hispanics, people diagnosed with cancer before age 18, and smokers were more likely to engage in risky drinking behaviors.
“We know that many people who are diagnosed with cancer continue to drink alcohol, but this study provides much more detailed information about that,” said Farhad Islami, MD, PhD, senior scientific director for cancer disparity research at the American Cancer Society, Atlanta, who was not involved in the study.
Given the degree of drinking identified in this population, Dr. Cao highlighted the importance of talking to patients about alcohol.
“Our findings highlight an opportunity for enhanced support and intervention concerning risky drinking behaviors” in oncology, Dr. Cao said. “Given the societal norms surrounding alcohol and the general lack of awareness of alcohol’s short- and long-term impact on cancer outcomes, gently educating patients/survivors about potential risks while understanding the cultural and societal contexts of drinking can make a difference.”
Dr. Islami agreed that oncologists should talk to their patients about alcohol, “especially those going through active treatment because alcohol may affect the treatment or may be associated with more complications of the treatment.”
“Many people now know that smoking causes cancer, but unfortunately, many people do not know about the association of alcohol with cancer,” he said.
Outside of an awareness gap, there are numerous risk factors for substance abuse among cancer survivors, Marleen Meyers, MD, director of the cancer survivorship program at NYU Langone Perlmutter Cancer Center, New York, explained.
Alcohol can help some cancer survivors dull feelings of isolation, fear, stress, and poor pain management that may accompany their diagnosis and treatment, said Dr. Meyers, who was not involved in the research. That is why “it is important for patients to be honest with their providers and for providers to ask about substance use in a nonjudgmental way.”
In these conversations, oncologists should educate patients about the safety risks associated with alcohol intake during or after treatment and that there is no established “safe” amount of alcohol. Incorporating a mental health screening and questions about a family history of substance abuse can also help identify patients “most at risk so providers can be proactive,” she said.
The study was supported by a grant from the NIH. Dr. Cao, Dr. Islami, and Dr. Meyers report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
An analysis of more than 15,000 adults with a cancer diagnosis revealed that nearly 80% were current drinkers. Among current drinkers, 13% consumed a moderate amount of alcohol in a typical day, while close to 40% engaged in hazardous drinking.
The numbers are “staggering,” Yin Cao, ScD, MPH, of Washington University in St. Louis, said in an interview. “Most concerning is that those on cancer treatment are engaged in a similar level of risky drinking.”
The study was published online in JAMA Network Open.
Drinking alcohol can increase a person’s risk for a variety of cancers, including oral and pharyngeal cancer as well as esophageal, colorectal, liver, and female breast cancers.
Consuming alcohol is also associated with numerous risks among people diagnosed with cancer. In the short term, alcohol consumption can worsen postsurgical outcomes as well as impair cognition and amplify cardiotoxicity in patients undergoing chemotherapy. In the long term, drinking alcohol can elevate a person’s risk of recurrence, secondary tumors, and mortality.
The American Society of Clinical Oncology recently issued a statement reinforcing the need to prioritize alcohol consumption as a key modifiable behavioral factor in the cancer control research agenda.
The current American Cancer Society guidelines indicate that it’s best to avoid or, at least, minimize alcohol consumption. Men should limit their intake to no more than two drinks per day and women should have no more than one drink per day.
Despite this data and guidelines, alcohol drinking patterns among cancer survivors in the United States remain poorly understood.
To explore further, the researchers identified 15,199 adult cancer survivors enrolled in the National Institutes of Health’s All of Us Research Program.
Overall, 78% of the cohort – more than 11,800 individuals – were current drinkers. In a typical day, 24% engaged in binge drinking – consuming six or more drinks on a single occasion – and 38% engaged in hazardous drinking. Using the Alcohol Use Disorders Identification Test–Consumption, the researchers classified hazardous drinking as scores of 4 or higher in men and 3 or higher in women.
Drinking patterns looked similar in the subset of 1,839 patients undergoing cancer treatment. In this group, 76% were current drinkers. Among current drinkers, 12% exceeded moderate drinking levels, 23% reported binge drinking, and 38% engaged in hazardous drinking. In this group, men, Hispanics, people diagnosed with cancer before age 18, and smokers were more likely to engage in risky drinking behaviors.
“We know that many people who are diagnosed with cancer continue to drink alcohol, but this study provides much more detailed information about that,” said Farhad Islami, MD, PhD, senior scientific director for cancer disparity research at the American Cancer Society, Atlanta, who was not involved in the study.
Given the degree of drinking identified in this population, Dr. Cao highlighted the importance of talking to patients about alcohol.
“Our findings highlight an opportunity for enhanced support and intervention concerning risky drinking behaviors” in oncology, Dr. Cao said. “Given the societal norms surrounding alcohol and the general lack of awareness of alcohol’s short- and long-term impact on cancer outcomes, gently educating patients/survivors about potential risks while understanding the cultural and societal contexts of drinking can make a difference.”
Dr. Islami agreed that oncologists should talk to their patients about alcohol, “especially those going through active treatment because alcohol may affect the treatment or may be associated with more complications of the treatment.”
“Many people now know that smoking causes cancer, but unfortunately, many people do not know about the association of alcohol with cancer,” he said.
Outside of an awareness gap, there are numerous risk factors for substance abuse among cancer survivors, Marleen Meyers, MD, director of the cancer survivorship program at NYU Langone Perlmutter Cancer Center, New York, explained.
Alcohol can help some cancer survivors dull feelings of isolation, fear, stress, and poor pain management that may accompany their diagnosis and treatment, said Dr. Meyers, who was not involved in the research. That is why “it is important for patients to be honest with their providers and for providers to ask about substance use in a nonjudgmental way.”
In these conversations, oncologists should educate patients about the safety risks associated with alcohol intake during or after treatment and that there is no established “safe” amount of alcohol. Incorporating a mental health screening and questions about a family history of substance abuse can also help identify patients “most at risk so providers can be proactive,” she said.
The study was supported by a grant from the NIH. Dr. Cao, Dr. Islami, and Dr. Meyers report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
An analysis of more than 15,000 adults with a cancer diagnosis revealed that nearly 80% were current drinkers. Among current drinkers, 13% consumed a moderate amount of alcohol in a typical day, while close to 40% engaged in hazardous drinking.
The numbers are “staggering,” Yin Cao, ScD, MPH, of Washington University in St. Louis, said in an interview. “Most concerning is that those on cancer treatment are engaged in a similar level of risky drinking.”
The study was published online in JAMA Network Open.
Drinking alcohol can increase a person’s risk for a variety of cancers, including oral and pharyngeal cancer as well as esophageal, colorectal, liver, and female breast cancers.
Consuming alcohol is also associated with numerous risks among people diagnosed with cancer. In the short term, alcohol consumption can worsen postsurgical outcomes as well as impair cognition and amplify cardiotoxicity in patients undergoing chemotherapy. In the long term, drinking alcohol can elevate a person’s risk of recurrence, secondary tumors, and mortality.
The American Society of Clinical Oncology recently issued a statement reinforcing the need to prioritize alcohol consumption as a key modifiable behavioral factor in the cancer control research agenda.
The current American Cancer Society guidelines indicate that it’s best to avoid or, at least, minimize alcohol consumption. Men should limit their intake to no more than two drinks per day and women should have no more than one drink per day.
Despite this data and guidelines, alcohol drinking patterns among cancer survivors in the United States remain poorly understood.
To explore further, the researchers identified 15,199 adult cancer survivors enrolled in the National Institutes of Health’s All of Us Research Program.
Overall, 78% of the cohort – more than 11,800 individuals – were current drinkers. In a typical day, 24% engaged in binge drinking – consuming six or more drinks on a single occasion – and 38% engaged in hazardous drinking. Using the Alcohol Use Disorders Identification Test–Consumption, the researchers classified hazardous drinking as scores of 4 or higher in men and 3 or higher in women.
Drinking patterns looked similar in the subset of 1,839 patients undergoing cancer treatment. In this group, 76% were current drinkers. Among current drinkers, 12% exceeded moderate drinking levels, 23% reported binge drinking, and 38% engaged in hazardous drinking. In this group, men, Hispanics, people diagnosed with cancer before age 18, and smokers were more likely to engage in risky drinking behaviors.
“We know that many people who are diagnosed with cancer continue to drink alcohol, but this study provides much more detailed information about that,” said Farhad Islami, MD, PhD, senior scientific director for cancer disparity research at the American Cancer Society, Atlanta, who was not involved in the study.
Given the degree of drinking identified in this population, Dr. Cao highlighted the importance of talking to patients about alcohol.
“Our findings highlight an opportunity for enhanced support and intervention concerning risky drinking behaviors” in oncology, Dr. Cao said. “Given the societal norms surrounding alcohol and the general lack of awareness of alcohol’s short- and long-term impact on cancer outcomes, gently educating patients/survivors about potential risks while understanding the cultural and societal contexts of drinking can make a difference.”
Dr. Islami agreed that oncologists should talk to their patients about alcohol, “especially those going through active treatment because alcohol may affect the treatment or may be associated with more complications of the treatment.”
“Many people now know that smoking causes cancer, but unfortunately, many people do not know about the association of alcohol with cancer,” he said.
Outside of an awareness gap, there are numerous risk factors for substance abuse among cancer survivors, Marleen Meyers, MD, director of the cancer survivorship program at NYU Langone Perlmutter Cancer Center, New York, explained.
Alcohol can help some cancer survivors dull feelings of isolation, fear, stress, and poor pain management that may accompany their diagnosis and treatment, said Dr. Meyers, who was not involved in the research. That is why “it is important for patients to be honest with their providers and for providers to ask about substance use in a nonjudgmental way.”
In these conversations, oncologists should educate patients about the safety risks associated with alcohol intake during or after treatment and that there is no established “safe” amount of alcohol. Incorporating a mental health screening and questions about a family history of substance abuse can also help identify patients “most at risk so providers can be proactive,” she said.
The study was supported by a grant from the NIH. Dr. Cao, Dr. Islami, and Dr. Meyers report no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN
Can caffeine improve thyroid function?
“Although the causal relationship between caffeine intake and thyroid function requires further verification, as an easily obtainable and widely consumed dietary ingredient, caffeine is a potential candidate for improving thyroid health in people with metabolic disorders,” reported the authors in the study, published in Nutritional Journal.
Caffeine intake, within established healthy ranges, showed a nonlinear association with thyroid levels.
Moderate caffeine intake has been associated with reducing the risk of metabolic disorders in addition to showing some mental health benefits. However, research on its effects on thyroid hormone, which importantly plays a key role in systemic metabolism and neurologic development, is lacking.
To investigate the effects, Yu Zhou, of the Department of Rehabilitation Medicine, School of Health, Fujian Medical University, Fuzhou, China, and colleagues evaluated data from the National Health and Nutrition Examination Survey (NHANES) III 2007-2012 study involving 2,582 participants for whom data were available regarding medical conditions, dietary intake, thyroid function, and demographic background.
The participants were divided into three subgroups based on sex, age, body mass index, hyperglycemia, hypertension, and cardio-cerebral vascular disease (CVD).
Group 1 (n = 208) was the most metabolically unhealthy. Patients in that group had the highest BMI and were of oldest age. In addition, that group had higher rates of hypertension, hyperglycemia, and CVD, but, notably, it had the lowest level of caffeine consumption.
In group 2 (n = 543), all participants were current smokers, and 90.4% had a habit of drinking alcohol. That group also had the highest percentage of men.
Group 3 (n = 1,183) was the most metabolically healthy, with more women, younger age, and lowest BMI. No participants in that group had hyperglycemia, hypertension, or CVD.
Group 1, the most metabolically unhealthy, had the highest serum thyroid-stimulating hormone (TSH) levels. Of note, while participants with thyroid diseases were initially excluded from the analysis, higher TSH levels are predictive of subclinical hypothyroidism or progression to overt hypothyroidism.
Overall, there was no association between caffeine and TSH levels.
However, a subgroup analysis of the groups showed that in group 1, caffeine intake correlated with TSH nonlinearly (P = .0019), with minimal average consumption of caffeine (< 9.97 mg/d). There was an association with slightly higher TSH levels (P = .035) after adjustment for age, sex, race, drink, disease state, micronutrients, and macronutrients.
However, in higher, moderate amounts of caffeine consumption (9.97 – 264.97 mg/d), there was an inverse association, with lower TSH (P = .001).
There was no association between daily caffeine consumption of more than 264.97 mg and TSH levels.
For context, a typical 8-ounce cup of coffee generally contains 80-100 mg of caffeine, and the Food and Drug Administration indicates that 400 mg/d of caffeine is safe for healthy adults.
Group 2 consumed the highest amount of caffeine. Notably, that group had the lowest serum TSH levels of the three groups. There were no significant associations between caffeine consumption and TSH levels in group 2 or group 3.
There were no significant associations between caffeine consumption and levels of serum FT4 or FT3, also linked to thyroid dysfunction, in any of the groups.
The findings show that “caffeine consumption was correlated with serum TSH nonlinearly, and when taken in moderate amounts (9.97-264.97 mg/d), caffeine demonstrated a positive correlation with serum TSH levels in patients with metabolic disorders,” the authors concluded.
Mechanisms?
Caffeine is believed to modulate pituitary hormone secretion, which has been shown to influence the hypothalamic-pituitary-adrenal axis. The authors speculated that caffeine could potentially affect thyroid activity by affecting pituitary function.
“However, the effects of transient and chronic caffeine administration on human thyroid function need to be verified further, and the related mechanisms remain unclear,” they noted.
Commenting on the study, Maik Pietzner, PhD, of the Berlin Institute of Health, noted that an important limitation of the study is that various patient groups were excluded, including those with abnormal TSH levels.
“What makes me wonder is the high number of exclusions and the focus on very specific groups of people. This almost certainly introduces bias, e.g., what is specific to people not reporting coffee consumption,” Dr. Pietzner said.
Furthermore, “we already know that patients with poor metabolic health do also have slight variations in thyroid hormone levels and also have different dietary patterns,” he explained.
“So reverse confounding might occur in which the poor metabolic health is associated with both poor thyroid hormone levels and coffee consumption,” Dr. Pietzner said.
He also noted the “somewhat odd” finding that the group with the highest metabolic disorders had the lowest coffee consumption, yet the highest TSH levels.
“My guess would be that this might also be a chance finding, given that the distribution of TSH values is very skewed, which can have a strong effect in linear regression models,” Dr. Pietzner said.
In general, “the evidence generated by the study is rather weak, but there is good evidence that higher coffee consumption is linked to better metabolic health, although the exact mechanisms is not known, if indeed causal,” Dr. Pietzner added. “Prospective studies are needed to evaluate whether higher coffee consumption indeed lowers the risk for thyroid disease.”
A version of this article first appeared on Medscape.com.
“Although the causal relationship between caffeine intake and thyroid function requires further verification, as an easily obtainable and widely consumed dietary ingredient, caffeine is a potential candidate for improving thyroid health in people with metabolic disorders,” reported the authors in the study, published in Nutritional Journal.
Caffeine intake, within established healthy ranges, showed a nonlinear association with thyroid levels.
Moderate caffeine intake has been associated with reducing the risk of metabolic disorders in addition to showing some mental health benefits. However, research on its effects on thyroid hormone, which importantly plays a key role in systemic metabolism and neurologic development, is lacking.
To investigate the effects, Yu Zhou, of the Department of Rehabilitation Medicine, School of Health, Fujian Medical University, Fuzhou, China, and colleagues evaluated data from the National Health and Nutrition Examination Survey (NHANES) III 2007-2012 study involving 2,582 participants for whom data were available regarding medical conditions, dietary intake, thyroid function, and demographic background.
The participants were divided into three subgroups based on sex, age, body mass index, hyperglycemia, hypertension, and cardio-cerebral vascular disease (CVD).
Group 1 (n = 208) was the most metabolically unhealthy. Patients in that group had the highest BMI and were of oldest age. In addition, that group had higher rates of hypertension, hyperglycemia, and CVD, but, notably, it had the lowest level of caffeine consumption.
In group 2 (n = 543), all participants were current smokers, and 90.4% had a habit of drinking alcohol. That group also had the highest percentage of men.
Group 3 (n = 1,183) was the most metabolically healthy, with more women, younger age, and lowest BMI. No participants in that group had hyperglycemia, hypertension, or CVD.
Group 1, the most metabolically unhealthy, had the highest serum thyroid-stimulating hormone (TSH) levels. Of note, while participants with thyroid diseases were initially excluded from the analysis, higher TSH levels are predictive of subclinical hypothyroidism or progression to overt hypothyroidism.
Overall, there was no association between caffeine and TSH levels.
However, a subgroup analysis of the groups showed that in group 1, caffeine intake correlated with TSH nonlinearly (P = .0019), with minimal average consumption of caffeine (< 9.97 mg/d). There was an association with slightly higher TSH levels (P = .035) after adjustment for age, sex, race, drink, disease state, micronutrients, and macronutrients.
However, in higher, moderate amounts of caffeine consumption (9.97 – 264.97 mg/d), there was an inverse association, with lower TSH (P = .001).
There was no association between daily caffeine consumption of more than 264.97 mg and TSH levels.
For context, a typical 8-ounce cup of coffee generally contains 80-100 mg of caffeine, and the Food and Drug Administration indicates that 400 mg/d of caffeine is safe for healthy adults.
Group 2 consumed the highest amount of caffeine. Notably, that group had the lowest serum TSH levels of the three groups. There were no significant associations between caffeine consumption and TSH levels in group 2 or group 3.
There were no significant associations between caffeine consumption and levels of serum FT4 or FT3, also linked to thyroid dysfunction, in any of the groups.
The findings show that “caffeine consumption was correlated with serum TSH nonlinearly, and when taken in moderate amounts (9.97-264.97 mg/d), caffeine demonstrated a positive correlation with serum TSH levels in patients with metabolic disorders,” the authors concluded.
Mechanisms?
Caffeine is believed to modulate pituitary hormone secretion, which has been shown to influence the hypothalamic-pituitary-adrenal axis. The authors speculated that caffeine could potentially affect thyroid activity by affecting pituitary function.
“However, the effects of transient and chronic caffeine administration on human thyroid function need to be verified further, and the related mechanisms remain unclear,” they noted.
Commenting on the study, Maik Pietzner, PhD, of the Berlin Institute of Health, noted that an important limitation of the study is that various patient groups were excluded, including those with abnormal TSH levels.
“What makes me wonder is the high number of exclusions and the focus on very specific groups of people. This almost certainly introduces bias, e.g., what is specific to people not reporting coffee consumption,” Dr. Pietzner said.
Furthermore, “we already know that patients with poor metabolic health do also have slight variations in thyroid hormone levels and also have different dietary patterns,” he explained.
“So reverse confounding might occur in which the poor metabolic health is associated with both poor thyroid hormone levels and coffee consumption,” Dr. Pietzner said.
He also noted the “somewhat odd” finding that the group with the highest metabolic disorders had the lowest coffee consumption, yet the highest TSH levels.
“My guess would be that this might also be a chance finding, given that the distribution of TSH values is very skewed, which can have a strong effect in linear regression models,” Dr. Pietzner said.
In general, “the evidence generated by the study is rather weak, but there is good evidence that higher coffee consumption is linked to better metabolic health, although the exact mechanisms is not known, if indeed causal,” Dr. Pietzner added. “Prospective studies are needed to evaluate whether higher coffee consumption indeed lowers the risk for thyroid disease.”
A version of this article first appeared on Medscape.com.
“Although the causal relationship between caffeine intake and thyroid function requires further verification, as an easily obtainable and widely consumed dietary ingredient, caffeine is a potential candidate for improving thyroid health in people with metabolic disorders,” reported the authors in the study, published in Nutritional Journal.
Caffeine intake, within established healthy ranges, showed a nonlinear association with thyroid levels.
Moderate caffeine intake has been associated with reducing the risk of metabolic disorders in addition to showing some mental health benefits. However, research on its effects on thyroid hormone, which importantly plays a key role in systemic metabolism and neurologic development, is lacking.
To investigate the effects, Yu Zhou, of the Department of Rehabilitation Medicine, School of Health, Fujian Medical University, Fuzhou, China, and colleagues evaluated data from the National Health and Nutrition Examination Survey (NHANES) III 2007-2012 study involving 2,582 participants for whom data were available regarding medical conditions, dietary intake, thyroid function, and demographic background.
The participants were divided into three subgroups based on sex, age, body mass index, hyperglycemia, hypertension, and cardio-cerebral vascular disease (CVD).
Group 1 (n = 208) was the most metabolically unhealthy. Patients in that group had the highest BMI and were of oldest age. In addition, that group had higher rates of hypertension, hyperglycemia, and CVD, but, notably, it had the lowest level of caffeine consumption.
In group 2 (n = 543), all participants were current smokers, and 90.4% had a habit of drinking alcohol. That group also had the highest percentage of men.
Group 3 (n = 1,183) was the most metabolically healthy, with more women, younger age, and lowest BMI. No participants in that group had hyperglycemia, hypertension, or CVD.
Group 1, the most metabolically unhealthy, had the highest serum thyroid-stimulating hormone (TSH) levels. Of note, while participants with thyroid diseases were initially excluded from the analysis, higher TSH levels are predictive of subclinical hypothyroidism or progression to overt hypothyroidism.
Overall, there was no association between caffeine and TSH levels.
However, a subgroup analysis of the groups showed that in group 1, caffeine intake correlated with TSH nonlinearly (P = .0019), with minimal average consumption of caffeine (< 9.97 mg/d). There was an association with slightly higher TSH levels (P = .035) after adjustment for age, sex, race, drink, disease state, micronutrients, and macronutrients.
However, in higher, moderate amounts of caffeine consumption (9.97 – 264.97 mg/d), there was an inverse association, with lower TSH (P = .001).
There was no association between daily caffeine consumption of more than 264.97 mg and TSH levels.
For context, a typical 8-ounce cup of coffee generally contains 80-100 mg of caffeine, and the Food and Drug Administration indicates that 400 mg/d of caffeine is safe for healthy adults.
Group 2 consumed the highest amount of caffeine. Notably, that group had the lowest serum TSH levels of the three groups. There were no significant associations between caffeine consumption and TSH levels in group 2 or group 3.
There were no significant associations between caffeine consumption and levels of serum FT4 or FT3, also linked to thyroid dysfunction, in any of the groups.
The findings show that “caffeine consumption was correlated with serum TSH nonlinearly, and when taken in moderate amounts (9.97-264.97 mg/d), caffeine demonstrated a positive correlation with serum TSH levels in patients with metabolic disorders,” the authors concluded.
Mechanisms?
Caffeine is believed to modulate pituitary hormone secretion, which has been shown to influence the hypothalamic-pituitary-adrenal axis. The authors speculated that caffeine could potentially affect thyroid activity by affecting pituitary function.
“However, the effects of transient and chronic caffeine administration on human thyroid function need to be verified further, and the related mechanisms remain unclear,” they noted.
Commenting on the study, Maik Pietzner, PhD, of the Berlin Institute of Health, noted that an important limitation of the study is that various patient groups were excluded, including those with abnormal TSH levels.
“What makes me wonder is the high number of exclusions and the focus on very specific groups of people. This almost certainly introduces bias, e.g., what is specific to people not reporting coffee consumption,” Dr. Pietzner said.
Furthermore, “we already know that patients with poor metabolic health do also have slight variations in thyroid hormone levels and also have different dietary patterns,” he explained.
“So reverse confounding might occur in which the poor metabolic health is associated with both poor thyroid hormone levels and coffee consumption,” Dr. Pietzner said.
He also noted the “somewhat odd” finding that the group with the highest metabolic disorders had the lowest coffee consumption, yet the highest TSH levels.
“My guess would be that this might also be a chance finding, given that the distribution of TSH values is very skewed, which can have a strong effect in linear regression models,” Dr. Pietzner said.
In general, “the evidence generated by the study is rather weak, but there is good evidence that higher coffee consumption is linked to better metabolic health, although the exact mechanisms is not known, if indeed causal,” Dr. Pietzner added. “Prospective studies are needed to evaluate whether higher coffee consumption indeed lowers the risk for thyroid disease.”
A version of this article first appeared on Medscape.com.
FROM NUTRITIONAL JOURNAL
Artificial sweeteners no help for weight loss: Review
It also shows evidence that these products are not beneficial for controlling excess weight.
Francisco Gómez-Delgado, MD, PhD, and Pablo Pérez-Martínez, MD, PhD, are members of the Spanish Society of Arteriosclerosis and of the Spanish Society of Internal Medicine. They have coordinated an updated review of the leading scientific evidence surrounding artificial sweeteners: evidence showing that far from positively affecting our health, they have “negative effects for the cardiometabolic system.”
The paper, published in Current Opinion in Cardiology, delves into the consumption of these sweeteners and their negative influence on the development of obesity and of several of the most important cardiometabolic risk factors (hypertension, dyslipidemia, and diabetes).
Globalization and the increase in consumption of ultraprocessed foods have led to a need for greater knowledge on the health impacts of certain nutrients such as artificial sweeteners (nutritive and nonnutritive). This review aims to analyze their role and their effect on cardiometabolic and cardiovascular disease risk.
Cardiovascular risk
The detrimental effects of a high-calorie, high-sugar diet have been well established. For this reason, health authorities recommend limiting sugar consumption. The recommendation has led the food industry to develop different artificial sweeteners with specific properties, such as flavor and stability (nutritive artificial sweeteners), and others aimed at limiting sugar in the diet (nonnutritive artificial sweeteners). Recent evidence explores the influence of these two types of artificial sweeteners on cardiovascular disease risk through risk factors such as obesity and type 2 diabetes, among others.
Initially, the consumption of artificial sweeteners was presented as an alternative for reducing calorie intake in the diet as an option for people with excess weight and obesity. However, as this paper explains, the consumption of these artificial sweeteners favors weight gain because of neuroendocrine mechanisms related to satiety that are abnormally activated when artificial sweeteners are consumed.
Weight gain
On the other hand, evidence shows that consuming artificial sweeteners does not encourage weight loss. “Quite the contrary,” Dr. Pérez-Martínez, scientific director at the Maimonides Biomedical Research Institute and internist at the University Hospital Reina Sofia, both in Córdoba, told this news organization. “There is evidence showing weight gain resulting from the effect that artificial sweetener consumption has at the neurohormonal level by altering the mechanisms involved in regulating the feeling of satiety.”
However, on the basis of current evidence, sugar cannot be claimed to be less harmful. “What we do know is that in both cases, we should reduce or remove them from our diets and replace them with other healthier alternatives for weight management, such as eating plant-based products or being physically active.”
Confronting ignorance
Nonetheless, these recommendations are conditional, “because the weight of the evidence is not extremely high, since there have not been a whole lot of studies. All nutritional studies must be viewed with caution,” Manuel Anguita, MD, PhD, said in an interview. Dr. Anguita is department head of clinical cardiology at the University Hospital Reina Sofia in Córdoba and past president of the Spanish Society of Cardiology.
“It’s something that should be included within the medical record when you’re assessing cardiovascular risk. In addition to identifying patients who use artificial sweeteners, it’s especially important to emphasize that it’s not an appropriate recommendation for weight management.” Healthier measures include moderate exercise and the Mediterranean diet.
Explaining why this research is valuable, he said, “It’s generally useful because there’s ignorance not only in the population but among physicians as well [about] these negative effects of sweeteners.”
Diabetes and metabolic syndrome
Artificial sweeteners cause significant disruptions in the endocrine system, leading our metabolism to function abnormally. The review revealed that consuming artificial sweeteners raises the risk for type 2 diabetes by between 18% and 24% and raises the risk for metabolic syndrome by up to 44%.
Dr. Gómez-Delgado, an internal medicine specialist at the University Hospital of Jaen in Spain and first author of the study, discussed the deleterious effects of sweeteners on metabolism. “On one hand, neurohormonal disorders impact appetite, and the feeling of satiety is abnormally delayed.” On the other hand, “they induce excessive insulin secretion in the pancreas,” which in the long run, encourages metabolic disorders that lead to diabetes. Ultimately, this process produces what we know as “dysbiosis, since our microbiota is unable to process these artificial sweeteners.” Dysbiosis triggers specific pathophysiologic processes that negatively affect cardiometabolic and cardiovascular systems.
No differences
Regarding the type of sweetener, Dr. Gómez-Delgado noted that currently available studies assess the consumption of special dietary products that, in most cases, include various types of artificial sweeteners. “So, it’s not possible to define specific differences between them as to how they impact our health.” Additional studies are needed to confirm this effect at the cardiometabolic level and to analyze the different types of artificial sweeteners individually.
“There’s enough evidence to confirm that consuming artificial sweeteners negatively interferes with our metabolism – especially glucose metabolism – and increases the risk of developing diabetes,” said Dr. Gómez-Delgado.
High-sodium drinks
When it comes to the influence of artificial sweeteners on hypertension, “there is no single explanation. The World Health Organization already discussed this issue 4-5 years ago, not only due to their carcinogenic risk, but also due to this cardiovascular risk in terms of a lack of control of obesity, diabetes, and hypertension,” said Dr. Anguita.
Another important point “is that this is not in reference to the sweeteners themselves, but to soft drinks containing those components, which is where we have more studies,” he added. There are two factors explaining this increase in hypertension, which poses a problem at the population level, with medium- to long-term follow-up. “The sugary beverages that we mentioned have a higher sodium content. That is, the sweeteners add this element, which is a factor that’s directly linked to the increase in blood pressure levels.” Another factor that can influence blood pressure is “the increase in insulin secretion that has been described as resulting from sweeteners. In the medium and long term, this is associated with increased blood pressure levels.”
Cardiovascular risk factor?
Are artificial sweeteners considered to be a new cardiovascular risk factor? “What they really do is increase the incidence of the other classic risk factors,” including obesity, said Dr. Anguita. It has been shown that artificial sweeteners don’t reduce obesity when used continuously. Nonetheless, “there is still not enough evidence to view it in the same light as the classic risk factors,” added Dr. Anguita. However, it is a factor that can clearly worsen the control of the other factors. Therefore, “it’s appropriate to sound an alarm and explain that it’s not the best way to lose weight; there are many other healthier choices.”
“We need more robust evidence to take a clear position on the use of this type of sweetener and its detrimental effect on health. Meanwhile, it would be ideal to limit their consumption or even avoid adding artificial sweeteners to coffee or teas,” added Dr. Pérez-Martínez.
Regulate consumption
Dr. Pérez-Martínez mentioned that the measures proposed to regulate the consumption of artificial sweeteners and to modify the current legislation must involve “minimizing the consumption of these special dietary products as much as possible and even avoiding adding these artificial sweeteners to the foods that we consume; for example, to coffee and tea.” On the other hand, “we must provide consumers with information that is as clear and simple as possible regarding the composition of the food they consume and how it impacts their health.”
However, “we need more evidence to be able to take a clear position on what type of sweeteners we can consume in our diet and also to what extent we should limit their presence in the foods we consume,” said Dr. Pérez-Martínez.
Last, “most of the evidence is from short-term observational studies that assess frequencies and patterns of consumption of foods containing these artificial sweeteners.” Of course, “we need studies that specifically analyze their effects at the metabolic level as well as longer-term studies where the nutritional follow-up of participants is more accurate and rigorous, especially when it comes to the consumption of this type of food,” concluded Dr. Gómez-Delgado.
This article was translated from the Medscape Spanish Edition. A version appeared on Medscape.com.
It also shows evidence that these products are not beneficial for controlling excess weight.
Francisco Gómez-Delgado, MD, PhD, and Pablo Pérez-Martínez, MD, PhD, are members of the Spanish Society of Arteriosclerosis and of the Spanish Society of Internal Medicine. They have coordinated an updated review of the leading scientific evidence surrounding artificial sweeteners: evidence showing that far from positively affecting our health, they have “negative effects for the cardiometabolic system.”
The paper, published in Current Opinion in Cardiology, delves into the consumption of these sweeteners and their negative influence on the development of obesity and of several of the most important cardiometabolic risk factors (hypertension, dyslipidemia, and diabetes).
Globalization and the increase in consumption of ultraprocessed foods have led to a need for greater knowledge on the health impacts of certain nutrients such as artificial sweeteners (nutritive and nonnutritive). This review aims to analyze their role and their effect on cardiometabolic and cardiovascular disease risk.
Cardiovascular risk
The detrimental effects of a high-calorie, high-sugar diet have been well established. For this reason, health authorities recommend limiting sugar consumption. The recommendation has led the food industry to develop different artificial sweeteners with specific properties, such as flavor and stability (nutritive artificial sweeteners), and others aimed at limiting sugar in the diet (nonnutritive artificial sweeteners). Recent evidence explores the influence of these two types of artificial sweeteners on cardiovascular disease risk through risk factors such as obesity and type 2 diabetes, among others.
Initially, the consumption of artificial sweeteners was presented as an alternative for reducing calorie intake in the diet as an option for people with excess weight and obesity. However, as this paper explains, the consumption of these artificial sweeteners favors weight gain because of neuroendocrine mechanisms related to satiety that are abnormally activated when artificial sweeteners are consumed.
Weight gain
On the other hand, evidence shows that consuming artificial sweeteners does not encourage weight loss. “Quite the contrary,” Dr. Pérez-Martínez, scientific director at the Maimonides Biomedical Research Institute and internist at the University Hospital Reina Sofia, both in Córdoba, told this news organization. “There is evidence showing weight gain resulting from the effect that artificial sweetener consumption has at the neurohormonal level by altering the mechanisms involved in regulating the feeling of satiety.”
However, on the basis of current evidence, sugar cannot be claimed to be less harmful. “What we do know is that in both cases, we should reduce or remove them from our diets and replace them with other healthier alternatives for weight management, such as eating plant-based products or being physically active.”
Confronting ignorance
Nonetheless, these recommendations are conditional, “because the weight of the evidence is not extremely high, since there have not been a whole lot of studies. All nutritional studies must be viewed with caution,” Manuel Anguita, MD, PhD, said in an interview. Dr. Anguita is department head of clinical cardiology at the University Hospital Reina Sofia in Córdoba and past president of the Spanish Society of Cardiology.
“It’s something that should be included within the medical record when you’re assessing cardiovascular risk. In addition to identifying patients who use artificial sweeteners, it’s especially important to emphasize that it’s not an appropriate recommendation for weight management.” Healthier measures include moderate exercise and the Mediterranean diet.
Explaining why this research is valuable, he said, “It’s generally useful because there’s ignorance not only in the population but among physicians as well [about] these negative effects of sweeteners.”
Diabetes and metabolic syndrome
Artificial sweeteners cause significant disruptions in the endocrine system, leading our metabolism to function abnormally. The review revealed that consuming artificial sweeteners raises the risk for type 2 diabetes by between 18% and 24% and raises the risk for metabolic syndrome by up to 44%.
Dr. Gómez-Delgado, an internal medicine specialist at the University Hospital of Jaen in Spain and first author of the study, discussed the deleterious effects of sweeteners on metabolism. “On one hand, neurohormonal disorders impact appetite, and the feeling of satiety is abnormally delayed.” On the other hand, “they induce excessive insulin secretion in the pancreas,” which in the long run, encourages metabolic disorders that lead to diabetes. Ultimately, this process produces what we know as “dysbiosis, since our microbiota is unable to process these artificial sweeteners.” Dysbiosis triggers specific pathophysiologic processes that negatively affect cardiometabolic and cardiovascular systems.
No differences
Regarding the type of sweetener, Dr. Gómez-Delgado noted that currently available studies assess the consumption of special dietary products that, in most cases, include various types of artificial sweeteners. “So, it’s not possible to define specific differences between them as to how they impact our health.” Additional studies are needed to confirm this effect at the cardiometabolic level and to analyze the different types of artificial sweeteners individually.
“There’s enough evidence to confirm that consuming artificial sweeteners negatively interferes with our metabolism – especially glucose metabolism – and increases the risk of developing diabetes,” said Dr. Gómez-Delgado.
High-sodium drinks
When it comes to the influence of artificial sweeteners on hypertension, “there is no single explanation. The World Health Organization already discussed this issue 4-5 years ago, not only due to their carcinogenic risk, but also due to this cardiovascular risk in terms of a lack of control of obesity, diabetes, and hypertension,” said Dr. Anguita.
Another important point “is that this is not in reference to the sweeteners themselves, but to soft drinks containing those components, which is where we have more studies,” he added. There are two factors explaining this increase in hypertension, which poses a problem at the population level, with medium- to long-term follow-up. “The sugary beverages that we mentioned have a higher sodium content. That is, the sweeteners add this element, which is a factor that’s directly linked to the increase in blood pressure levels.” Another factor that can influence blood pressure is “the increase in insulin secretion that has been described as resulting from sweeteners. In the medium and long term, this is associated with increased blood pressure levels.”
Cardiovascular risk factor?
Are artificial sweeteners considered to be a new cardiovascular risk factor? “What they really do is increase the incidence of the other classic risk factors,” including obesity, said Dr. Anguita. It has been shown that artificial sweeteners don’t reduce obesity when used continuously. Nonetheless, “there is still not enough evidence to view it in the same light as the classic risk factors,” added Dr. Anguita. However, it is a factor that can clearly worsen the control of the other factors. Therefore, “it’s appropriate to sound an alarm and explain that it’s not the best way to lose weight; there are many other healthier choices.”
“We need more robust evidence to take a clear position on the use of this type of sweetener and its detrimental effect on health. Meanwhile, it would be ideal to limit their consumption or even avoid adding artificial sweeteners to coffee or teas,” added Dr. Pérez-Martínez.
Regulate consumption
Dr. Pérez-Martínez mentioned that the measures proposed to regulate the consumption of artificial sweeteners and to modify the current legislation must involve “minimizing the consumption of these special dietary products as much as possible and even avoiding adding these artificial sweeteners to the foods that we consume; for example, to coffee and tea.” On the other hand, “we must provide consumers with information that is as clear and simple as possible regarding the composition of the food they consume and how it impacts their health.”
However, “we need more evidence to be able to take a clear position on what type of sweeteners we can consume in our diet and also to what extent we should limit their presence in the foods we consume,” said Dr. Pérez-Martínez.
Last, “most of the evidence is from short-term observational studies that assess frequencies and patterns of consumption of foods containing these artificial sweeteners.” Of course, “we need studies that specifically analyze their effects at the metabolic level as well as longer-term studies where the nutritional follow-up of participants is more accurate and rigorous, especially when it comes to the consumption of this type of food,” concluded Dr. Gómez-Delgado.
This article was translated from the Medscape Spanish Edition. A version appeared on Medscape.com.
It also shows evidence that these products are not beneficial for controlling excess weight.
Francisco Gómez-Delgado, MD, PhD, and Pablo Pérez-Martínez, MD, PhD, are members of the Spanish Society of Arteriosclerosis and of the Spanish Society of Internal Medicine. They have coordinated an updated review of the leading scientific evidence surrounding artificial sweeteners: evidence showing that far from positively affecting our health, they have “negative effects for the cardiometabolic system.”
The paper, published in Current Opinion in Cardiology, delves into the consumption of these sweeteners and their negative influence on the development of obesity and of several of the most important cardiometabolic risk factors (hypertension, dyslipidemia, and diabetes).
Globalization and the increase in consumption of ultraprocessed foods have led to a need for greater knowledge on the health impacts of certain nutrients such as artificial sweeteners (nutritive and nonnutritive). This review aims to analyze their role and their effect on cardiometabolic and cardiovascular disease risk.
Cardiovascular risk
The detrimental effects of a high-calorie, high-sugar diet have been well established. For this reason, health authorities recommend limiting sugar consumption. The recommendation has led the food industry to develop different artificial sweeteners with specific properties, such as flavor and stability (nutritive artificial sweeteners), and others aimed at limiting sugar in the diet (nonnutritive artificial sweeteners). Recent evidence explores the influence of these two types of artificial sweeteners on cardiovascular disease risk through risk factors such as obesity and type 2 diabetes, among others.
Initially, the consumption of artificial sweeteners was presented as an alternative for reducing calorie intake in the diet as an option for people with excess weight and obesity. However, as this paper explains, the consumption of these artificial sweeteners favors weight gain because of neuroendocrine mechanisms related to satiety that are abnormally activated when artificial sweeteners are consumed.
Weight gain
On the other hand, evidence shows that consuming artificial sweeteners does not encourage weight loss. “Quite the contrary,” Dr. Pérez-Martínez, scientific director at the Maimonides Biomedical Research Institute and internist at the University Hospital Reina Sofia, both in Córdoba, told this news organization. “There is evidence showing weight gain resulting from the effect that artificial sweetener consumption has at the neurohormonal level by altering the mechanisms involved in regulating the feeling of satiety.”
However, on the basis of current evidence, sugar cannot be claimed to be less harmful. “What we do know is that in both cases, we should reduce or remove them from our diets and replace them with other healthier alternatives for weight management, such as eating plant-based products or being physically active.”
Confronting ignorance
Nonetheless, these recommendations are conditional, “because the weight of the evidence is not extremely high, since there have not been a whole lot of studies. All nutritional studies must be viewed with caution,” Manuel Anguita, MD, PhD, said in an interview. Dr. Anguita is department head of clinical cardiology at the University Hospital Reina Sofia in Córdoba and past president of the Spanish Society of Cardiology.
“It’s something that should be included within the medical record when you’re assessing cardiovascular risk. In addition to identifying patients who use artificial sweeteners, it’s especially important to emphasize that it’s not an appropriate recommendation for weight management.” Healthier measures include moderate exercise and the Mediterranean diet.
Explaining why this research is valuable, he said, “It’s generally useful because there’s ignorance not only in the population but among physicians as well [about] these negative effects of sweeteners.”
Diabetes and metabolic syndrome
Artificial sweeteners cause significant disruptions in the endocrine system, leading our metabolism to function abnormally. The review revealed that consuming artificial sweeteners raises the risk for type 2 diabetes by between 18% and 24% and raises the risk for metabolic syndrome by up to 44%.
Dr. Gómez-Delgado, an internal medicine specialist at the University Hospital of Jaen in Spain and first author of the study, discussed the deleterious effects of sweeteners on metabolism. “On one hand, neurohormonal disorders impact appetite, and the feeling of satiety is abnormally delayed.” On the other hand, “they induce excessive insulin secretion in the pancreas,” which in the long run, encourages metabolic disorders that lead to diabetes. Ultimately, this process produces what we know as “dysbiosis, since our microbiota is unable to process these artificial sweeteners.” Dysbiosis triggers specific pathophysiologic processes that negatively affect cardiometabolic and cardiovascular systems.
No differences
Regarding the type of sweetener, Dr. Gómez-Delgado noted that currently available studies assess the consumption of special dietary products that, in most cases, include various types of artificial sweeteners. “So, it’s not possible to define specific differences between them as to how they impact our health.” Additional studies are needed to confirm this effect at the cardiometabolic level and to analyze the different types of artificial sweeteners individually.
“There’s enough evidence to confirm that consuming artificial sweeteners negatively interferes with our metabolism – especially glucose metabolism – and increases the risk of developing diabetes,” said Dr. Gómez-Delgado.
High-sodium drinks
When it comes to the influence of artificial sweeteners on hypertension, “there is no single explanation. The World Health Organization already discussed this issue 4-5 years ago, not only due to their carcinogenic risk, but also due to this cardiovascular risk in terms of a lack of control of obesity, diabetes, and hypertension,” said Dr. Anguita.
Another important point “is that this is not in reference to the sweeteners themselves, but to soft drinks containing those components, which is where we have more studies,” he added. There are two factors explaining this increase in hypertension, which poses a problem at the population level, with medium- to long-term follow-up. “The sugary beverages that we mentioned have a higher sodium content. That is, the sweeteners add this element, which is a factor that’s directly linked to the increase in blood pressure levels.” Another factor that can influence blood pressure is “the increase in insulin secretion that has been described as resulting from sweeteners. In the medium and long term, this is associated with increased blood pressure levels.”
Cardiovascular risk factor?
Are artificial sweeteners considered to be a new cardiovascular risk factor? “What they really do is increase the incidence of the other classic risk factors,” including obesity, said Dr. Anguita. It has been shown that artificial sweeteners don’t reduce obesity when used continuously. Nonetheless, “there is still not enough evidence to view it in the same light as the classic risk factors,” added Dr. Anguita. However, it is a factor that can clearly worsen the control of the other factors. Therefore, “it’s appropriate to sound an alarm and explain that it’s not the best way to lose weight; there are many other healthier choices.”
“We need more robust evidence to take a clear position on the use of this type of sweetener and its detrimental effect on health. Meanwhile, it would be ideal to limit their consumption or even avoid adding artificial sweeteners to coffee or teas,” added Dr. Pérez-Martínez.
Regulate consumption
Dr. Pérez-Martínez mentioned that the measures proposed to regulate the consumption of artificial sweeteners and to modify the current legislation must involve “minimizing the consumption of these special dietary products as much as possible and even avoiding adding these artificial sweeteners to the foods that we consume; for example, to coffee and tea.” On the other hand, “we must provide consumers with information that is as clear and simple as possible regarding the composition of the food they consume and how it impacts their health.”
However, “we need more evidence to be able to take a clear position on what type of sweeteners we can consume in our diet and also to what extent we should limit their presence in the foods we consume,” said Dr. Pérez-Martínez.
Last, “most of the evidence is from short-term observational studies that assess frequencies and patterns of consumption of foods containing these artificial sweeteners.” Of course, “we need studies that specifically analyze their effects at the metabolic level as well as longer-term studies where the nutritional follow-up of participants is more accurate and rigorous, especially when it comes to the consumption of this type of food,” concluded Dr. Gómez-Delgado.
This article was translated from the Medscape Spanish Edition. A version appeared on Medscape.com.
FROM CURRENT OPINION IN CARDIOLOGY
Gene therapy offers new way to fight alcohol use disorder
Researchers from Oregon Health & Science University, Portland implanted the therapy directly into the brains of rhesus monkeys that had been conditioned to drink 8-10 alcoholic drinks a day. A harmless virus that carried a specific gene was placed in the region of the brain that regulates dopamine, which provides feelings of reward and pleasure.
“We wanted to see if we could normalize the dopamine in these motivational areas – if, indeed, motivation to overdrink or drink heavily would be mitigated,” said study author Kathleen Grant, PhD, a professor and chief of the division of neuroscience at the university’s Oregon National Primate Research Center.
The need for new alcohol use disorder treatments may be more dire than ever. Alcohol-related deaths in the United States increased dramatically between 2007 and 2020, especially in women, according to research published in the journal JAMA Network Open. The next year, they spiked again, to 108,791 alcohol-related deaths in 2021 alone, according to the National Institutes of Health. That’s slightly more than the number of drug overdoses recorded in 2021.
For the 29.5 million Americans with alcohol use disorder, also known as alcohol abuse or dependence, the road to recovery can be challenging. One reason is that the reward systems in their brains are working against them.
At the first taste of alcohol, the body releases dopamine. But if a person drinks too much for too long, the brain reduces dopamine production and even more alcohol is needed to feel good again.
The gene researchers placed in the monkeys’ brains is called glial-derived neurotrophic factor. It is a growth factor, stimulating cells to multiply. It may help improve function of brain cells that synthesize dopamine, effectively resetting the whole system and reducing the urge to drink.
The study was surprisingly successful. Compared with primates that received a placebo, those that received the growth factor gene decreased their drinking by about 90%. They basically quit drinking, while the primates that got the placebo resumed their habit.
A similar procedure is already used in patients with Parkinson’s disease. But more animal studies, and human clinical trials, would be needed before this therapy could be used in humans with alcohol use disorder. This invasive treatment involves brain surgery, which has risks, so it would likely be reserved for those with the most severe, dangerous drinking habits.
“I think it’d be appropriate for individuals where other treatment modalities just weren’t effective, and they’re worried for their lives,” Dr. Grant said.
Alcohol use disorder treatments
Today, treatment for alcohol use disorder ranges from a brief conversation with a health care provider, in mild cases, to psychiatric treatment or medication in moderate or severe cases.
There are four Food and Drug Administration–approved treatments for alcohol use disorder and a few more medications that health care providers can prescribe off label.
“They’re not widely used,” said Henry Kranzler, MD, a professor of psychiatry and director of the Center for Studies of Addiction at the University of Pennsylvania, Philadelphia. “They’re shockingly underutilized.”
One reason: Just 4.6% of people with alcohol use disorder seek treatment each year, according to NIH data.
“Some of the issues include the ubiquity of alcohol, and its acceptance in American culture – and the fact that that makes it difficult for people to acknowledge that they have a problem with alcohol,” said Dr. Kranzler.
But another problem is that many health care professionals don’t recognize and treat alcohol use disorder in patients who do seek care. Those seeking treatment for alcohol use disorder can find a qualified provider at the American Academy of Addiction Psychiatry or American Society of Addiction Medicine directories.
The future of treatment
Ongoing research could lead to more treatments, and make them more available and more appealing.
Unlike many other drugs that work on a single receptor in the body – like opioids that target opioid receptors, or nicotine, which targets choline receptors – alcohol affects many different receptors, said Robert Swift, MD, PhD, a professor of psychiatry and human behavior at Brown University, Providence, R.I. It also penetrates cells at high doses.
“There are so many different effects of alcohol, which makes it very hard to treat,” he said. “But on the other hand, it gives us an advantage, and there are probably different points that we can attack.”
Other exciting developments are underway, although more research, including clinical trials in humans, is needed before they arrive.
Some of the most promising:
- Hallucinogens. In the 1950s, before they became illegal, these drugs helped people drink less. Even Bill Wilson, cofounder of Alcoholics Anonymous, used hallucinogenic treatment in his recovery; it helped him envision overcoming a challenge. Today, there is renewed interest in hallucinogens for alcohol use disorder. In a study published in , people with alcohol use disorder who were given the hallucinogen psilocybin along with therapy spent fewer days drinking heavily over the following 32 weeks than people who received a different medication. Don’t try to do this yourself, though. “It’s not just taking a hallucinogen and having a trip,” Dr. Swift said. “It’s a therapy-guided session, so it’s a combination of using the hallucinogenic substance with a skilled therapist, and sometimes two skilled therapists, helping to guide the experience.”
- Epigenetic editing. Alcohol exposure can affect the activity of a gene in the amygdala, a brain region involved in emotional processing. found that, by editing that gene in rats through an intravenous line of genetic material, they reduced the rodents’ drinking and anxiety.
- Oxytocin. The so-called love hormone could help reset the dopamine system to make alcohol less appealing. “There are oxytocin receptors on dopamine neurons, and oxytocin makes your dopamine system more effective,” Dr. Swift said. In a from the Medical University of South Carolina, Charleston, mice injected with oxytocin didn’t drink during a stressful situation that could have otherwise led to relapse.
- Ghrelin. This stomach hormone could help curb drinking. In a study published in , mice that received drugs that increased ghrelin reduced their alcohol intake.
A version of this article first appeared on WebMD.com.
Researchers from Oregon Health & Science University, Portland implanted the therapy directly into the brains of rhesus monkeys that had been conditioned to drink 8-10 alcoholic drinks a day. A harmless virus that carried a specific gene was placed in the region of the brain that regulates dopamine, which provides feelings of reward and pleasure.
“We wanted to see if we could normalize the dopamine in these motivational areas – if, indeed, motivation to overdrink or drink heavily would be mitigated,” said study author Kathleen Grant, PhD, a professor and chief of the division of neuroscience at the university’s Oregon National Primate Research Center.
The need for new alcohol use disorder treatments may be more dire than ever. Alcohol-related deaths in the United States increased dramatically between 2007 and 2020, especially in women, according to research published in the journal JAMA Network Open. The next year, they spiked again, to 108,791 alcohol-related deaths in 2021 alone, according to the National Institutes of Health. That’s slightly more than the number of drug overdoses recorded in 2021.
For the 29.5 million Americans with alcohol use disorder, also known as alcohol abuse or dependence, the road to recovery can be challenging. One reason is that the reward systems in their brains are working against them.
At the first taste of alcohol, the body releases dopamine. But if a person drinks too much for too long, the brain reduces dopamine production and even more alcohol is needed to feel good again.
The gene researchers placed in the monkeys’ brains is called glial-derived neurotrophic factor. It is a growth factor, stimulating cells to multiply. It may help improve function of brain cells that synthesize dopamine, effectively resetting the whole system and reducing the urge to drink.
The study was surprisingly successful. Compared with primates that received a placebo, those that received the growth factor gene decreased their drinking by about 90%. They basically quit drinking, while the primates that got the placebo resumed their habit.
A similar procedure is already used in patients with Parkinson’s disease. But more animal studies, and human clinical trials, would be needed before this therapy could be used in humans with alcohol use disorder. This invasive treatment involves brain surgery, which has risks, so it would likely be reserved for those with the most severe, dangerous drinking habits.
“I think it’d be appropriate for individuals where other treatment modalities just weren’t effective, and they’re worried for their lives,” Dr. Grant said.
Alcohol use disorder treatments
Today, treatment for alcohol use disorder ranges from a brief conversation with a health care provider, in mild cases, to psychiatric treatment or medication in moderate or severe cases.
There are four Food and Drug Administration–approved treatments for alcohol use disorder and a few more medications that health care providers can prescribe off label.
“They’re not widely used,” said Henry Kranzler, MD, a professor of psychiatry and director of the Center for Studies of Addiction at the University of Pennsylvania, Philadelphia. “They’re shockingly underutilized.”
One reason: Just 4.6% of people with alcohol use disorder seek treatment each year, according to NIH data.
“Some of the issues include the ubiquity of alcohol, and its acceptance in American culture – and the fact that that makes it difficult for people to acknowledge that they have a problem with alcohol,” said Dr. Kranzler.
But another problem is that many health care professionals don’t recognize and treat alcohol use disorder in patients who do seek care. Those seeking treatment for alcohol use disorder can find a qualified provider at the American Academy of Addiction Psychiatry or American Society of Addiction Medicine directories.
The future of treatment
Ongoing research could lead to more treatments, and make them more available and more appealing.
Unlike many other drugs that work on a single receptor in the body – like opioids that target opioid receptors, or nicotine, which targets choline receptors – alcohol affects many different receptors, said Robert Swift, MD, PhD, a professor of psychiatry and human behavior at Brown University, Providence, R.I. It also penetrates cells at high doses.
“There are so many different effects of alcohol, which makes it very hard to treat,” he said. “But on the other hand, it gives us an advantage, and there are probably different points that we can attack.”
Other exciting developments are underway, although more research, including clinical trials in humans, is needed before they arrive.
Some of the most promising:
- Hallucinogens. In the 1950s, before they became illegal, these drugs helped people drink less. Even Bill Wilson, cofounder of Alcoholics Anonymous, used hallucinogenic treatment in his recovery; it helped him envision overcoming a challenge. Today, there is renewed interest in hallucinogens for alcohol use disorder. In a study published in , people with alcohol use disorder who were given the hallucinogen psilocybin along with therapy spent fewer days drinking heavily over the following 32 weeks than people who received a different medication. Don’t try to do this yourself, though. “It’s not just taking a hallucinogen and having a trip,” Dr. Swift said. “It’s a therapy-guided session, so it’s a combination of using the hallucinogenic substance with a skilled therapist, and sometimes two skilled therapists, helping to guide the experience.”
- Epigenetic editing. Alcohol exposure can affect the activity of a gene in the amygdala, a brain region involved in emotional processing. found that, by editing that gene in rats through an intravenous line of genetic material, they reduced the rodents’ drinking and anxiety.
- Oxytocin. The so-called love hormone could help reset the dopamine system to make alcohol less appealing. “There are oxytocin receptors on dopamine neurons, and oxytocin makes your dopamine system more effective,” Dr. Swift said. In a from the Medical University of South Carolina, Charleston, mice injected with oxytocin didn’t drink during a stressful situation that could have otherwise led to relapse.
- Ghrelin. This stomach hormone could help curb drinking. In a study published in , mice that received drugs that increased ghrelin reduced their alcohol intake.
A version of this article first appeared on WebMD.com.
Researchers from Oregon Health & Science University, Portland implanted the therapy directly into the brains of rhesus monkeys that had been conditioned to drink 8-10 alcoholic drinks a day. A harmless virus that carried a specific gene was placed in the region of the brain that regulates dopamine, which provides feelings of reward and pleasure.
“We wanted to see if we could normalize the dopamine in these motivational areas – if, indeed, motivation to overdrink or drink heavily would be mitigated,” said study author Kathleen Grant, PhD, a professor and chief of the division of neuroscience at the university’s Oregon National Primate Research Center.
The need for new alcohol use disorder treatments may be more dire than ever. Alcohol-related deaths in the United States increased dramatically between 2007 and 2020, especially in women, according to research published in the journal JAMA Network Open. The next year, they spiked again, to 108,791 alcohol-related deaths in 2021 alone, according to the National Institutes of Health. That’s slightly more than the number of drug overdoses recorded in 2021.
For the 29.5 million Americans with alcohol use disorder, also known as alcohol abuse or dependence, the road to recovery can be challenging. One reason is that the reward systems in their brains are working against them.
At the first taste of alcohol, the body releases dopamine. But if a person drinks too much for too long, the brain reduces dopamine production and even more alcohol is needed to feel good again.
The gene researchers placed in the monkeys’ brains is called glial-derived neurotrophic factor. It is a growth factor, stimulating cells to multiply. It may help improve function of brain cells that synthesize dopamine, effectively resetting the whole system and reducing the urge to drink.
The study was surprisingly successful. Compared with primates that received a placebo, those that received the growth factor gene decreased their drinking by about 90%. They basically quit drinking, while the primates that got the placebo resumed their habit.
A similar procedure is already used in patients with Parkinson’s disease. But more animal studies, and human clinical trials, would be needed before this therapy could be used in humans with alcohol use disorder. This invasive treatment involves brain surgery, which has risks, so it would likely be reserved for those with the most severe, dangerous drinking habits.
“I think it’d be appropriate for individuals where other treatment modalities just weren’t effective, and they’re worried for their lives,” Dr. Grant said.
Alcohol use disorder treatments
Today, treatment for alcohol use disorder ranges from a brief conversation with a health care provider, in mild cases, to psychiatric treatment or medication in moderate or severe cases.
There are four Food and Drug Administration–approved treatments for alcohol use disorder and a few more medications that health care providers can prescribe off label.
“They’re not widely used,” said Henry Kranzler, MD, a professor of psychiatry and director of the Center for Studies of Addiction at the University of Pennsylvania, Philadelphia. “They’re shockingly underutilized.”
One reason: Just 4.6% of people with alcohol use disorder seek treatment each year, according to NIH data.
“Some of the issues include the ubiquity of alcohol, and its acceptance in American culture – and the fact that that makes it difficult for people to acknowledge that they have a problem with alcohol,” said Dr. Kranzler.
But another problem is that many health care professionals don’t recognize and treat alcohol use disorder in patients who do seek care. Those seeking treatment for alcohol use disorder can find a qualified provider at the American Academy of Addiction Psychiatry or American Society of Addiction Medicine directories.
The future of treatment
Ongoing research could lead to more treatments, and make them more available and more appealing.
Unlike many other drugs that work on a single receptor in the body – like opioids that target opioid receptors, or nicotine, which targets choline receptors – alcohol affects many different receptors, said Robert Swift, MD, PhD, a professor of psychiatry and human behavior at Brown University, Providence, R.I. It also penetrates cells at high doses.
“There are so many different effects of alcohol, which makes it very hard to treat,” he said. “But on the other hand, it gives us an advantage, and there are probably different points that we can attack.”
Other exciting developments are underway, although more research, including clinical trials in humans, is needed before they arrive.
Some of the most promising:
- Hallucinogens. In the 1950s, before they became illegal, these drugs helped people drink less. Even Bill Wilson, cofounder of Alcoholics Anonymous, used hallucinogenic treatment in his recovery; it helped him envision overcoming a challenge. Today, there is renewed interest in hallucinogens for alcohol use disorder. In a study published in , people with alcohol use disorder who were given the hallucinogen psilocybin along with therapy spent fewer days drinking heavily over the following 32 weeks than people who received a different medication. Don’t try to do this yourself, though. “It’s not just taking a hallucinogen and having a trip,” Dr. Swift said. “It’s a therapy-guided session, so it’s a combination of using the hallucinogenic substance with a skilled therapist, and sometimes two skilled therapists, helping to guide the experience.”
- Epigenetic editing. Alcohol exposure can affect the activity of a gene in the amygdala, a brain region involved in emotional processing. found that, by editing that gene in rats through an intravenous line of genetic material, they reduced the rodents’ drinking and anxiety.
- Oxytocin. The so-called love hormone could help reset the dopamine system to make alcohol less appealing. “There are oxytocin receptors on dopamine neurons, and oxytocin makes your dopamine system more effective,” Dr. Swift said. In a from the Medical University of South Carolina, Charleston, mice injected with oxytocin didn’t drink during a stressful situation that could have otherwise led to relapse.
- Ghrelin. This stomach hormone could help curb drinking. In a study published in , mice that received drugs that increased ghrelin reduced their alcohol intake.
A version of this article first appeared on WebMD.com.
FROM NATURE MEDICINE
Study questions if blue light–blocking glasses really work
Despite claims by their makers, The glasses probably don’t improve wearers’ sleep habits either, according to the study.
Blue light glasses are usually marketed as being able to filter out the potentially harmful effects of blue light from screens, such as eyestrain, dry eye, and sleep problems. Interest in blue light glasses increased during the COVID-19 pandemic as more people stayed home and looked at their computers and phones. They’re often prescribed by optometrists.
The study, published in the Cochrane Database of Systematic Reviews, looked at data collected from 17 clinical trials in six countries that recruited 619 people.
“We found there may be no short-term advantages with using blue light–filtering spectacle lenses to reduce visual fatigue associated with computer use, compared to non–blue-light–filtering lenses,” senior author Laura Downie, PhD, an associate professor of optometry and vision sciences at the University of Melbourne, said in a statement.
“It is also currently unclear whether these lenses affect vision quality or sleep-related outcomes, and no conclusions could be drawn about any potential effects on retinal health in the longer term. People should be aware of these findings when deciding whether to purchase these spectacles.”
Researchers noted that one reason the glasses don’t help is that the amount of blue light received from computer screens and other artificial sources is only about a thousandth of what people get from natural daylight. On top of that, blue light lenses usually filter out only about 10%-25% of blue light.
“Our findings do not support the prescription of blue light–filtering lenses to the general population,” Dr. Downie said.
Eye experts say people can cut down on eyestrain by simply cutting down on the amount of time they look at screens, or by taking regular breaks. To improve sleep, stop looking at screens for a few hours before bedtime.
The researchers noted limitations in their analysis. None of the studies investigated contrast sensitivity, color discrimination, discomfort glare, macular health, serum melatonin levels, or overall patient visual satisfaction.
Also, the length of the different studies varied. More studies of the use of blue light–filtering glasses is needed, the researchers said.
The study received funding from Australia’s National Health and Medical Research Council, the Public Health Agency in the United Kingdom, and Queen’s University Belfast. Two coauthors reported receiving payment from the College of Optometrists.
A version of this article first appeared on WebMD.com.
Despite claims by their makers, The glasses probably don’t improve wearers’ sleep habits either, according to the study.
Blue light glasses are usually marketed as being able to filter out the potentially harmful effects of blue light from screens, such as eyestrain, dry eye, and sleep problems. Interest in blue light glasses increased during the COVID-19 pandemic as more people stayed home and looked at their computers and phones. They’re often prescribed by optometrists.
The study, published in the Cochrane Database of Systematic Reviews, looked at data collected from 17 clinical trials in six countries that recruited 619 people.
“We found there may be no short-term advantages with using blue light–filtering spectacle lenses to reduce visual fatigue associated with computer use, compared to non–blue-light–filtering lenses,” senior author Laura Downie, PhD, an associate professor of optometry and vision sciences at the University of Melbourne, said in a statement.
“It is also currently unclear whether these lenses affect vision quality or sleep-related outcomes, and no conclusions could be drawn about any potential effects on retinal health in the longer term. People should be aware of these findings when deciding whether to purchase these spectacles.”
Researchers noted that one reason the glasses don’t help is that the amount of blue light received from computer screens and other artificial sources is only about a thousandth of what people get from natural daylight. On top of that, blue light lenses usually filter out only about 10%-25% of blue light.
“Our findings do not support the prescription of blue light–filtering lenses to the general population,” Dr. Downie said.
Eye experts say people can cut down on eyestrain by simply cutting down on the amount of time they look at screens, or by taking regular breaks. To improve sleep, stop looking at screens for a few hours before bedtime.
The researchers noted limitations in their analysis. None of the studies investigated contrast sensitivity, color discrimination, discomfort glare, macular health, serum melatonin levels, or overall patient visual satisfaction.
Also, the length of the different studies varied. More studies of the use of blue light–filtering glasses is needed, the researchers said.
The study received funding from Australia’s National Health and Medical Research Council, the Public Health Agency in the United Kingdom, and Queen’s University Belfast. Two coauthors reported receiving payment from the College of Optometrists.
A version of this article first appeared on WebMD.com.
Despite claims by their makers, The glasses probably don’t improve wearers’ sleep habits either, according to the study.
Blue light glasses are usually marketed as being able to filter out the potentially harmful effects of blue light from screens, such as eyestrain, dry eye, and sleep problems. Interest in blue light glasses increased during the COVID-19 pandemic as more people stayed home and looked at their computers and phones. They’re often prescribed by optometrists.
The study, published in the Cochrane Database of Systematic Reviews, looked at data collected from 17 clinical trials in six countries that recruited 619 people.
“We found there may be no short-term advantages with using blue light–filtering spectacle lenses to reduce visual fatigue associated with computer use, compared to non–blue-light–filtering lenses,” senior author Laura Downie, PhD, an associate professor of optometry and vision sciences at the University of Melbourne, said in a statement.
“It is also currently unclear whether these lenses affect vision quality or sleep-related outcomes, and no conclusions could be drawn about any potential effects on retinal health in the longer term. People should be aware of these findings when deciding whether to purchase these spectacles.”
Researchers noted that one reason the glasses don’t help is that the amount of blue light received from computer screens and other artificial sources is only about a thousandth of what people get from natural daylight. On top of that, blue light lenses usually filter out only about 10%-25% of blue light.
“Our findings do not support the prescription of blue light–filtering lenses to the general population,” Dr. Downie said.
Eye experts say people can cut down on eyestrain by simply cutting down on the amount of time they look at screens, or by taking regular breaks. To improve sleep, stop looking at screens for a few hours before bedtime.
The researchers noted limitations in their analysis. None of the studies investigated contrast sensitivity, color discrimination, discomfort glare, macular health, serum melatonin levels, or overall patient visual satisfaction.
Also, the length of the different studies varied. More studies of the use of blue light–filtering glasses is needed, the researchers said.
The study received funding from Australia’s National Health and Medical Research Council, the Public Health Agency in the United Kingdom, and Queen’s University Belfast. Two coauthors reported receiving payment from the College of Optometrists.
A version of this article first appeared on WebMD.com.
FROM COCHRANE DATABASE OF SYSTEMATIC REVIEWS
Short, intense bursts of physical activity may cut cancer risk
The results of a recent study in JAMA Oncology suggest that This activity could be a promising measure for cancer prevention in people who otherwise find it difficult to exercise regularly.
Periods of intense, intermittent physical activity are short phases of strenuous physical exercise that normally last for 1 or 2 minutes, such as a short sprint for the bus or walking up the stairs. In the prospective cohort study conducted in a large group of unathletic adults, researchers investigated a potential dose-effect relationship between intense and daily intermittent physical activity and the cancer incidence rate.
Using data gathered from wearable arm trackers, the researchers analyzed the physical activity of 22,398 people with an average age of 62 years from the UK Biobank. Of these participants, 54.8% were women. After a median follow-up of 6.7 years, corresponding to 149,650 person-years, they determined the general cancer incidence rate in this cohort and the incidence rate of 13 kinds of cancer associated with minimal physical activity (physical-activity related cancers).
Over the study period, 2,356 cancer events occurred, of which 1,084 could be attributed to kinds of cancer associated with minimal physical activity. Nearly all of the intense physical activity (92.3%) was achieved in bursts of up to 1 minute.
Four minutes
The daily duration of activity was almost linearly associated with the outcome, wrote Emmanuel Stamatakis, PhD, professor of physical activity, lifestyle, and population health at the University of Sydney. “The dose-effect curve was more vertical, and the extent of the risk reduction for kinds of cancer associated with minimal activity was larger than for the overall cancer incidence rate.”
For example, the lowest dose of intense, intermittent physical activity of up to 1 minute was generally 3.4 minutes per day for cancer in general and 3.7 minutes per day for cancer associated with minimal activity (hazard ratio, 0.83 and 0.72, respectively).
“The results of the study with an average follow-up time of almost 7 years suggest that people with a little less than 4 minutes per day of sporadic intense activity had an overall 17% lower risk of cancer,” wrote Yvonne Wengström, PhD, professor of nursing at Karolinska Institutet in Stockholm, in an accompanying editorial.
For kinds of cancer possibly associated with minimal activity, the researchers found the risk to be reduced by 28% through daily intermittent physical activity. “Even a few minutes of short, intense physical exercise in people with less leisure activity could lower their cancer risk,” wrote Dr. Wengström and colleagues.
Only at the end of 2022 did the data from Dr. Stamatakis and his colleagues suggest a correlation between a little more than 4 minutes of intense physical activity per day and a lower risk for cardiovascular diseases, cancer, and overall mortality in athletes and nonathletes.
Wearable arm trackers
The authors of the recent study used an existing cohort’s activity data from an earlier substudy of the UK Biobank that measured acceleration in the wrist. The movement behavior here was recorded over a period of 7 days in more than 90,000 people between 2013 and 2015.
Dr. Wengström and her colleagues rated the arm trackers to be more reliable than the questionnaires that were completed by the subjects. “One strength of the present study is that physical activity was evaluated with the help of wrist acceleration meters, even though nonathletes were defined using the questionnaire data.”
Information about the general lifestyle of healthy living people also had to be included. Dr. Wengström believes that the researchers succeeded in this, because they adjusted the analyses for the following important factors:
- Age.
- Sex.
- Body mass index.
- Level of education.
- Smoking status.
- Alcohol consumption.
- Duration of sleep.
- Fruit and vegetable consumption.
- Medication intake.
- Parental cancer history.
Clinical implications
According to Dr. Wengström, more studies are required to see whether the results of this study can also be transferred to patients who already have a cancer disease. This is because patients with cancer such as premenopausal and postmenopausal women with breast cancer diseases, who have different biologies and hormonal environments, are affected differently by physical activity.
However, physical activity does play a role in patients with cancer “since physical fitness improves muscle strength, cancer-related fatigue, and the survivors’ quality of life,” said Dr. Wengström. However, it is still important to find the correct amount of physical activity for each group of patients and for each patient. Nevertheless, “any physical activity is better than none,” wrote Dr. Wengström and her colleagues.
This article was translated from Medscape’s German edition. A version of this article appeared on Medscape.com.
The results of a recent study in JAMA Oncology suggest that This activity could be a promising measure for cancer prevention in people who otherwise find it difficult to exercise regularly.
Periods of intense, intermittent physical activity are short phases of strenuous physical exercise that normally last for 1 or 2 minutes, such as a short sprint for the bus or walking up the stairs. In the prospective cohort study conducted in a large group of unathletic adults, researchers investigated a potential dose-effect relationship between intense and daily intermittent physical activity and the cancer incidence rate.
Using data gathered from wearable arm trackers, the researchers analyzed the physical activity of 22,398 people with an average age of 62 years from the UK Biobank. Of these participants, 54.8% were women. After a median follow-up of 6.7 years, corresponding to 149,650 person-years, they determined the general cancer incidence rate in this cohort and the incidence rate of 13 kinds of cancer associated with minimal physical activity (physical-activity related cancers).
Over the study period, 2,356 cancer events occurred, of which 1,084 could be attributed to kinds of cancer associated with minimal physical activity. Nearly all of the intense physical activity (92.3%) was achieved in bursts of up to 1 minute.
Four minutes
The daily duration of activity was almost linearly associated with the outcome, wrote Emmanuel Stamatakis, PhD, professor of physical activity, lifestyle, and population health at the University of Sydney. “The dose-effect curve was more vertical, and the extent of the risk reduction for kinds of cancer associated with minimal activity was larger than for the overall cancer incidence rate.”
For example, the lowest dose of intense, intermittent physical activity of up to 1 minute was generally 3.4 minutes per day for cancer in general and 3.7 minutes per day for cancer associated with minimal activity (hazard ratio, 0.83 and 0.72, respectively).
“The results of the study with an average follow-up time of almost 7 years suggest that people with a little less than 4 minutes per day of sporadic intense activity had an overall 17% lower risk of cancer,” wrote Yvonne Wengström, PhD, professor of nursing at Karolinska Institutet in Stockholm, in an accompanying editorial.
For kinds of cancer possibly associated with minimal activity, the researchers found the risk to be reduced by 28% through daily intermittent physical activity. “Even a few minutes of short, intense physical exercise in people with less leisure activity could lower their cancer risk,” wrote Dr. Wengström and colleagues.
Only at the end of 2022 did the data from Dr. Stamatakis and his colleagues suggest a correlation between a little more than 4 minutes of intense physical activity per day and a lower risk for cardiovascular diseases, cancer, and overall mortality in athletes and nonathletes.
Wearable arm trackers
The authors of the recent study used an existing cohort’s activity data from an earlier substudy of the UK Biobank that measured acceleration in the wrist. The movement behavior here was recorded over a period of 7 days in more than 90,000 people between 2013 and 2015.
Dr. Wengström and her colleagues rated the arm trackers to be more reliable than the questionnaires that were completed by the subjects. “One strength of the present study is that physical activity was evaluated with the help of wrist acceleration meters, even though nonathletes were defined using the questionnaire data.”
Information about the general lifestyle of healthy living people also had to be included. Dr. Wengström believes that the researchers succeeded in this, because they adjusted the analyses for the following important factors:
- Age.
- Sex.
- Body mass index.
- Level of education.
- Smoking status.
- Alcohol consumption.
- Duration of sleep.
- Fruit and vegetable consumption.
- Medication intake.
- Parental cancer history.
Clinical implications
According to Dr. Wengström, more studies are required to see whether the results of this study can also be transferred to patients who already have a cancer disease. This is because patients with cancer such as premenopausal and postmenopausal women with breast cancer diseases, who have different biologies and hormonal environments, are affected differently by physical activity.
However, physical activity does play a role in patients with cancer “since physical fitness improves muscle strength, cancer-related fatigue, and the survivors’ quality of life,” said Dr. Wengström. However, it is still important to find the correct amount of physical activity for each group of patients and for each patient. Nevertheless, “any physical activity is better than none,” wrote Dr. Wengström and her colleagues.
This article was translated from Medscape’s German edition. A version of this article appeared on Medscape.com.
The results of a recent study in JAMA Oncology suggest that This activity could be a promising measure for cancer prevention in people who otherwise find it difficult to exercise regularly.
Periods of intense, intermittent physical activity are short phases of strenuous physical exercise that normally last for 1 or 2 minutes, such as a short sprint for the bus or walking up the stairs. In the prospective cohort study conducted in a large group of unathletic adults, researchers investigated a potential dose-effect relationship between intense and daily intermittent physical activity and the cancer incidence rate.
Using data gathered from wearable arm trackers, the researchers analyzed the physical activity of 22,398 people with an average age of 62 years from the UK Biobank. Of these participants, 54.8% were women. After a median follow-up of 6.7 years, corresponding to 149,650 person-years, they determined the general cancer incidence rate in this cohort and the incidence rate of 13 kinds of cancer associated with minimal physical activity (physical-activity related cancers).
Over the study period, 2,356 cancer events occurred, of which 1,084 could be attributed to kinds of cancer associated with minimal physical activity. Nearly all of the intense physical activity (92.3%) was achieved in bursts of up to 1 minute.
Four minutes
The daily duration of activity was almost linearly associated with the outcome, wrote Emmanuel Stamatakis, PhD, professor of physical activity, lifestyle, and population health at the University of Sydney. “The dose-effect curve was more vertical, and the extent of the risk reduction for kinds of cancer associated with minimal activity was larger than for the overall cancer incidence rate.”
For example, the lowest dose of intense, intermittent physical activity of up to 1 minute was generally 3.4 minutes per day for cancer in general and 3.7 minutes per day for cancer associated with minimal activity (hazard ratio, 0.83 and 0.72, respectively).
“The results of the study with an average follow-up time of almost 7 years suggest that people with a little less than 4 minutes per day of sporadic intense activity had an overall 17% lower risk of cancer,” wrote Yvonne Wengström, PhD, professor of nursing at Karolinska Institutet in Stockholm, in an accompanying editorial.
For kinds of cancer possibly associated with minimal activity, the researchers found the risk to be reduced by 28% through daily intermittent physical activity. “Even a few minutes of short, intense physical exercise in people with less leisure activity could lower their cancer risk,” wrote Dr. Wengström and colleagues.
Only at the end of 2022 did the data from Dr. Stamatakis and his colleagues suggest a correlation between a little more than 4 minutes of intense physical activity per day and a lower risk for cardiovascular diseases, cancer, and overall mortality in athletes and nonathletes.
Wearable arm trackers
The authors of the recent study used an existing cohort’s activity data from an earlier substudy of the UK Biobank that measured acceleration in the wrist. The movement behavior here was recorded over a period of 7 days in more than 90,000 people between 2013 and 2015.
Dr. Wengström and her colleagues rated the arm trackers to be more reliable than the questionnaires that were completed by the subjects. “One strength of the present study is that physical activity was evaluated with the help of wrist acceleration meters, even though nonathletes were defined using the questionnaire data.”
Information about the general lifestyle of healthy living people also had to be included. Dr. Wengström believes that the researchers succeeded in this, because they adjusted the analyses for the following important factors:
- Age.
- Sex.
- Body mass index.
- Level of education.
- Smoking status.
- Alcohol consumption.
- Duration of sleep.
- Fruit and vegetable consumption.
- Medication intake.
- Parental cancer history.
Clinical implications
According to Dr. Wengström, more studies are required to see whether the results of this study can also be transferred to patients who already have a cancer disease. This is because patients with cancer such as premenopausal and postmenopausal women with breast cancer diseases, who have different biologies and hormonal environments, are affected differently by physical activity.
However, physical activity does play a role in patients with cancer “since physical fitness improves muscle strength, cancer-related fatigue, and the survivors’ quality of life,” said Dr. Wengström. However, it is still important to find the correct amount of physical activity for each group of patients and for each patient. Nevertheless, “any physical activity is better than none,” wrote Dr. Wengström and her colleagues.
This article was translated from Medscape’s German edition. A version of this article appeared on Medscape.com.
FROM JAMA ONCOLOGY
Can this common herb help grow hair?
If you’re looking to grow hair, you might just have a solution in your kitchen cabinet – if TikTok and some dermatologists are correct.
The herb might also protect hair from the sun, pollution, and other environmental elements, according to an article in Insider.
The study published in Skinmed found that rosemary oil was similar to the effectiveness of minoxidil for regrowing hair in men with androgenetic alopecia. The scalp was also less itchy after 3-6 months of use.
The study included only men.
Still, dermatologist Shilpi Khetarpal, MD, told the Cleveland Clinic that it seems to work.
“The study really prompted people to look at rosemary oil for hair growth,” she said. “It became much more common in over-the-counter products after that, too.”
The Cleveland Clinic also reports that rosemary oil might help against dandruff and premature graying.
Dr. Khetarpal suggested massaging rosemary oil into the scalp, letting it soak overnight, and then washing it out. This should be done two or three times a week.
She also noted that only a few drops of rosemary oil are needed, and that the focus should be on the scalp rather than the hair, which rosemary oil makes look greasy.
It may take 6 months for “meaningful improvement,” Dr. Khetarpal said.
Meanwhile, TikTok users love hyping the oil’s hair care qualities. On the social media platform, videos with the hashtag #rosemaryoil have been viewed more than 2 billion times.
A version of this article appeared on WebMD.com.
If you’re looking to grow hair, you might just have a solution in your kitchen cabinet – if TikTok and some dermatologists are correct.
The herb might also protect hair from the sun, pollution, and other environmental elements, according to an article in Insider.
The study published in Skinmed found that rosemary oil was similar to the effectiveness of minoxidil for regrowing hair in men with androgenetic alopecia. The scalp was also less itchy after 3-6 months of use.
The study included only men.
Still, dermatologist Shilpi Khetarpal, MD, told the Cleveland Clinic that it seems to work.
“The study really prompted people to look at rosemary oil for hair growth,” she said. “It became much more common in over-the-counter products after that, too.”
The Cleveland Clinic also reports that rosemary oil might help against dandruff and premature graying.
Dr. Khetarpal suggested massaging rosemary oil into the scalp, letting it soak overnight, and then washing it out. This should be done two or three times a week.
She also noted that only a few drops of rosemary oil are needed, and that the focus should be on the scalp rather than the hair, which rosemary oil makes look greasy.
It may take 6 months for “meaningful improvement,” Dr. Khetarpal said.
Meanwhile, TikTok users love hyping the oil’s hair care qualities. On the social media platform, videos with the hashtag #rosemaryoil have been viewed more than 2 billion times.
A version of this article appeared on WebMD.com.
If you’re looking to grow hair, you might just have a solution in your kitchen cabinet – if TikTok and some dermatologists are correct.
The herb might also protect hair from the sun, pollution, and other environmental elements, according to an article in Insider.
The study published in Skinmed found that rosemary oil was similar to the effectiveness of minoxidil for regrowing hair in men with androgenetic alopecia. The scalp was also less itchy after 3-6 months of use.
The study included only men.
Still, dermatologist Shilpi Khetarpal, MD, told the Cleveland Clinic that it seems to work.
“The study really prompted people to look at rosemary oil for hair growth,” she said. “It became much more common in over-the-counter products after that, too.”
The Cleveland Clinic also reports that rosemary oil might help against dandruff and premature graying.
Dr. Khetarpal suggested massaging rosemary oil into the scalp, letting it soak overnight, and then washing it out. This should be done two or three times a week.
She also noted that only a few drops of rosemary oil are needed, and that the focus should be on the scalp rather than the hair, which rosemary oil makes look greasy.
It may take 6 months for “meaningful improvement,” Dr. Khetarpal said.
Meanwhile, TikTok users love hyping the oil’s hair care qualities. On the social media platform, videos with the hashtag #rosemaryoil have been viewed more than 2 billion times.
A version of this article appeared on WebMD.com.
CDC tracking new COVID strain
On Aug. 17, the agency posted on X, formerly known as Twitter, that the lineage has been detected in the United States, Denmark, and Israel.
“As we learn more about BA.2.86, CDC’s advice on protecting yourself from COVID-19 remains the same,” the CDC said on X.
A case of BA.2.86 was detected at a laboratory at the University of Michigan, CBS News reported. It’s not clear how the university obtained the sample that was sequenced. A case was also detected in the United Kingdom, the news outlet said.
The World Health Organization is also tracking BA.2.86 and has classified it as a “variant under monitoring.”
“More data are needed to understand this COVID-19 variant and the extent of its spread, but the number of mutations warrants attention. WHO will update countries and the public as we learn more,” the WHO said on X.
The strain is so new that scientists don’t know if BA.2.86 is more easily spread, causes more severe symptoms than existing strains, or will be more resistant to vaccines and natural immunity developed over the last few years.
Early research indicates BA.2.86 “will have equal or greater escape than XBB.1.5 from antibodies elicited by pre-Omicron and first-generation Omicron variants,” Jesse Bloom, PhD, a virologist at the Fred Hutchinson Cancer Center, said in a slide deck published Aug. 17. (XBB.1.5 is the Omicron subvariant that is targeted in the updated COVID booster shot to be released soon.)
Still, Dr. Bloom noted that “even if a highly mutated new variant like BA.2.86 starts to spread, we will be in a far better place than we were in 2020 and 2021, since most people have some immunity to SARS-CoV-2 now.”
A version of this article first appeared on WebMD.com.
On Aug. 17, the agency posted on X, formerly known as Twitter, that the lineage has been detected in the United States, Denmark, and Israel.
“As we learn more about BA.2.86, CDC’s advice on protecting yourself from COVID-19 remains the same,” the CDC said on X.
A case of BA.2.86 was detected at a laboratory at the University of Michigan, CBS News reported. It’s not clear how the university obtained the sample that was sequenced. A case was also detected in the United Kingdom, the news outlet said.
The World Health Organization is also tracking BA.2.86 and has classified it as a “variant under monitoring.”
“More data are needed to understand this COVID-19 variant and the extent of its spread, but the number of mutations warrants attention. WHO will update countries and the public as we learn more,” the WHO said on X.
The strain is so new that scientists don’t know if BA.2.86 is more easily spread, causes more severe symptoms than existing strains, or will be more resistant to vaccines and natural immunity developed over the last few years.
Early research indicates BA.2.86 “will have equal or greater escape than XBB.1.5 from antibodies elicited by pre-Omicron and first-generation Omicron variants,” Jesse Bloom, PhD, a virologist at the Fred Hutchinson Cancer Center, said in a slide deck published Aug. 17. (XBB.1.5 is the Omicron subvariant that is targeted in the updated COVID booster shot to be released soon.)
Still, Dr. Bloom noted that “even if a highly mutated new variant like BA.2.86 starts to spread, we will be in a far better place than we were in 2020 and 2021, since most people have some immunity to SARS-CoV-2 now.”
A version of this article first appeared on WebMD.com.
On Aug. 17, the agency posted on X, formerly known as Twitter, that the lineage has been detected in the United States, Denmark, and Israel.
“As we learn more about BA.2.86, CDC’s advice on protecting yourself from COVID-19 remains the same,” the CDC said on X.
A case of BA.2.86 was detected at a laboratory at the University of Michigan, CBS News reported. It’s not clear how the university obtained the sample that was sequenced. A case was also detected in the United Kingdom, the news outlet said.
The World Health Organization is also tracking BA.2.86 and has classified it as a “variant under monitoring.”
“More data are needed to understand this COVID-19 variant and the extent of its spread, but the number of mutations warrants attention. WHO will update countries and the public as we learn more,” the WHO said on X.
The strain is so new that scientists don’t know if BA.2.86 is more easily spread, causes more severe symptoms than existing strains, or will be more resistant to vaccines and natural immunity developed over the last few years.
Early research indicates BA.2.86 “will have equal or greater escape than XBB.1.5 from antibodies elicited by pre-Omicron and first-generation Omicron variants,” Jesse Bloom, PhD, a virologist at the Fred Hutchinson Cancer Center, said in a slide deck published Aug. 17. (XBB.1.5 is the Omicron subvariant that is targeted in the updated COVID booster shot to be released soon.)
Still, Dr. Bloom noted that “even if a highly mutated new variant like BA.2.86 starts to spread, we will be in a far better place than we were in 2020 and 2021, since most people have some immunity to SARS-CoV-2 now.”
A version of this article first appeared on WebMD.com.
Few meet eligibility for newer Alzheimer’s drugs
, a cross sectional study has found.
Reporting in the journal Neurology, researchers from the Mayo Clinic in Rochester, Minn., and the University of Chicago found that only a small percentage of patients in the Mayo Clinic Study of Aging (MCSA) with mild cognitive impairment (MCI) or mild dementia due to Alzheimer’s disease would meet the clinical trial eligibility requirements of either agent.
“Our study results show only a small percentage of people with early Alzheimer’s disease may be eligible to receive treatment, mostly due to chronic health conditions and brain scan abnormalities common in older adults,” said lead researcher Maria Vassilaki, MD, PhD, an epidemiologist at Mayo Clinic in Rochester, Minn.
Applying clinical trial exclusion criteria to a broader population
The study included 237 people aged 50-90, 222 who had MCI and 15 with mild dementia, and whose brain scans showed increased amounts of amyloid-beta plaques. Average age of the participants was 80.9 years and 97.5% were White (99.6% not Hispanic or Latino).
The researchers then looked at the eligibility criteria for the pivotal clinical trials for lecanemab, which the U.S. Food and Drug Administration approved in January this year, and aducanumab, which the FDA cleared in 2021. Both drugs received FDA accelerated approval.
For lecanemab, clinical trial inclusion required specific scores for the Clinical Dementia Rating (CDR) (other than 0.5 or 1.0), Wechsler Memory Scale (WMS-R) Logical Memory II (which varied with age group), or Mini-Mental State Examination (MMSE) (22 to 30). A body mass index between 17 and 35 kg/m2 was also an inclusion criteria. Only 112 people, or 47%, met the inclusion criteria. Exclusion criteria included a history of cardiovascular disease or cancer, Parkinson’s disease, or brain injury, or a positive brain scan. When the exclusion criteria were applied, only 19 people, or 8%, qualified for the lecanemab trial.
When the researchers modified the exclusion criteria to include all study participants with MCI but not applying results from additional cognitive tests, 17.4% of MCSA patients would have been eligible for the lecanemab trial.
Aducanumab clinical trial inclusion criteria were a CDR global score other than 0.5 and an MMSE below 24, with an age cutoff of 85 years. Only 104 of the MCSA population, or 44%, met the clinical trial criteria. When the researchers applied the exclusion criteria for cardiovascular disease, central nervous system-related exclusions (such as brain cancer or epilepsy), a history of cancer, or brain scan abnormalities, they found that only 12 people, or 5%, would have been eligible for an aducanumab trial.
“Clinical trials often have strict eligibility criteria and could exclude those with other conditions that could be common in older adults,” Dr. Vassilaki said in emailed comments. “Thus, we wanted to examine if we apply these criteria to a study that recruits participants from the community, how many of the individuals in the early symptomatic stages, mild cognitive impairment or mild dementia due to Alzheimer’s disease, would be eligible for the treatment.”
Dr. Vassilaki said these drugs need to be studied in larger, more diverse populations, as well as in less healthy populations, before they’re more widely available to people with Alzheimer’s disease. “In addition,” she said, “we can learn more from the postmarketing surveillance of side effects and also from registries of patients receiving these treatments.”
One limitation of the study Dr. Vassilaki pointed out is the overwhelmingly White population. Evaluating the clinical trial eligibility criteria in more diverse populations is crucial, she said.
Estimating the number of patients who would qualify for treatment
In an accompanying commentary, Matthew Howes, MD, of Butler Hospital and Brown University in Providence, R.I., and colleagues wrote that the study findings provide health systems planning to offer amyloid-lowering antibodies for Alzheimer’s disease an estimate of how many patients would be eligible for the treatments. “Providers must exercise clinical judgment in selecting patients for treatment with shared decision-making with patients and families,” the commentators wrote.
The study was supported by the National Institutes of Health, the National Institute on Aging, the Alexander Family Alzheimer’s Disease Research Professorship of the Mayo Clinic, the Mayo Foundation for Medical Education and Research, the Liston Award, the GHR Foundation, and the Schuler Foundation. Dr. Vassilaki disclosed relationships with F. Hoffmann-La Roche, Abbott Laboratories, Johnson & Johnson, Medtronic, Merck, and Amgen. Dr. Howe has no relevant disclosures.
, a cross sectional study has found.
Reporting in the journal Neurology, researchers from the Mayo Clinic in Rochester, Minn., and the University of Chicago found that only a small percentage of patients in the Mayo Clinic Study of Aging (MCSA) with mild cognitive impairment (MCI) or mild dementia due to Alzheimer’s disease would meet the clinical trial eligibility requirements of either agent.
“Our study results show only a small percentage of people with early Alzheimer’s disease may be eligible to receive treatment, mostly due to chronic health conditions and brain scan abnormalities common in older adults,” said lead researcher Maria Vassilaki, MD, PhD, an epidemiologist at Mayo Clinic in Rochester, Minn.
Applying clinical trial exclusion criteria to a broader population
The study included 237 people aged 50-90, 222 who had MCI and 15 with mild dementia, and whose brain scans showed increased amounts of amyloid-beta plaques. Average age of the participants was 80.9 years and 97.5% were White (99.6% not Hispanic or Latino).
The researchers then looked at the eligibility criteria for the pivotal clinical trials for lecanemab, which the U.S. Food and Drug Administration approved in January this year, and aducanumab, which the FDA cleared in 2021. Both drugs received FDA accelerated approval.
For lecanemab, clinical trial inclusion required specific scores for the Clinical Dementia Rating (CDR) (other than 0.5 or 1.0), Wechsler Memory Scale (WMS-R) Logical Memory II (which varied with age group), or Mini-Mental State Examination (MMSE) (22 to 30). A body mass index between 17 and 35 kg/m2 was also an inclusion criteria. Only 112 people, or 47%, met the inclusion criteria. Exclusion criteria included a history of cardiovascular disease or cancer, Parkinson’s disease, or brain injury, or a positive brain scan. When the exclusion criteria were applied, only 19 people, or 8%, qualified for the lecanemab trial.
When the researchers modified the exclusion criteria to include all study participants with MCI but not applying results from additional cognitive tests, 17.4% of MCSA patients would have been eligible for the lecanemab trial.
Aducanumab clinical trial inclusion criteria were a CDR global score other than 0.5 and an MMSE below 24, with an age cutoff of 85 years. Only 104 of the MCSA population, or 44%, met the clinical trial criteria. When the researchers applied the exclusion criteria for cardiovascular disease, central nervous system-related exclusions (such as brain cancer or epilepsy), a history of cancer, or brain scan abnormalities, they found that only 12 people, or 5%, would have been eligible for an aducanumab trial.
“Clinical trials often have strict eligibility criteria and could exclude those with other conditions that could be common in older adults,” Dr. Vassilaki said in emailed comments. “Thus, we wanted to examine if we apply these criteria to a study that recruits participants from the community, how many of the individuals in the early symptomatic stages, mild cognitive impairment or mild dementia due to Alzheimer’s disease, would be eligible for the treatment.”
Dr. Vassilaki said these drugs need to be studied in larger, more diverse populations, as well as in less healthy populations, before they’re more widely available to people with Alzheimer’s disease. “In addition,” she said, “we can learn more from the postmarketing surveillance of side effects and also from registries of patients receiving these treatments.”
One limitation of the study Dr. Vassilaki pointed out is the overwhelmingly White population. Evaluating the clinical trial eligibility criteria in more diverse populations is crucial, she said.
Estimating the number of patients who would qualify for treatment
In an accompanying commentary, Matthew Howes, MD, of Butler Hospital and Brown University in Providence, R.I., and colleagues wrote that the study findings provide health systems planning to offer amyloid-lowering antibodies for Alzheimer’s disease an estimate of how many patients would be eligible for the treatments. “Providers must exercise clinical judgment in selecting patients for treatment with shared decision-making with patients and families,” the commentators wrote.
The study was supported by the National Institutes of Health, the National Institute on Aging, the Alexander Family Alzheimer’s Disease Research Professorship of the Mayo Clinic, the Mayo Foundation for Medical Education and Research, the Liston Award, the GHR Foundation, and the Schuler Foundation. Dr. Vassilaki disclosed relationships with F. Hoffmann-La Roche, Abbott Laboratories, Johnson & Johnson, Medtronic, Merck, and Amgen. Dr. Howe has no relevant disclosures.
, a cross sectional study has found.
Reporting in the journal Neurology, researchers from the Mayo Clinic in Rochester, Minn., and the University of Chicago found that only a small percentage of patients in the Mayo Clinic Study of Aging (MCSA) with mild cognitive impairment (MCI) or mild dementia due to Alzheimer’s disease would meet the clinical trial eligibility requirements of either agent.
“Our study results show only a small percentage of people with early Alzheimer’s disease may be eligible to receive treatment, mostly due to chronic health conditions and brain scan abnormalities common in older adults,” said lead researcher Maria Vassilaki, MD, PhD, an epidemiologist at Mayo Clinic in Rochester, Minn.
Applying clinical trial exclusion criteria to a broader population
The study included 237 people aged 50-90, 222 who had MCI and 15 with mild dementia, and whose brain scans showed increased amounts of amyloid-beta plaques. Average age of the participants was 80.9 years and 97.5% were White (99.6% not Hispanic or Latino).
The researchers then looked at the eligibility criteria for the pivotal clinical trials for lecanemab, which the U.S. Food and Drug Administration approved in January this year, and aducanumab, which the FDA cleared in 2021. Both drugs received FDA accelerated approval.
For lecanemab, clinical trial inclusion required specific scores for the Clinical Dementia Rating (CDR) (other than 0.5 or 1.0), Wechsler Memory Scale (WMS-R) Logical Memory II (which varied with age group), or Mini-Mental State Examination (MMSE) (22 to 30). A body mass index between 17 and 35 kg/m2 was also an inclusion criteria. Only 112 people, or 47%, met the inclusion criteria. Exclusion criteria included a history of cardiovascular disease or cancer, Parkinson’s disease, or brain injury, or a positive brain scan. When the exclusion criteria were applied, only 19 people, or 8%, qualified for the lecanemab trial.
When the researchers modified the exclusion criteria to include all study participants with MCI but not applying results from additional cognitive tests, 17.4% of MCSA patients would have been eligible for the lecanemab trial.
Aducanumab clinical trial inclusion criteria were a CDR global score other than 0.5 and an MMSE below 24, with an age cutoff of 85 years. Only 104 of the MCSA population, or 44%, met the clinical trial criteria. When the researchers applied the exclusion criteria for cardiovascular disease, central nervous system-related exclusions (such as brain cancer or epilepsy), a history of cancer, or brain scan abnormalities, they found that only 12 people, or 5%, would have been eligible for an aducanumab trial.
“Clinical trials often have strict eligibility criteria and could exclude those with other conditions that could be common in older adults,” Dr. Vassilaki said in emailed comments. “Thus, we wanted to examine if we apply these criteria to a study that recruits participants from the community, how many of the individuals in the early symptomatic stages, mild cognitive impairment or mild dementia due to Alzheimer’s disease, would be eligible for the treatment.”
Dr. Vassilaki said these drugs need to be studied in larger, more diverse populations, as well as in less healthy populations, before they’re more widely available to people with Alzheimer’s disease. “In addition,” she said, “we can learn more from the postmarketing surveillance of side effects and also from registries of patients receiving these treatments.”
One limitation of the study Dr. Vassilaki pointed out is the overwhelmingly White population. Evaluating the clinical trial eligibility criteria in more diverse populations is crucial, she said.
Estimating the number of patients who would qualify for treatment
In an accompanying commentary, Matthew Howes, MD, of Butler Hospital and Brown University in Providence, R.I., and colleagues wrote that the study findings provide health systems planning to offer amyloid-lowering antibodies for Alzheimer’s disease an estimate of how many patients would be eligible for the treatments. “Providers must exercise clinical judgment in selecting patients for treatment with shared decision-making with patients and families,” the commentators wrote.
The study was supported by the National Institutes of Health, the National Institute on Aging, the Alexander Family Alzheimer’s Disease Research Professorship of the Mayo Clinic, the Mayo Foundation for Medical Education and Research, the Liston Award, the GHR Foundation, and the Schuler Foundation. Dr. Vassilaki disclosed relationships with F. Hoffmann-La Roche, Abbott Laboratories, Johnson & Johnson, Medtronic, Merck, and Amgen. Dr. Howe has no relevant disclosures.
FROM NEUROLOGY
On the trail of a new vaccine for Lyme disease
The results of their study were published in the journal Microbiome.
Ticks are vectors of many harmful pathogens that can cause life-threatening illnesses. Ixodes ricinus (in Europe) and Ixodes scapularis (in Canada and the United States) carry Borrelia, the bacteria that cause Lyme disease. At the moment, there is no vaccine for this disease. But that could all change, thanks to the findings of scientists at the National Research Institute for Agriculture, Food, and Environment (INRAE), in collaboration with the Agency for Food, Environmental, and Occupational Health and Safety and the National Veterinary School of Alfort, France.
“Ticks can transmit a broad variety of pathogens of medical importance, including Borrelia afzelii, the causative agent of Lyme borreliosis in Europe. Tick microbiota is an important factor modulating not only vector physiology, but also the vector competence,” the team reported. They focused their efforts on developing a vaccine that would disturb the tick microbiota and thus reduce Borrelia colonization.
To explore this indirect approach, they injected a harmless strain of Escherichia coli bacteria into mice, which then produced antibodies. Their reasoning was that when a tick bites one of these mice, the antibodies would pass into the arachnid’s microbiota and disturb it, thereby making the tick less harmful. And indeed, the researchers’ work showed that in the ticks that fed on vaccinated mice, levels of Borrelia levels were much lower than in than ticks that fed on unvaccinated mice (see video for an explanation). So, when given to a mouse, this vaccine “protects” the tick against colonization by Borrelia but does not protect the mouse against the disease.
The study has advanced this area of research in two significant ways: It provides new information on the importance of the microbiota when it comes to ticks that are infected with Borrelia, and it suggests an innovative vaccination strategy. Indeed, the results confirm that tick microbiota is essential for the development of Borrelia in the arachnid. As noted in an INRAE press release, “This is a key piece of data that opens the door to one day having an innovative vaccination strategy aimed at perturbing the microbiota of the vector of the Lyme disease agent.”
Dengue, Zika virus, and malaria are also transmitted by a vector – the mosquito. Innovative antimicrobiota vaccines may be able to control these diseases as well.
This article was translated from the Medscape French Edition. A version of this article appeared on Medscape.com.
The results of their study were published in the journal Microbiome.
Ticks are vectors of many harmful pathogens that can cause life-threatening illnesses. Ixodes ricinus (in Europe) and Ixodes scapularis (in Canada and the United States) carry Borrelia, the bacteria that cause Lyme disease. At the moment, there is no vaccine for this disease. But that could all change, thanks to the findings of scientists at the National Research Institute for Agriculture, Food, and Environment (INRAE), in collaboration with the Agency for Food, Environmental, and Occupational Health and Safety and the National Veterinary School of Alfort, France.
“Ticks can transmit a broad variety of pathogens of medical importance, including Borrelia afzelii, the causative agent of Lyme borreliosis in Europe. Tick microbiota is an important factor modulating not only vector physiology, but also the vector competence,” the team reported. They focused their efforts on developing a vaccine that would disturb the tick microbiota and thus reduce Borrelia colonization.
To explore this indirect approach, they injected a harmless strain of Escherichia coli bacteria into mice, which then produced antibodies. Their reasoning was that when a tick bites one of these mice, the antibodies would pass into the arachnid’s microbiota and disturb it, thereby making the tick less harmful. And indeed, the researchers’ work showed that in the ticks that fed on vaccinated mice, levels of Borrelia levels were much lower than in than ticks that fed on unvaccinated mice (see video for an explanation). So, when given to a mouse, this vaccine “protects” the tick against colonization by Borrelia but does not protect the mouse against the disease.
The study has advanced this area of research in two significant ways: It provides new information on the importance of the microbiota when it comes to ticks that are infected with Borrelia, and it suggests an innovative vaccination strategy. Indeed, the results confirm that tick microbiota is essential for the development of Borrelia in the arachnid. As noted in an INRAE press release, “This is a key piece of data that opens the door to one day having an innovative vaccination strategy aimed at perturbing the microbiota of the vector of the Lyme disease agent.”
Dengue, Zika virus, and malaria are also transmitted by a vector – the mosquito. Innovative antimicrobiota vaccines may be able to control these diseases as well.
This article was translated from the Medscape French Edition. A version of this article appeared on Medscape.com.
The results of their study were published in the journal Microbiome.
Ticks are vectors of many harmful pathogens that can cause life-threatening illnesses. Ixodes ricinus (in Europe) and Ixodes scapularis (in Canada and the United States) carry Borrelia, the bacteria that cause Lyme disease. At the moment, there is no vaccine for this disease. But that could all change, thanks to the findings of scientists at the National Research Institute for Agriculture, Food, and Environment (INRAE), in collaboration with the Agency for Food, Environmental, and Occupational Health and Safety and the National Veterinary School of Alfort, France.
“Ticks can transmit a broad variety of pathogens of medical importance, including Borrelia afzelii, the causative agent of Lyme borreliosis in Europe. Tick microbiota is an important factor modulating not only vector physiology, but also the vector competence,” the team reported. They focused their efforts on developing a vaccine that would disturb the tick microbiota and thus reduce Borrelia colonization.
To explore this indirect approach, they injected a harmless strain of Escherichia coli bacteria into mice, which then produced antibodies. Their reasoning was that when a tick bites one of these mice, the antibodies would pass into the arachnid’s microbiota and disturb it, thereby making the tick less harmful. And indeed, the researchers’ work showed that in the ticks that fed on vaccinated mice, levels of Borrelia levels were much lower than in than ticks that fed on unvaccinated mice (see video for an explanation). So, when given to a mouse, this vaccine “protects” the tick against colonization by Borrelia but does not protect the mouse against the disease.
The study has advanced this area of research in two significant ways: It provides new information on the importance of the microbiota when it comes to ticks that are infected with Borrelia, and it suggests an innovative vaccination strategy. Indeed, the results confirm that tick microbiota is essential for the development of Borrelia in the arachnid. As noted in an INRAE press release, “This is a key piece of data that opens the door to one day having an innovative vaccination strategy aimed at perturbing the microbiota of the vector of the Lyme disease agent.”
Dengue, Zika virus, and malaria are also transmitted by a vector – the mosquito. Innovative antimicrobiota vaccines may be able to control these diseases as well.
This article was translated from the Medscape French Edition. A version of this article appeared on Medscape.com.
FROM MICROBIOME