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FDA Removes Harmful Chemicals From Food Packaging
Issued on February 28, 2024, “this means the major source of dietary exposure to PFAS from food packaging like fast-food wrappers, microwave popcorn bags, take-out paperboard containers, and pet food bags is being eliminated,” the FDA said in a statement.
In 2020, the FDA had secured commitments from manufacturers to stop selling products containing PFAS used in the food packaging for grease-proofing. “Today’s announcement marks the fulfillment of these voluntary commitments,” according to the agency.
PFAS, a class of thousands of chemicals also called “forever chemicals” are widely used in consumer and industrial products. People may be exposed via contaminated food packaging (although perhaps no longer in the United States) or occupationally. Studies have found that some PFAS disrupt hormones including estrogen and testosterone, whereas others may impair thyroid function.
Endocrine Society Report Sounds the Alarm About PFAS and Others
The FDA’s announcement came just 2 days after the Endocrine Society issued a new alarm about the human health dangers from environmental EDCs including PFAS in a report covering the latest science.
“Endocrine disrupting chemicals” are individual substances or mixtures that can interfere with natural hormonal function, leading to disease or even death. Many are ubiquitous in the modern environment and contribute to a wide range of human diseases.
The new report Endocrine Disrupting Chemicals: Threats to Human Health was issued jointly with the International Pollutants Elimination Network (IPEN), a global advocacy organization. It’s an update to the Endocrine Society’s 2015 report, providing new data on the endocrine-disrupting substances previously covered and adding four EDCs not discussed in that document: Pesticides, plastics, PFAS, and children’s products containing arsenic.
At a briefing held during the United Nations Environment Assembly meeting in Nairobi, Kenya, last week, the new report’s lead author Andrea C. Gore, PhD, of the University of Texas at Austin, noted, “A well-established body of scientific research indicates that endocrine-disrupting chemicals that are part of our daily lives are making us more susceptible to reproductive disorders, cancer, diabetes, obesity, heart disease, and other serious health conditions.”
Added Dr. Gore, who is also a member of the Endocrine Society’s Board of Directors, “These chemicals pose particularly serious risks to pregnant women and children. Now is the time for the UN Environment Assembly and other global policymakers to take action to address this threat to public health.”
While the science has been emerging rapidly, global and national chemical control policies haven’t kept up, the authors said. Of particular concern is that EDCs behave differently from other chemicals in many ways, including that even very low-dose exposures can pose health threats, but policies thus far haven’t dealt with that aspect.
Moreover, “the effects of low doses cannot be predicted by the effects observed at high doses. This means there may be no safe dose for exposure to EDCs,” according to the report.
Exposures can come from household products, including furniture, toys, and food packages, as well as electronics building materials and cosmetics. These chemicals are also in the outdoor environment, via pesticides, air pollution, and industrial waste.
“IPEN and the Endocrine Society call for chemical regulations based on the most modern scientific understanding of how hormones act and how EDCs can perturb these actions. We work to educate policy makers in global, regional, and national government assemblies and help ensure that regulations correlate with current scientific understanding,” they said in the report.
New Data on Four Classes of EDCs
Chapters of the report summarized the latest information about the science of EDCs and their links to endocrine disease and real-world exposure. It included a special section about “EDCs throughout the plastics life cycle” and a summary of the links between EDCs and climate change.
The report reviewed three pesticides, including the world’s most heavily applied herbicide, glycophosphate. Exposures can occur directly from the air, water, dust, and food residues. Recent data linked glycophosphate to adverse reproductive health outcomes.
Two toxic plastic chemicals, phthalates and bisphenols, are present in personal care products, among others. Emerging evidence links them with impaired neurodevelopment, leading to impaired cognitive function, learning, attention, and impulsivity.
Arsenic has long been linked to human health conditions including cancer, but more recent evidence finds it can disrupt multiple endocrine systems and lead to metabolic conditions including diabetes, reproductive dysfunction, and cardiovascular and neurocognitive conditions.
The special section about plastics noted that they are made from fossil fuels and chemicals, including many toxic substances that are known or suspected EDCs. People who live near plastic production facilities or waste dumps may be at greatest risk, but anyone can be exposed using any plastic product. Plastic waste disposal is increasingly problematic and often foisted on lower- and middle-income countries.
‘Additional Education and Awareness-Raising Among Stakeholders Remain Necessary’
Policies aimed at reducing human health risks from EDCs have included the 2022 Plastics Treaty, a resolution adopted by 175 countries at the United Nations Environmental Assembly that “may be a significant step toward global control of plastics and elimination of threats from exposures to EDCs in plastics,” the report said.
The authors added, “While significant progress has been made in recent years connecting scientific advances on EDCs with health-protective policies, additional education and awareness-raising among stakeholders remain necessary to achieve a safer and more sustainable environment that minimizes exposure to these harmful chemicals.”
The document was produced with financial contributions from the Government of Sweden, the Tides Foundation, Passport Foundation, and other donors.
A version of this article appeared on Medscape.com.
Issued on February 28, 2024, “this means the major source of dietary exposure to PFAS from food packaging like fast-food wrappers, microwave popcorn bags, take-out paperboard containers, and pet food bags is being eliminated,” the FDA said in a statement.
In 2020, the FDA had secured commitments from manufacturers to stop selling products containing PFAS used in the food packaging for grease-proofing. “Today’s announcement marks the fulfillment of these voluntary commitments,” according to the agency.
PFAS, a class of thousands of chemicals also called “forever chemicals” are widely used in consumer and industrial products. People may be exposed via contaminated food packaging (although perhaps no longer in the United States) or occupationally. Studies have found that some PFAS disrupt hormones including estrogen and testosterone, whereas others may impair thyroid function.
Endocrine Society Report Sounds the Alarm About PFAS and Others
The FDA’s announcement came just 2 days after the Endocrine Society issued a new alarm about the human health dangers from environmental EDCs including PFAS in a report covering the latest science.
“Endocrine disrupting chemicals” are individual substances or mixtures that can interfere with natural hormonal function, leading to disease or even death. Many are ubiquitous in the modern environment and contribute to a wide range of human diseases.
The new report Endocrine Disrupting Chemicals: Threats to Human Health was issued jointly with the International Pollutants Elimination Network (IPEN), a global advocacy organization. It’s an update to the Endocrine Society’s 2015 report, providing new data on the endocrine-disrupting substances previously covered and adding four EDCs not discussed in that document: Pesticides, plastics, PFAS, and children’s products containing arsenic.
At a briefing held during the United Nations Environment Assembly meeting in Nairobi, Kenya, last week, the new report’s lead author Andrea C. Gore, PhD, of the University of Texas at Austin, noted, “A well-established body of scientific research indicates that endocrine-disrupting chemicals that are part of our daily lives are making us more susceptible to reproductive disorders, cancer, diabetes, obesity, heart disease, and other serious health conditions.”
Added Dr. Gore, who is also a member of the Endocrine Society’s Board of Directors, “These chemicals pose particularly serious risks to pregnant women and children. Now is the time for the UN Environment Assembly and other global policymakers to take action to address this threat to public health.”
While the science has been emerging rapidly, global and national chemical control policies haven’t kept up, the authors said. Of particular concern is that EDCs behave differently from other chemicals in many ways, including that even very low-dose exposures can pose health threats, but policies thus far haven’t dealt with that aspect.
Moreover, “the effects of low doses cannot be predicted by the effects observed at high doses. This means there may be no safe dose for exposure to EDCs,” according to the report.
Exposures can come from household products, including furniture, toys, and food packages, as well as electronics building materials and cosmetics. These chemicals are also in the outdoor environment, via pesticides, air pollution, and industrial waste.
“IPEN and the Endocrine Society call for chemical regulations based on the most modern scientific understanding of how hormones act and how EDCs can perturb these actions. We work to educate policy makers in global, regional, and national government assemblies and help ensure that regulations correlate with current scientific understanding,” they said in the report.
New Data on Four Classes of EDCs
Chapters of the report summarized the latest information about the science of EDCs and their links to endocrine disease and real-world exposure. It included a special section about “EDCs throughout the plastics life cycle” and a summary of the links between EDCs and climate change.
The report reviewed three pesticides, including the world’s most heavily applied herbicide, glycophosphate. Exposures can occur directly from the air, water, dust, and food residues. Recent data linked glycophosphate to adverse reproductive health outcomes.
Two toxic plastic chemicals, phthalates and bisphenols, are present in personal care products, among others. Emerging evidence links them with impaired neurodevelopment, leading to impaired cognitive function, learning, attention, and impulsivity.
Arsenic has long been linked to human health conditions including cancer, but more recent evidence finds it can disrupt multiple endocrine systems and lead to metabolic conditions including diabetes, reproductive dysfunction, and cardiovascular and neurocognitive conditions.
The special section about plastics noted that they are made from fossil fuels and chemicals, including many toxic substances that are known or suspected EDCs. People who live near plastic production facilities or waste dumps may be at greatest risk, but anyone can be exposed using any plastic product. Plastic waste disposal is increasingly problematic and often foisted on lower- and middle-income countries.
‘Additional Education and Awareness-Raising Among Stakeholders Remain Necessary’
Policies aimed at reducing human health risks from EDCs have included the 2022 Plastics Treaty, a resolution adopted by 175 countries at the United Nations Environmental Assembly that “may be a significant step toward global control of plastics and elimination of threats from exposures to EDCs in plastics,” the report said.
The authors added, “While significant progress has been made in recent years connecting scientific advances on EDCs with health-protective policies, additional education and awareness-raising among stakeholders remain necessary to achieve a safer and more sustainable environment that minimizes exposure to these harmful chemicals.”
The document was produced with financial contributions from the Government of Sweden, the Tides Foundation, Passport Foundation, and other donors.
A version of this article appeared on Medscape.com.
Issued on February 28, 2024, “this means the major source of dietary exposure to PFAS from food packaging like fast-food wrappers, microwave popcorn bags, take-out paperboard containers, and pet food bags is being eliminated,” the FDA said in a statement.
In 2020, the FDA had secured commitments from manufacturers to stop selling products containing PFAS used in the food packaging for grease-proofing. “Today’s announcement marks the fulfillment of these voluntary commitments,” according to the agency.
PFAS, a class of thousands of chemicals also called “forever chemicals” are widely used in consumer and industrial products. People may be exposed via contaminated food packaging (although perhaps no longer in the United States) or occupationally. Studies have found that some PFAS disrupt hormones including estrogen and testosterone, whereas others may impair thyroid function.
Endocrine Society Report Sounds the Alarm About PFAS and Others
The FDA’s announcement came just 2 days after the Endocrine Society issued a new alarm about the human health dangers from environmental EDCs including PFAS in a report covering the latest science.
“Endocrine disrupting chemicals” are individual substances or mixtures that can interfere with natural hormonal function, leading to disease or even death. Many are ubiquitous in the modern environment and contribute to a wide range of human diseases.
The new report Endocrine Disrupting Chemicals: Threats to Human Health was issued jointly with the International Pollutants Elimination Network (IPEN), a global advocacy organization. It’s an update to the Endocrine Society’s 2015 report, providing new data on the endocrine-disrupting substances previously covered and adding four EDCs not discussed in that document: Pesticides, plastics, PFAS, and children’s products containing arsenic.
At a briefing held during the United Nations Environment Assembly meeting in Nairobi, Kenya, last week, the new report’s lead author Andrea C. Gore, PhD, of the University of Texas at Austin, noted, “A well-established body of scientific research indicates that endocrine-disrupting chemicals that are part of our daily lives are making us more susceptible to reproductive disorders, cancer, diabetes, obesity, heart disease, and other serious health conditions.”
Added Dr. Gore, who is also a member of the Endocrine Society’s Board of Directors, “These chemicals pose particularly serious risks to pregnant women and children. Now is the time for the UN Environment Assembly and other global policymakers to take action to address this threat to public health.”
While the science has been emerging rapidly, global and national chemical control policies haven’t kept up, the authors said. Of particular concern is that EDCs behave differently from other chemicals in many ways, including that even very low-dose exposures can pose health threats, but policies thus far haven’t dealt with that aspect.
Moreover, “the effects of low doses cannot be predicted by the effects observed at high doses. This means there may be no safe dose for exposure to EDCs,” according to the report.
Exposures can come from household products, including furniture, toys, and food packages, as well as electronics building materials and cosmetics. These chemicals are also in the outdoor environment, via pesticides, air pollution, and industrial waste.
“IPEN and the Endocrine Society call for chemical regulations based on the most modern scientific understanding of how hormones act and how EDCs can perturb these actions. We work to educate policy makers in global, regional, and national government assemblies and help ensure that regulations correlate with current scientific understanding,” they said in the report.
New Data on Four Classes of EDCs
Chapters of the report summarized the latest information about the science of EDCs and their links to endocrine disease and real-world exposure. It included a special section about “EDCs throughout the plastics life cycle” and a summary of the links between EDCs and climate change.
The report reviewed three pesticides, including the world’s most heavily applied herbicide, glycophosphate. Exposures can occur directly from the air, water, dust, and food residues. Recent data linked glycophosphate to adverse reproductive health outcomes.
Two toxic plastic chemicals, phthalates and bisphenols, are present in personal care products, among others. Emerging evidence links them with impaired neurodevelopment, leading to impaired cognitive function, learning, attention, and impulsivity.
Arsenic has long been linked to human health conditions including cancer, but more recent evidence finds it can disrupt multiple endocrine systems and lead to metabolic conditions including diabetes, reproductive dysfunction, and cardiovascular and neurocognitive conditions.
The special section about plastics noted that they are made from fossil fuels and chemicals, including many toxic substances that are known or suspected EDCs. People who live near plastic production facilities or waste dumps may be at greatest risk, but anyone can be exposed using any plastic product. Plastic waste disposal is increasingly problematic and often foisted on lower- and middle-income countries.
‘Additional Education and Awareness-Raising Among Stakeholders Remain Necessary’
Policies aimed at reducing human health risks from EDCs have included the 2022 Plastics Treaty, a resolution adopted by 175 countries at the United Nations Environmental Assembly that “may be a significant step toward global control of plastics and elimination of threats from exposures to EDCs in plastics,” the report said.
The authors added, “While significant progress has been made in recent years connecting scientific advances on EDCs with health-protective policies, additional education and awareness-raising among stakeholders remain necessary to achieve a safer and more sustainable environment that minimizes exposure to these harmful chemicals.”
The document was produced with financial contributions from the Government of Sweden, the Tides Foundation, Passport Foundation, and other donors.
A version of this article appeared on Medscape.com.
Does Bariatric Surgery Increase or Decrease Cancer Risk? It Depends.
Bariatric surgery appears to decrease the risk for some cancers, but it may increase the risk for others, particularly colorectal cancer (CRC), according to a synthesis of current evidence.
“There has been a recent burst of studies examining the association between bariatric surgery and the longitudinal risks of developing cancer,” corresponding author Zhi Ven Fong, MD, MPH, DrPH, surgical oncologist, Mayo Clinic Arizona, Phoenix, said in an interview. “However, there has not been a rigorous and critical analysis of the data published to date.”
In evaluating research showing an association between bariatric surgery and longitudinal cancer risk, the investigators found that the quality of the studies and their findings are “heterogeneous and might be susceptible to bias,” Dr. Fong said.
Bariatric surgery appears to have the strongest and most consistent association with the reduction of breast, ovarian, and endometrial cancer risk, first author Pei-Wen Lim, MD, MS, bariatric surgeon at Mayo Clinic Arizona, Phoenix, told this news organization. “However, there have been concerning signals from preclinical and epidemiological studies that bariatric surgery may be associated with a higher risk of developing colorectal cancers,” she added.
The authors cautioned against certain changes in clinical management.
“First, cancer surveillance frequency should not be altered after bariatric surgery because of any assumed reduction in longitudinal cancer risk, and surveillance strategy should mirror that of an average-risk individual,” they wrote. “Secondly, the indications for bariatric surgery should not be expanded for the purpose of cancer-risk mitigation.”
The review was published online in JAMA Surgery.
Protection Against Hormone-Related Cancers
The authors pointed to several studies that appear to support the association between bariatric surgery and decreased risk for hormone-related cancers.
Among them is an observational study of 6781 patients in Canada that showed a significant reduction in breast cancer risk at a median follow-up of 5 years in those who had bariatric surgery vs those who did not (P = .01).
The largest study to date on risk for hormone-related cancer after bariatric surgery was conducted using New York State data for 302,883 women.
It showed a lower rate of breast, endometrial, and ovarian cancers after bariatric surgery (hazard ratio [HR], 0.78; P < .001), with Roux-en-Y gastric bypass conferring the greatest benefit compared with laparoscopic sleeve gastrectomy (HR, 0.66; P = .006) and laparoscopic adjustable gastric banding (HR, 0.83; P = .006).
Beyond the shared mechanisms explaining obesity and cancer risk, a proposed explanation for the strong, consistent association between bariatric surgery and hormone-sensitive cancers is the role obesity-related changes in estrogen stimulation play in development of such cancers, the authors noted.
Association With GI Cancers
The association between bariatric surgery and development of esophageal, gastric, liver, and pancreas cancers is less clear. The data are heterogeneous, with studies showing either no association or decreased longitudinal incidence, the authors reported.
The data are also mixed when it comes to CRC. Epidemiological studies have demonstrated decreased longitudinal incidence of colon and rectal cancer after bariatric surgery; however, two studies have suggested an increased CRC risk after bariatric surgery, the authors noted.
A 15-year study from England that matched 8794 patients with obesity who underwent bariatric surgery with 8794 patients with obesity who did not have the surgery showed that gastric bypass (but not gastric banding or sleeve gastrectomy) was associated with a greater than twofold increased risk of developing colon and rectal cancer (odds ratio, 2.63).
These findings were corroborated in a Swedish cohort study with more than 10 years of follow-up data.
One potential explanation for the heterogeneous findings is that “present studies do not discriminate the sub-types of colon and rectal cancer, with bariatric surgery possibly increasing the incidence of colitis-associated cancers but not hereditary cancers,” the authors wrote.
“The mechanism by which gastric bypass may increase the risk of colorectal cancer is through changes in the gut’s microbiome. These changes in gut flora may triumph the protective effect of weight loss on the development of colorectal cancers,” Dr. Fong said.
Prospective studies are necessary to better delineate CRC risk after bariatric surgery, the authors wrote.
Benefits Outweigh Risk
“Ultimately, it has been proven that bariatric surgery saves lives by improving the metabolic profile of patients with obesity through reduction in cardiovascular risk factors such as hypertension, diabetes, and nonalcoholic fatty liver disease,” Dr. Lim said.
“If patients qualify for bariatric surgery on the basis of their BMI or comorbidities, they should pursue it for its metabolic benefits, but perhaps consider timely or closer-interval screening colonoscopies to monitor for potential colorectal cancer development,” Dr. Lim added.
When asked to comment on the review, Marina Kurian, MD, president, American Society for Metabolic and Bariatric Surgery, also pointed to the advantages of bariatric surgery in reducing major adverse cardiovascular events and improving hypertension, hyperlipidemia, and diabetes.
Bariatric surgery reduces many types of cancers, although the data specific to CRC risk with bariatric surgery are mixed, she added.
“The jury is still out,” said Dr. Kurian, clinical professor of surgery at NYU Langone Health in New York, who was not involved in the review. “There are papers and meta-analyses that show benefit even in colorectal cancer, but then there are a couple of papers out there that suggest a risk that seems to be specific to men.
“It could just be a numbers game, where we may not have enough data. We need more granular data that will help address these nuances and really determine what is the actual risk,” Dr. Kurian said. “But overall, for cancer, bariatric surgery is a win.”
This research had no specific funding. Dr. Fong and Dr. Lim had no relevant disclosures. Dr. Kurian disclosed relationships with Allergan, Allurion, CineMed, CSATS, Ezisurg Medical, Hernon, Johnson & Johnson, Medtronic, Novo, Stryker, and Vivus.
A version of this article appeared on Medscape.com.
Bariatric surgery appears to decrease the risk for some cancers, but it may increase the risk for others, particularly colorectal cancer (CRC), according to a synthesis of current evidence.
“There has been a recent burst of studies examining the association between bariatric surgery and the longitudinal risks of developing cancer,” corresponding author Zhi Ven Fong, MD, MPH, DrPH, surgical oncologist, Mayo Clinic Arizona, Phoenix, said in an interview. “However, there has not been a rigorous and critical analysis of the data published to date.”
In evaluating research showing an association between bariatric surgery and longitudinal cancer risk, the investigators found that the quality of the studies and their findings are “heterogeneous and might be susceptible to bias,” Dr. Fong said.
Bariatric surgery appears to have the strongest and most consistent association with the reduction of breast, ovarian, and endometrial cancer risk, first author Pei-Wen Lim, MD, MS, bariatric surgeon at Mayo Clinic Arizona, Phoenix, told this news organization. “However, there have been concerning signals from preclinical and epidemiological studies that bariatric surgery may be associated with a higher risk of developing colorectal cancers,” she added.
The authors cautioned against certain changes in clinical management.
“First, cancer surveillance frequency should not be altered after bariatric surgery because of any assumed reduction in longitudinal cancer risk, and surveillance strategy should mirror that of an average-risk individual,” they wrote. “Secondly, the indications for bariatric surgery should not be expanded for the purpose of cancer-risk mitigation.”
The review was published online in JAMA Surgery.
Protection Against Hormone-Related Cancers
The authors pointed to several studies that appear to support the association between bariatric surgery and decreased risk for hormone-related cancers.
Among them is an observational study of 6781 patients in Canada that showed a significant reduction in breast cancer risk at a median follow-up of 5 years in those who had bariatric surgery vs those who did not (P = .01).
The largest study to date on risk for hormone-related cancer after bariatric surgery was conducted using New York State data for 302,883 women.
It showed a lower rate of breast, endometrial, and ovarian cancers after bariatric surgery (hazard ratio [HR], 0.78; P < .001), with Roux-en-Y gastric bypass conferring the greatest benefit compared with laparoscopic sleeve gastrectomy (HR, 0.66; P = .006) and laparoscopic adjustable gastric banding (HR, 0.83; P = .006).
Beyond the shared mechanisms explaining obesity and cancer risk, a proposed explanation for the strong, consistent association between bariatric surgery and hormone-sensitive cancers is the role obesity-related changes in estrogen stimulation play in development of such cancers, the authors noted.
Association With GI Cancers
The association between bariatric surgery and development of esophageal, gastric, liver, and pancreas cancers is less clear. The data are heterogeneous, with studies showing either no association or decreased longitudinal incidence, the authors reported.
The data are also mixed when it comes to CRC. Epidemiological studies have demonstrated decreased longitudinal incidence of colon and rectal cancer after bariatric surgery; however, two studies have suggested an increased CRC risk after bariatric surgery, the authors noted.
A 15-year study from England that matched 8794 patients with obesity who underwent bariatric surgery with 8794 patients with obesity who did not have the surgery showed that gastric bypass (but not gastric banding or sleeve gastrectomy) was associated with a greater than twofold increased risk of developing colon and rectal cancer (odds ratio, 2.63).
These findings were corroborated in a Swedish cohort study with more than 10 years of follow-up data.
One potential explanation for the heterogeneous findings is that “present studies do not discriminate the sub-types of colon and rectal cancer, with bariatric surgery possibly increasing the incidence of colitis-associated cancers but not hereditary cancers,” the authors wrote.
“The mechanism by which gastric bypass may increase the risk of colorectal cancer is through changes in the gut’s microbiome. These changes in gut flora may triumph the protective effect of weight loss on the development of colorectal cancers,” Dr. Fong said.
Prospective studies are necessary to better delineate CRC risk after bariatric surgery, the authors wrote.
Benefits Outweigh Risk
“Ultimately, it has been proven that bariatric surgery saves lives by improving the metabolic profile of patients with obesity through reduction in cardiovascular risk factors such as hypertension, diabetes, and nonalcoholic fatty liver disease,” Dr. Lim said.
“If patients qualify for bariatric surgery on the basis of their BMI or comorbidities, they should pursue it for its metabolic benefits, but perhaps consider timely or closer-interval screening colonoscopies to monitor for potential colorectal cancer development,” Dr. Lim added.
When asked to comment on the review, Marina Kurian, MD, president, American Society for Metabolic and Bariatric Surgery, also pointed to the advantages of bariatric surgery in reducing major adverse cardiovascular events and improving hypertension, hyperlipidemia, and diabetes.
Bariatric surgery reduces many types of cancers, although the data specific to CRC risk with bariatric surgery are mixed, she added.
“The jury is still out,” said Dr. Kurian, clinical professor of surgery at NYU Langone Health in New York, who was not involved in the review. “There are papers and meta-analyses that show benefit even in colorectal cancer, but then there are a couple of papers out there that suggest a risk that seems to be specific to men.
“It could just be a numbers game, where we may not have enough data. We need more granular data that will help address these nuances and really determine what is the actual risk,” Dr. Kurian said. “But overall, for cancer, bariatric surgery is a win.”
This research had no specific funding. Dr. Fong and Dr. Lim had no relevant disclosures. Dr. Kurian disclosed relationships with Allergan, Allurion, CineMed, CSATS, Ezisurg Medical, Hernon, Johnson & Johnson, Medtronic, Novo, Stryker, and Vivus.
A version of this article appeared on Medscape.com.
Bariatric surgery appears to decrease the risk for some cancers, but it may increase the risk for others, particularly colorectal cancer (CRC), according to a synthesis of current evidence.
“There has been a recent burst of studies examining the association between bariatric surgery and the longitudinal risks of developing cancer,” corresponding author Zhi Ven Fong, MD, MPH, DrPH, surgical oncologist, Mayo Clinic Arizona, Phoenix, said in an interview. “However, there has not been a rigorous and critical analysis of the data published to date.”
In evaluating research showing an association between bariatric surgery and longitudinal cancer risk, the investigators found that the quality of the studies and their findings are “heterogeneous and might be susceptible to bias,” Dr. Fong said.
Bariatric surgery appears to have the strongest and most consistent association with the reduction of breast, ovarian, and endometrial cancer risk, first author Pei-Wen Lim, MD, MS, bariatric surgeon at Mayo Clinic Arizona, Phoenix, told this news organization. “However, there have been concerning signals from preclinical and epidemiological studies that bariatric surgery may be associated with a higher risk of developing colorectal cancers,” she added.
The authors cautioned against certain changes in clinical management.
“First, cancer surveillance frequency should not be altered after bariatric surgery because of any assumed reduction in longitudinal cancer risk, and surveillance strategy should mirror that of an average-risk individual,” they wrote. “Secondly, the indications for bariatric surgery should not be expanded for the purpose of cancer-risk mitigation.”
The review was published online in JAMA Surgery.
Protection Against Hormone-Related Cancers
The authors pointed to several studies that appear to support the association between bariatric surgery and decreased risk for hormone-related cancers.
Among them is an observational study of 6781 patients in Canada that showed a significant reduction in breast cancer risk at a median follow-up of 5 years in those who had bariatric surgery vs those who did not (P = .01).
The largest study to date on risk for hormone-related cancer after bariatric surgery was conducted using New York State data for 302,883 women.
It showed a lower rate of breast, endometrial, and ovarian cancers after bariatric surgery (hazard ratio [HR], 0.78; P < .001), with Roux-en-Y gastric bypass conferring the greatest benefit compared with laparoscopic sleeve gastrectomy (HR, 0.66; P = .006) and laparoscopic adjustable gastric banding (HR, 0.83; P = .006).
Beyond the shared mechanisms explaining obesity and cancer risk, a proposed explanation for the strong, consistent association between bariatric surgery and hormone-sensitive cancers is the role obesity-related changes in estrogen stimulation play in development of such cancers, the authors noted.
Association With GI Cancers
The association between bariatric surgery and development of esophageal, gastric, liver, and pancreas cancers is less clear. The data are heterogeneous, with studies showing either no association or decreased longitudinal incidence, the authors reported.
The data are also mixed when it comes to CRC. Epidemiological studies have demonstrated decreased longitudinal incidence of colon and rectal cancer after bariatric surgery; however, two studies have suggested an increased CRC risk after bariatric surgery, the authors noted.
A 15-year study from England that matched 8794 patients with obesity who underwent bariatric surgery with 8794 patients with obesity who did not have the surgery showed that gastric bypass (but not gastric banding or sleeve gastrectomy) was associated with a greater than twofold increased risk of developing colon and rectal cancer (odds ratio, 2.63).
These findings were corroborated in a Swedish cohort study with more than 10 years of follow-up data.
One potential explanation for the heterogeneous findings is that “present studies do not discriminate the sub-types of colon and rectal cancer, with bariatric surgery possibly increasing the incidence of colitis-associated cancers but not hereditary cancers,” the authors wrote.
“The mechanism by which gastric bypass may increase the risk of colorectal cancer is through changes in the gut’s microbiome. These changes in gut flora may triumph the protective effect of weight loss on the development of colorectal cancers,” Dr. Fong said.
Prospective studies are necessary to better delineate CRC risk after bariatric surgery, the authors wrote.
Benefits Outweigh Risk
“Ultimately, it has been proven that bariatric surgery saves lives by improving the metabolic profile of patients with obesity through reduction in cardiovascular risk factors such as hypertension, diabetes, and nonalcoholic fatty liver disease,” Dr. Lim said.
“If patients qualify for bariatric surgery on the basis of their BMI or comorbidities, they should pursue it for its metabolic benefits, but perhaps consider timely or closer-interval screening colonoscopies to monitor for potential colorectal cancer development,” Dr. Lim added.
When asked to comment on the review, Marina Kurian, MD, president, American Society for Metabolic and Bariatric Surgery, also pointed to the advantages of bariatric surgery in reducing major adverse cardiovascular events and improving hypertension, hyperlipidemia, and diabetes.
Bariatric surgery reduces many types of cancers, although the data specific to CRC risk with bariatric surgery are mixed, she added.
“The jury is still out,” said Dr. Kurian, clinical professor of surgery at NYU Langone Health in New York, who was not involved in the review. “There are papers and meta-analyses that show benefit even in colorectal cancer, but then there are a couple of papers out there that suggest a risk that seems to be specific to men.
“It could just be a numbers game, where we may not have enough data. We need more granular data that will help address these nuances and really determine what is the actual risk,” Dr. Kurian said. “But overall, for cancer, bariatric surgery is a win.”
This research had no specific funding. Dr. Fong and Dr. Lim had no relevant disclosures. Dr. Kurian disclosed relationships with Allergan, Allurion, CineMed, CSATS, Ezisurg Medical, Hernon, Johnson & Johnson, Medtronic, Novo, Stryker, and Vivus.
A version of this article appeared on Medscape.com.
GLP-1s’ Next Target: Male Infertility?
The explosion of interest in glucagon-like peptide 1 receptor agonists (GLP-1 RAs), such as semaglutide and tirzepatide, has raised questions about what therapeutic effects this class of medication might have beyond their current indications for type 2 diabetes and obesity.
Recent clinical trials have recently identified benefits from GLP-1 agents for the heart, liver, and kidneys, but the current evidence base is murkier regarding how the drugs may affect male fertility.
For starters, overweight and obesity are strongly associated with male infertility in several overlapping ways. Obesity can disrupt hormones linked to fertility, increase the risk for defective sperm, adversely affect semen quality, and even make sexual intercourse more difficult due to obesity’s link to erectile dysfunction. As a result, GLP-1 RAs should at least in theory boost male fertility in men who take the drugs to lose weight.
But animal studies and a handful of small trials and observational data point to the potential for GLP-1 RAs to improve male fertility in other ways.
A recent narrative review on GLP-1 RAs and male reproductive health, published in the journal Medicina in December 2023, surveyed the potential of the drugs for male infertility and offered reason for optimism.
Hossein Sadeghi-Nejad, MD, director of urology at NYU Langone Health, New York, and a coauthor of the article, said that one reason he and his colleagues conducted their analysis was the known association between weight loss and an increase in testosterone.
“Most of the animal studies that are out there show that this class of drugs does affect testosterone levels,” Dr. Sadeghi-Nejad said; they wanted to better understand what other evidence showed about GLP-1 agonists and other fertility factors.
Link Between Obesity and Fertility
The recent paper first reviews the well-established link between obesity and poorer fertility outcomes.
“Certainly, obesity poses a significant societal problem with substantial impacts on both overall health and economic aspects,” senior author Ranjith Ramasamy, MD, associate professor of urology and director of the reproductive urology Fellowship program at the University of Miami’s Miller School of Medicine, told this news organization. “The escalating global obesity rates raise concerns, especially in the field of male infertility, where excessive body fat induces intrinsic hormonal changes leading to alterations, eventually, in semen parameters.”
The authors noted that obesity has been linked in the research to worse assisted reproductive technology (ART) outcomes and to subfecundity, taking more than 12 months to achieve pregnancy. They also referenced a systematic review that found men with obesity were more likely to have lower sperm counts and less viable sperm.
“From our standpoint, I think the key point was to raise awareness about the fact that obesity, because of the aromatization of testosterone to estradiol [from excess adipose tissue], will affect the hormonal axis and the availability of testosterone and, therefore, indirectly affects spermatogenesis,” Dr. Sadeghi-Nejad said.
Obesity is also linked to lower levels of inhibin B, which stimulates testosterone secretion in Sertoli cells, which, when combined with the proinflammatory state of obesity, “results in a less favorable environment for sperm production,” he said. Finally, the link between obesity and poorer sexual function further inhibits fertility potential, he added.
Until recently, the primary treatments for obesity in men experiencing fertility problems have been lifestyle modifications or surgical interventions. But the recent approval of GLP-1 RA drugs for obesity present an additional option depending on how these drugs affect other fertility parameters.
Direct or Indirect Effects?
Most of the available evidence on GLP-RAs and sperm parameters comes from preclinical research. One of the few clinical trials, published last year in the Journal of Clinical Medicine, investigated the effects of liraglutide in men with metabolic hypogonadism, a body mass index between (BMI) 30 and 40, and severe erectile dysfunction.
Among the 110 men enrolled in the study, only the 35 participants who said that they were not seeking fatherhood received liraglutide. After 4 months of treatment, these men had significantly improved semen concentration, motility, and morphology than did those wanting to conceive who received conventional fertility treatment. Erectile dysfunction was also more improved in the liraglutide group, according to the researchers.
Though this study demonstrated the potential for liraglutide to treat metabolic hypogonadism, the men in that group also had greater weight loss and BMI reduction than the other participants. The review cited several other studies — albeit small ones — in which weight loss was associated with improvements in sperm parameters, including one randomized controlled trial in which one group lost weight with liraglutide and the other with lifestyle modifications; both groups showed increases in the concentration and number of sperm.
One of the key questions requiring further research, then, is whether GLP-1 agents have direct effects on male fertility independent of a reduction in obesity. The randomized controlled trials comparing liraglutide and lifestyle modifications failed to find additional effects on semen in the men taking liraglutide; however, the study had only 56 participants, and results from liraglutide cannot be generalized to potential effects of semaglutide or tirzepatide, Dr. Sadeghi-Nejad said.
“Determining the relative contributions of weight loss versus direct drug actions on fertility outcomes remains challenging without robust data,” Dr. Ramasamy said. “While acknowledged that diet and physical activity positively impact fertility, confirming the synergistic role of GLP-1 receptor agonists requires evidence from well-designed randomized clinical trials.”
Rodent studies suggest that GLP-1 RAs may independently affect testicular function because GLP-1 receptors exist in Sertoli and Leydig cells of the testes. In one study, for example, obese mice who received the GLP-1 agonist exenatide for 8 weeks had “improved sperm motility, DNA integrity, and decreased expression of pro-inflammatory cytokines,” the authors of the review reported. But the precise mechanisms aren’t well understood.
“We know that there are GLP-1 receptors in the reproductive tract, but the extent of the downstream effect of stimulating those receptors, I don’t think we know well,” said John P. Lindsey II, MD, MEng, assistant professor of urology at University of California San Francisco Health.
Other hormonal effects of GLP-1 agonists, such as stimulating insulin production and better regulating blood glucose levels, are better understood, said Raevti Bole, MD, a urologist at Cleveland Clinic, in Ohio, but still other effects of the drugs may not yet be identified.
“I think the really big unknown is whether these types of drugs have effects that are not hormonal on male fertility and what those effects are, and how those affect sperm,” Dr. Bole said. “For example, we know that these drugs slow gastric emptying. Is it possible that slow gastric emptying affects some of the nutrients that you absorb, and that could affect fertility?” Similarly, she said, it’s not clear whether GLP-1 agonists would have any effects on the thyroid that could then affect fertility.
Effects on Offspring
Another open question about GLP-1 RAs and male fertility is their potential effects on the offspring, said Sriram Machineni, MBBS, associate professor of endocrinology at the Albert Einstein College of Medicine in New York City. The clinical trials involving the drugs for treating type 2 diabetes and obesity required both men and women to use contraception. If sperm contributing to a pregnancy are exposed to a GLP-1 agent, “we don’t know what the consequences could be,” Dr. Machineni said. “Just increasing the fertility of the man is not enough. We need to make sure it’s safe long-term for the fetus.”
Dr. Bole also pointed out the need for understanding potential effects in the fetus.
“We know that there are epigenetic changes that can happen to sperm that are influenced by the lifestyle and the physical health and environment of the parent,” Dr. Bole said. “So how could these drugs potentially affect those epigenetic changes that then potentially are passed on to the offspring? We don’t know that.”
An ideal source for that data would be a cohort registry of people who are taking the medication and then cause a pregnancy. “They have a registry for pregnant women,” Dr. Machineni said, “but we need something similar for men.”
Dr. Sadeghi-Nejad said that he and his coauthors are working on developing a registry for men who take GLP-1 RAs that would enable long-term tracking of multiple andrologic outcomes, including fertility and sexual dysfunction. Such a registry could theoretically be useful in tracking pregnancy and offspring outcomes as well.
Too Soon for Prescribing
Additional options for treating fertility in men with obesity would be welcome. Current treatments include the selective estrogen receptor modulator (SERM) clomiphene citrate and the aromatase inhibitor anastrozole. But these have their drawbacks, Dr. Sadeghi-Nejad pointed out; in the overweight population in particular, they “are not necessarily ideal,” he said.
“Although both are viable treatments for enhancing hormonal balance and semen parameters, clomiphene citrate has rare but documented side effects, including thromboembolism, gastrointestinal distress and occasional weight gain in men,” Dr. Sadeghi-Nejad and his colleagues wrote. “Furthermore, despite clomiphene citrate’s association with significant increases in sperm concentration, it is not universally effective, with a meta-analysis indicating a significant increase in sperm concentration in approximately 60% of men.”
For men who have obesity and oligospermia but normal levels of testosterone and estradiol, “conventional pharmaceutical approaches like clomiphene may not be suitable,” the authors wrote.
Still, GLP-1 RAs may have a role to play for this population.
“I think it is within the wheelhouse of a reproductive urologist to consider those types of medications,” Dr. Lindsey said. For example, for a patient who has overweight or obesity, “does it make sense to think about doing clomiphene therapy, which we often do for someone who has low testosterone, in conjunction [with a GLP-1 agonist]? Maybe there’s a kind of an additive effect of having both on board.”
Dr. Ramasamy similarly noted that GLP-1 agonists cannot replace SERMs but may work “synergistically” with them.
“Despite the established popularity of GLP-1 receptor agonists, there may be some reluctance among urologists and fertility specialists to prescribe them, with some others advocating for their use to enhance semen parameters,” Dr. Ramasamy said. “However, robust scientific evidence is still lacking, necessitating caution and a wait for more substantial data.”
Even if GLP-1 RAs prove to have therapeutic benefit for fertility, considerations such as availability and cost may affect prescribing.
“We do currently have safe and effective drugs that we use for male fertility, and those are generally nowhere near as expensive,” Dr. Bole said. “When we start talking about another drug that we can add, we have to think about the efficacy and the potential side effect but also, is this affordable for patients?”
Eventually, once more evidence become available, all of the urologists who spoke with this news organization said that they expect discussion about the possible therapeutic utility of GLP-1 agonists to make its way into clinical guidelines.
“Obesity is such a huge impediment for fertility in the modern environment,” Dr. Machineni said. “We will have to clarify the use of these agents, so I think this will be a part of the guidelines some point, but I think we need more information.”
The research was funded by the National Institute of Diabetes and Digestive and Kidney Diseases and the American Cancer Society. The review authors and other quoted physicians reported no disclosures. Dr. Machineni has consulted for Novo Nordisk and Lilly and has conducted clinical trials with semaglutide and tirzepatide for those companies.
A version of this article appeared on Medscape.com.
The explosion of interest in glucagon-like peptide 1 receptor agonists (GLP-1 RAs), such as semaglutide and tirzepatide, has raised questions about what therapeutic effects this class of medication might have beyond their current indications for type 2 diabetes and obesity.
Recent clinical trials have recently identified benefits from GLP-1 agents for the heart, liver, and kidneys, but the current evidence base is murkier regarding how the drugs may affect male fertility.
For starters, overweight and obesity are strongly associated with male infertility in several overlapping ways. Obesity can disrupt hormones linked to fertility, increase the risk for defective sperm, adversely affect semen quality, and even make sexual intercourse more difficult due to obesity’s link to erectile dysfunction. As a result, GLP-1 RAs should at least in theory boost male fertility in men who take the drugs to lose weight.
But animal studies and a handful of small trials and observational data point to the potential for GLP-1 RAs to improve male fertility in other ways.
A recent narrative review on GLP-1 RAs and male reproductive health, published in the journal Medicina in December 2023, surveyed the potential of the drugs for male infertility and offered reason for optimism.
Hossein Sadeghi-Nejad, MD, director of urology at NYU Langone Health, New York, and a coauthor of the article, said that one reason he and his colleagues conducted their analysis was the known association between weight loss and an increase in testosterone.
“Most of the animal studies that are out there show that this class of drugs does affect testosterone levels,” Dr. Sadeghi-Nejad said; they wanted to better understand what other evidence showed about GLP-1 agonists and other fertility factors.
Link Between Obesity and Fertility
The recent paper first reviews the well-established link between obesity and poorer fertility outcomes.
“Certainly, obesity poses a significant societal problem with substantial impacts on both overall health and economic aspects,” senior author Ranjith Ramasamy, MD, associate professor of urology and director of the reproductive urology Fellowship program at the University of Miami’s Miller School of Medicine, told this news organization. “The escalating global obesity rates raise concerns, especially in the field of male infertility, where excessive body fat induces intrinsic hormonal changes leading to alterations, eventually, in semen parameters.”
The authors noted that obesity has been linked in the research to worse assisted reproductive technology (ART) outcomes and to subfecundity, taking more than 12 months to achieve pregnancy. They also referenced a systematic review that found men with obesity were more likely to have lower sperm counts and less viable sperm.
“From our standpoint, I think the key point was to raise awareness about the fact that obesity, because of the aromatization of testosterone to estradiol [from excess adipose tissue], will affect the hormonal axis and the availability of testosterone and, therefore, indirectly affects spermatogenesis,” Dr. Sadeghi-Nejad said.
Obesity is also linked to lower levels of inhibin B, which stimulates testosterone secretion in Sertoli cells, which, when combined with the proinflammatory state of obesity, “results in a less favorable environment for sperm production,” he said. Finally, the link between obesity and poorer sexual function further inhibits fertility potential, he added.
Until recently, the primary treatments for obesity in men experiencing fertility problems have been lifestyle modifications or surgical interventions. But the recent approval of GLP-1 RA drugs for obesity present an additional option depending on how these drugs affect other fertility parameters.
Direct or Indirect Effects?
Most of the available evidence on GLP-RAs and sperm parameters comes from preclinical research. One of the few clinical trials, published last year in the Journal of Clinical Medicine, investigated the effects of liraglutide in men with metabolic hypogonadism, a body mass index between (BMI) 30 and 40, and severe erectile dysfunction.
Among the 110 men enrolled in the study, only the 35 participants who said that they were not seeking fatherhood received liraglutide. After 4 months of treatment, these men had significantly improved semen concentration, motility, and morphology than did those wanting to conceive who received conventional fertility treatment. Erectile dysfunction was also more improved in the liraglutide group, according to the researchers.
Though this study demonstrated the potential for liraglutide to treat metabolic hypogonadism, the men in that group also had greater weight loss and BMI reduction than the other participants. The review cited several other studies — albeit small ones — in which weight loss was associated with improvements in sperm parameters, including one randomized controlled trial in which one group lost weight with liraglutide and the other with lifestyle modifications; both groups showed increases in the concentration and number of sperm.
One of the key questions requiring further research, then, is whether GLP-1 agents have direct effects on male fertility independent of a reduction in obesity. The randomized controlled trials comparing liraglutide and lifestyle modifications failed to find additional effects on semen in the men taking liraglutide; however, the study had only 56 participants, and results from liraglutide cannot be generalized to potential effects of semaglutide or tirzepatide, Dr. Sadeghi-Nejad said.
“Determining the relative contributions of weight loss versus direct drug actions on fertility outcomes remains challenging without robust data,” Dr. Ramasamy said. “While acknowledged that diet and physical activity positively impact fertility, confirming the synergistic role of GLP-1 receptor agonists requires evidence from well-designed randomized clinical trials.”
Rodent studies suggest that GLP-1 RAs may independently affect testicular function because GLP-1 receptors exist in Sertoli and Leydig cells of the testes. In one study, for example, obese mice who received the GLP-1 agonist exenatide for 8 weeks had “improved sperm motility, DNA integrity, and decreased expression of pro-inflammatory cytokines,” the authors of the review reported. But the precise mechanisms aren’t well understood.
“We know that there are GLP-1 receptors in the reproductive tract, but the extent of the downstream effect of stimulating those receptors, I don’t think we know well,” said John P. Lindsey II, MD, MEng, assistant professor of urology at University of California San Francisco Health.
Other hormonal effects of GLP-1 agonists, such as stimulating insulin production and better regulating blood glucose levels, are better understood, said Raevti Bole, MD, a urologist at Cleveland Clinic, in Ohio, but still other effects of the drugs may not yet be identified.
“I think the really big unknown is whether these types of drugs have effects that are not hormonal on male fertility and what those effects are, and how those affect sperm,” Dr. Bole said. “For example, we know that these drugs slow gastric emptying. Is it possible that slow gastric emptying affects some of the nutrients that you absorb, and that could affect fertility?” Similarly, she said, it’s not clear whether GLP-1 agonists would have any effects on the thyroid that could then affect fertility.
Effects on Offspring
Another open question about GLP-1 RAs and male fertility is their potential effects on the offspring, said Sriram Machineni, MBBS, associate professor of endocrinology at the Albert Einstein College of Medicine in New York City. The clinical trials involving the drugs for treating type 2 diabetes and obesity required both men and women to use contraception. If sperm contributing to a pregnancy are exposed to a GLP-1 agent, “we don’t know what the consequences could be,” Dr. Machineni said. “Just increasing the fertility of the man is not enough. We need to make sure it’s safe long-term for the fetus.”
Dr. Bole also pointed out the need for understanding potential effects in the fetus.
“We know that there are epigenetic changes that can happen to sperm that are influenced by the lifestyle and the physical health and environment of the parent,” Dr. Bole said. “So how could these drugs potentially affect those epigenetic changes that then potentially are passed on to the offspring? We don’t know that.”
An ideal source for that data would be a cohort registry of people who are taking the medication and then cause a pregnancy. “They have a registry for pregnant women,” Dr. Machineni said, “but we need something similar for men.”
Dr. Sadeghi-Nejad said that he and his coauthors are working on developing a registry for men who take GLP-1 RAs that would enable long-term tracking of multiple andrologic outcomes, including fertility and sexual dysfunction. Such a registry could theoretically be useful in tracking pregnancy and offspring outcomes as well.
Too Soon for Prescribing
Additional options for treating fertility in men with obesity would be welcome. Current treatments include the selective estrogen receptor modulator (SERM) clomiphene citrate and the aromatase inhibitor anastrozole. But these have their drawbacks, Dr. Sadeghi-Nejad pointed out; in the overweight population in particular, they “are not necessarily ideal,” he said.
“Although both are viable treatments for enhancing hormonal balance and semen parameters, clomiphene citrate has rare but documented side effects, including thromboembolism, gastrointestinal distress and occasional weight gain in men,” Dr. Sadeghi-Nejad and his colleagues wrote. “Furthermore, despite clomiphene citrate’s association with significant increases in sperm concentration, it is not universally effective, with a meta-analysis indicating a significant increase in sperm concentration in approximately 60% of men.”
For men who have obesity and oligospermia but normal levels of testosterone and estradiol, “conventional pharmaceutical approaches like clomiphene may not be suitable,” the authors wrote.
Still, GLP-1 RAs may have a role to play for this population.
“I think it is within the wheelhouse of a reproductive urologist to consider those types of medications,” Dr. Lindsey said. For example, for a patient who has overweight or obesity, “does it make sense to think about doing clomiphene therapy, which we often do for someone who has low testosterone, in conjunction [with a GLP-1 agonist]? Maybe there’s a kind of an additive effect of having both on board.”
Dr. Ramasamy similarly noted that GLP-1 agonists cannot replace SERMs but may work “synergistically” with them.
“Despite the established popularity of GLP-1 receptor agonists, there may be some reluctance among urologists and fertility specialists to prescribe them, with some others advocating for their use to enhance semen parameters,” Dr. Ramasamy said. “However, robust scientific evidence is still lacking, necessitating caution and a wait for more substantial data.”
Even if GLP-1 RAs prove to have therapeutic benefit for fertility, considerations such as availability and cost may affect prescribing.
“We do currently have safe and effective drugs that we use for male fertility, and those are generally nowhere near as expensive,” Dr. Bole said. “When we start talking about another drug that we can add, we have to think about the efficacy and the potential side effect but also, is this affordable for patients?”
Eventually, once more evidence become available, all of the urologists who spoke with this news organization said that they expect discussion about the possible therapeutic utility of GLP-1 agonists to make its way into clinical guidelines.
“Obesity is such a huge impediment for fertility in the modern environment,” Dr. Machineni said. “We will have to clarify the use of these agents, so I think this will be a part of the guidelines some point, but I think we need more information.”
The research was funded by the National Institute of Diabetes and Digestive and Kidney Diseases and the American Cancer Society. The review authors and other quoted physicians reported no disclosures. Dr. Machineni has consulted for Novo Nordisk and Lilly and has conducted clinical trials with semaglutide and tirzepatide for those companies.
A version of this article appeared on Medscape.com.
The explosion of interest in glucagon-like peptide 1 receptor agonists (GLP-1 RAs), such as semaglutide and tirzepatide, has raised questions about what therapeutic effects this class of medication might have beyond their current indications for type 2 diabetes and obesity.
Recent clinical trials have recently identified benefits from GLP-1 agents for the heart, liver, and kidneys, but the current evidence base is murkier regarding how the drugs may affect male fertility.
For starters, overweight and obesity are strongly associated with male infertility in several overlapping ways. Obesity can disrupt hormones linked to fertility, increase the risk for defective sperm, adversely affect semen quality, and even make sexual intercourse more difficult due to obesity’s link to erectile dysfunction. As a result, GLP-1 RAs should at least in theory boost male fertility in men who take the drugs to lose weight.
But animal studies and a handful of small trials and observational data point to the potential for GLP-1 RAs to improve male fertility in other ways.
A recent narrative review on GLP-1 RAs and male reproductive health, published in the journal Medicina in December 2023, surveyed the potential of the drugs for male infertility and offered reason for optimism.
Hossein Sadeghi-Nejad, MD, director of urology at NYU Langone Health, New York, and a coauthor of the article, said that one reason he and his colleagues conducted their analysis was the known association between weight loss and an increase in testosterone.
“Most of the animal studies that are out there show that this class of drugs does affect testosterone levels,” Dr. Sadeghi-Nejad said; they wanted to better understand what other evidence showed about GLP-1 agonists and other fertility factors.
Link Between Obesity and Fertility
The recent paper first reviews the well-established link between obesity and poorer fertility outcomes.
“Certainly, obesity poses a significant societal problem with substantial impacts on both overall health and economic aspects,” senior author Ranjith Ramasamy, MD, associate professor of urology and director of the reproductive urology Fellowship program at the University of Miami’s Miller School of Medicine, told this news organization. “The escalating global obesity rates raise concerns, especially in the field of male infertility, where excessive body fat induces intrinsic hormonal changes leading to alterations, eventually, in semen parameters.”
The authors noted that obesity has been linked in the research to worse assisted reproductive technology (ART) outcomes and to subfecundity, taking more than 12 months to achieve pregnancy. They also referenced a systematic review that found men with obesity were more likely to have lower sperm counts and less viable sperm.
“From our standpoint, I think the key point was to raise awareness about the fact that obesity, because of the aromatization of testosterone to estradiol [from excess adipose tissue], will affect the hormonal axis and the availability of testosterone and, therefore, indirectly affects spermatogenesis,” Dr. Sadeghi-Nejad said.
Obesity is also linked to lower levels of inhibin B, which stimulates testosterone secretion in Sertoli cells, which, when combined with the proinflammatory state of obesity, “results in a less favorable environment for sperm production,” he said. Finally, the link between obesity and poorer sexual function further inhibits fertility potential, he added.
Until recently, the primary treatments for obesity in men experiencing fertility problems have been lifestyle modifications or surgical interventions. But the recent approval of GLP-1 RA drugs for obesity present an additional option depending on how these drugs affect other fertility parameters.
Direct or Indirect Effects?
Most of the available evidence on GLP-RAs and sperm parameters comes from preclinical research. One of the few clinical trials, published last year in the Journal of Clinical Medicine, investigated the effects of liraglutide in men with metabolic hypogonadism, a body mass index between (BMI) 30 and 40, and severe erectile dysfunction.
Among the 110 men enrolled in the study, only the 35 participants who said that they were not seeking fatherhood received liraglutide. After 4 months of treatment, these men had significantly improved semen concentration, motility, and morphology than did those wanting to conceive who received conventional fertility treatment. Erectile dysfunction was also more improved in the liraglutide group, according to the researchers.
Though this study demonstrated the potential for liraglutide to treat metabolic hypogonadism, the men in that group also had greater weight loss and BMI reduction than the other participants. The review cited several other studies — albeit small ones — in which weight loss was associated with improvements in sperm parameters, including one randomized controlled trial in which one group lost weight with liraglutide and the other with lifestyle modifications; both groups showed increases in the concentration and number of sperm.
One of the key questions requiring further research, then, is whether GLP-1 agents have direct effects on male fertility independent of a reduction in obesity. The randomized controlled trials comparing liraglutide and lifestyle modifications failed to find additional effects on semen in the men taking liraglutide; however, the study had only 56 participants, and results from liraglutide cannot be generalized to potential effects of semaglutide or tirzepatide, Dr. Sadeghi-Nejad said.
“Determining the relative contributions of weight loss versus direct drug actions on fertility outcomes remains challenging without robust data,” Dr. Ramasamy said. “While acknowledged that diet and physical activity positively impact fertility, confirming the synergistic role of GLP-1 receptor agonists requires evidence from well-designed randomized clinical trials.”
Rodent studies suggest that GLP-1 RAs may independently affect testicular function because GLP-1 receptors exist in Sertoli and Leydig cells of the testes. In one study, for example, obese mice who received the GLP-1 agonist exenatide for 8 weeks had “improved sperm motility, DNA integrity, and decreased expression of pro-inflammatory cytokines,” the authors of the review reported. But the precise mechanisms aren’t well understood.
“We know that there are GLP-1 receptors in the reproductive tract, but the extent of the downstream effect of stimulating those receptors, I don’t think we know well,” said John P. Lindsey II, MD, MEng, assistant professor of urology at University of California San Francisco Health.
Other hormonal effects of GLP-1 agonists, such as stimulating insulin production and better regulating blood glucose levels, are better understood, said Raevti Bole, MD, a urologist at Cleveland Clinic, in Ohio, but still other effects of the drugs may not yet be identified.
“I think the really big unknown is whether these types of drugs have effects that are not hormonal on male fertility and what those effects are, and how those affect sperm,” Dr. Bole said. “For example, we know that these drugs slow gastric emptying. Is it possible that slow gastric emptying affects some of the nutrients that you absorb, and that could affect fertility?” Similarly, she said, it’s not clear whether GLP-1 agonists would have any effects on the thyroid that could then affect fertility.
Effects on Offspring
Another open question about GLP-1 RAs and male fertility is their potential effects on the offspring, said Sriram Machineni, MBBS, associate professor of endocrinology at the Albert Einstein College of Medicine in New York City. The clinical trials involving the drugs for treating type 2 diabetes and obesity required both men and women to use contraception. If sperm contributing to a pregnancy are exposed to a GLP-1 agent, “we don’t know what the consequences could be,” Dr. Machineni said. “Just increasing the fertility of the man is not enough. We need to make sure it’s safe long-term for the fetus.”
Dr. Bole also pointed out the need for understanding potential effects in the fetus.
“We know that there are epigenetic changes that can happen to sperm that are influenced by the lifestyle and the physical health and environment of the parent,” Dr. Bole said. “So how could these drugs potentially affect those epigenetic changes that then potentially are passed on to the offspring? We don’t know that.”
An ideal source for that data would be a cohort registry of people who are taking the medication and then cause a pregnancy. “They have a registry for pregnant women,” Dr. Machineni said, “but we need something similar for men.”
Dr. Sadeghi-Nejad said that he and his coauthors are working on developing a registry for men who take GLP-1 RAs that would enable long-term tracking of multiple andrologic outcomes, including fertility and sexual dysfunction. Such a registry could theoretically be useful in tracking pregnancy and offspring outcomes as well.
Too Soon for Prescribing
Additional options for treating fertility in men with obesity would be welcome. Current treatments include the selective estrogen receptor modulator (SERM) clomiphene citrate and the aromatase inhibitor anastrozole. But these have their drawbacks, Dr. Sadeghi-Nejad pointed out; in the overweight population in particular, they “are not necessarily ideal,” he said.
“Although both are viable treatments for enhancing hormonal balance and semen parameters, clomiphene citrate has rare but documented side effects, including thromboembolism, gastrointestinal distress and occasional weight gain in men,” Dr. Sadeghi-Nejad and his colleagues wrote. “Furthermore, despite clomiphene citrate’s association with significant increases in sperm concentration, it is not universally effective, with a meta-analysis indicating a significant increase in sperm concentration in approximately 60% of men.”
For men who have obesity and oligospermia but normal levels of testosterone and estradiol, “conventional pharmaceutical approaches like clomiphene may not be suitable,” the authors wrote.
Still, GLP-1 RAs may have a role to play for this population.
“I think it is within the wheelhouse of a reproductive urologist to consider those types of medications,” Dr. Lindsey said. For example, for a patient who has overweight or obesity, “does it make sense to think about doing clomiphene therapy, which we often do for someone who has low testosterone, in conjunction [with a GLP-1 agonist]? Maybe there’s a kind of an additive effect of having both on board.”
Dr. Ramasamy similarly noted that GLP-1 agonists cannot replace SERMs but may work “synergistically” with them.
“Despite the established popularity of GLP-1 receptor agonists, there may be some reluctance among urologists and fertility specialists to prescribe them, with some others advocating for their use to enhance semen parameters,” Dr. Ramasamy said. “However, robust scientific evidence is still lacking, necessitating caution and a wait for more substantial data.”
Even if GLP-1 RAs prove to have therapeutic benefit for fertility, considerations such as availability and cost may affect prescribing.
“We do currently have safe and effective drugs that we use for male fertility, and those are generally nowhere near as expensive,” Dr. Bole said. “When we start talking about another drug that we can add, we have to think about the efficacy and the potential side effect but also, is this affordable for patients?”
Eventually, once more evidence become available, all of the urologists who spoke with this news organization said that they expect discussion about the possible therapeutic utility of GLP-1 agonists to make its way into clinical guidelines.
“Obesity is such a huge impediment for fertility in the modern environment,” Dr. Machineni said. “We will have to clarify the use of these agents, so I think this will be a part of the guidelines some point, but I think we need more information.”
The research was funded by the National Institute of Diabetes and Digestive and Kidney Diseases and the American Cancer Society. The review authors and other quoted physicians reported no disclosures. Dr. Machineni has consulted for Novo Nordisk and Lilly and has conducted clinical trials with semaglutide and tirzepatide for those companies.
A version of this article appeared on Medscape.com.
Beyond the Shots: Focusing on Gut Health Can Aid Weight Loss
Injectable weight loss drugs like Wegovy, Saxenda, and Zepbound have been getting all the glory lately, but they’re not for everyone. If the inconvenience or cost of weight-loss drugs isn’t for you, another approach may be boosting your gut microbiome.
So how does one do that, and how does it work?
“There are a lot of different factors naturally in weight gain and weight loss, so the gut microbiome is certainly not the only thing,” said Chris Damman, MD, a gastroenterologist at the University of Washington. He studies how food and the microbiome affect your health. “With that caveat, it probably is playing an important role.”
Trillions of Microbes
The idea that your gut is home to an enormous range of tiny organisms — microbes — has existed for more than 100 years, but only in the 21st century have scientists had the ability to delve into specifics.
We now know you want a robust assortment of microbes in your gut, especially in the lower gut, your colon. They feast on fiber from the food you eat and turn it into substances your body needs. Those substances send signals all over your body.
If you don’t have enough microbes or have too many of the wrong kinds, it influences those signals, which can lead to health problems.
Thanks to these efforts, we know a lot about the interactions between your gut and the rest of your body, but we don’t know exactly how many things happen — whether some teeny critters within your microbiome cause the issues or vice versa.
“That’s the problem with so much of the microbiome stuff,” said Elizabeth Hohmann, MD, a physician investigator at the Massachusetts General Research Institute. “Olympic athletes have a better gut microbiome than most people. Well, sure they do — because they’re paying attention to their diet, they’re getting enough rest. Correlation does not causation make.”
The American Diet Messes With Your Gut
If you’re a typical American, you eat a lot of ultra-processed foods — manufactured with a long ingredients list that includes additives or preservatives. According to one study, those foods make up 73% of our food supply. That can have a serious impact on gut health.
“When you process a food and mill it, it turns a whole food into tiny particles,” Dr. Damman said. “That makes the food highly digestible. But if you eat a stalk of broccoli, a large amount of that broccoli in the form of fiber and other things will make its way to your lower gut, where it will feed microbes.”
With heavily processed foods, on the other hand, most of it gets digested before it can reach your lower gut, which leaves your microbes without the energy they need to survive.
Rosa Krajmalnik-Brown, PhD, is director of the Biodesign Center for Health Through Microbiomes at Arizona State University. Her lab has done research into how microbes use the undigested food that reaches your gut. She describes the problem with processed foods this way:
“Think about a Coke. When you drink it, all the sugar goes to your bloodstream, and the microbes in your gut don’t even know you’ve had it. Instead of drinking a Coke, if you eat an apple or something with fiber, some will go to you and some to the microbes. You’re feeding them, giving them energy.”
Weight and Your Gut Microbiome
The link between gut health and body weight has received a lot of attention. Research has shown, for example, that people with obesity have less diversity in their gut microbiome, and certain specific bacteria have been linked to obesity. In animal studies, transplanting gut microbes from obese mice to “germ-free” mice led those GF mice to gain weight. This suggests excess weight is, in fact, caused by certain microbes, but to date there’s scant evidence that the same is true with humans.
Dr. Krajmalnik-Brown’s group did an experiment in which they had people follow two different diets for 23 days each, with a break in between. Both provided similar amounts of calories and macronutrients each day but via different foods. The study’s typical Western menu featured processed foods — think grape juice, sandwiches made with deli turkey and white bread, and spaghetti with jarred sauce and ground beef. The other menu, what researchers called a “microbiome enhancer diet,” included foods like whole fruit, veggie sandwiches on multigrain buns, and steak with a side of whole wheat spaghetti.
While the study wasn’t designed for weight loss, an interesting thing happened when researchers analyzed participants’ bowel movements.
“We found that when you feed subjects a diet designed to provide more energy to the microbes and not to the [body], our subjects lost a little weight,” Dr. Krajmalnik-Brown said. “It looks like by feeding your microbes, it seems to make people healthier and potentially even lose a little.”
Another possible mechanism involves the same hormone that powers those injectable weight loss drugs. The lower part of your gut makes hormones that tell the entire gut to slow down and also help orchestrate metabolism and appetite. Among them is GLP-1. The drugs use a synthetic version, semaglutide or tirzepatide, to trigger the same effect.
According to Dr. Damman, you can stimulate your gut to make those helpful hormones with the food you eat — by giving your microbes the right fuel.
Eat to Feed Your Microbes
The foods you eat can affect your gut microbiome and so your weight. But don’t go looking for that one perfect ingredient, experts warn.
“Oftentimes we get this micro-focus, is this a good food or a bad food?” warned Katie Chapmon, a registered dietitian whose practice focuses on gut health. “You just want to make sure your microbiome is robust and healthy, so it communicates that your body is running, you’ve got it.”
Instead, try to give your body more of the kinds of food research has shown can feed your microbiome, many of which are plant-based. “Those are the things that are largely taken out during processing,” Dr. Damman said. He calls them the “Four Fs”:
Fiber: When you eat fiber-rich foods like fruits, vegetables, whole grains, nuts, and beans, your body can’t digest the fiber while it’s in the upper parts of your GI tract. It passes through to your lower gut, where healthy bacteria ferment it. That produces short-chain fatty acids, which send signals throughout your body, including ones related to appetite and feeling full.
Phenols: Phenolic compounds are antioxidants that give plant-based foods their color — when you talk about eating the rainbow, you’re talking about phenols. The microbes in your gut feed on them, too. “My goal for a meal is five distinct colors on the plate,” Ms. Chapmon said. “That rounds out the bases for the different polyphenols.”
Fermented foods: You can get a different kind of health benefit by eating food that’s already fermented — like sauerkraut, kimchi, kefir, yogurt, miso, tempeh, and kombucha. Fermentation can make the phenols in foods more accessible to your body. Plus, each mouthful introduces good bacteria into your body, some of which make it down to your gut. The bacteria that are already there feed on these new strains, which helps to increase the diversity of your microbiome.
Healthy fats: Here, it’s not so much about feeding the good bacteria in your microbiome. Dr. Damman says that omega-3 fatty acids, found in fatty fish, canola oil, some nuts, and other foods, decrease inflammation in the lining of your gut. Plus, healthy fat sources like extra-virgin olive oil and avocados are full of phenols.
Eating for gut health isn’t a magic bullet in terms of weight loss. But the benefits of a healthy gut go far beyond shedding a few pounds.
“I think we need to strive for health, not weight loss.” Dr. Krajmalnik-Brown said. “Keep your gut healthy and your microbes healthy, and that should eventually lead to a healthy weight. You’ll make your microbes happy, and your microbes do a lot for your health.”
A version of this article appeared on WebMD.com.
Injectable weight loss drugs like Wegovy, Saxenda, and Zepbound have been getting all the glory lately, but they’re not for everyone. If the inconvenience or cost of weight-loss drugs isn’t for you, another approach may be boosting your gut microbiome.
So how does one do that, and how does it work?
“There are a lot of different factors naturally in weight gain and weight loss, so the gut microbiome is certainly not the only thing,” said Chris Damman, MD, a gastroenterologist at the University of Washington. He studies how food and the microbiome affect your health. “With that caveat, it probably is playing an important role.”
Trillions of Microbes
The idea that your gut is home to an enormous range of tiny organisms — microbes — has existed for more than 100 years, but only in the 21st century have scientists had the ability to delve into specifics.
We now know you want a robust assortment of microbes in your gut, especially in the lower gut, your colon. They feast on fiber from the food you eat and turn it into substances your body needs. Those substances send signals all over your body.
If you don’t have enough microbes or have too many of the wrong kinds, it influences those signals, which can lead to health problems.
Thanks to these efforts, we know a lot about the interactions between your gut and the rest of your body, but we don’t know exactly how many things happen — whether some teeny critters within your microbiome cause the issues or vice versa.
“That’s the problem with so much of the microbiome stuff,” said Elizabeth Hohmann, MD, a physician investigator at the Massachusetts General Research Institute. “Olympic athletes have a better gut microbiome than most people. Well, sure they do — because they’re paying attention to their diet, they’re getting enough rest. Correlation does not causation make.”
The American Diet Messes With Your Gut
If you’re a typical American, you eat a lot of ultra-processed foods — manufactured with a long ingredients list that includes additives or preservatives. According to one study, those foods make up 73% of our food supply. That can have a serious impact on gut health.
“When you process a food and mill it, it turns a whole food into tiny particles,” Dr. Damman said. “That makes the food highly digestible. But if you eat a stalk of broccoli, a large amount of that broccoli in the form of fiber and other things will make its way to your lower gut, where it will feed microbes.”
With heavily processed foods, on the other hand, most of it gets digested before it can reach your lower gut, which leaves your microbes without the energy they need to survive.
Rosa Krajmalnik-Brown, PhD, is director of the Biodesign Center for Health Through Microbiomes at Arizona State University. Her lab has done research into how microbes use the undigested food that reaches your gut. She describes the problem with processed foods this way:
“Think about a Coke. When you drink it, all the sugar goes to your bloodstream, and the microbes in your gut don’t even know you’ve had it. Instead of drinking a Coke, if you eat an apple or something with fiber, some will go to you and some to the microbes. You’re feeding them, giving them energy.”
Weight and Your Gut Microbiome
The link between gut health and body weight has received a lot of attention. Research has shown, for example, that people with obesity have less diversity in their gut microbiome, and certain specific bacteria have been linked to obesity. In animal studies, transplanting gut microbes from obese mice to “germ-free” mice led those GF mice to gain weight. This suggests excess weight is, in fact, caused by certain microbes, but to date there’s scant evidence that the same is true with humans.
Dr. Krajmalnik-Brown’s group did an experiment in which they had people follow two different diets for 23 days each, with a break in between. Both provided similar amounts of calories and macronutrients each day but via different foods. The study’s typical Western menu featured processed foods — think grape juice, sandwiches made with deli turkey and white bread, and spaghetti with jarred sauce and ground beef. The other menu, what researchers called a “microbiome enhancer diet,” included foods like whole fruit, veggie sandwiches on multigrain buns, and steak with a side of whole wheat spaghetti.
While the study wasn’t designed for weight loss, an interesting thing happened when researchers analyzed participants’ bowel movements.
“We found that when you feed subjects a diet designed to provide more energy to the microbes and not to the [body], our subjects lost a little weight,” Dr. Krajmalnik-Brown said. “It looks like by feeding your microbes, it seems to make people healthier and potentially even lose a little.”
Another possible mechanism involves the same hormone that powers those injectable weight loss drugs. The lower part of your gut makes hormones that tell the entire gut to slow down and also help orchestrate metabolism and appetite. Among them is GLP-1. The drugs use a synthetic version, semaglutide or tirzepatide, to trigger the same effect.
According to Dr. Damman, you can stimulate your gut to make those helpful hormones with the food you eat — by giving your microbes the right fuel.
Eat to Feed Your Microbes
The foods you eat can affect your gut microbiome and so your weight. But don’t go looking for that one perfect ingredient, experts warn.
“Oftentimes we get this micro-focus, is this a good food or a bad food?” warned Katie Chapmon, a registered dietitian whose practice focuses on gut health. “You just want to make sure your microbiome is robust and healthy, so it communicates that your body is running, you’ve got it.”
Instead, try to give your body more of the kinds of food research has shown can feed your microbiome, many of which are plant-based. “Those are the things that are largely taken out during processing,” Dr. Damman said. He calls them the “Four Fs”:
Fiber: When you eat fiber-rich foods like fruits, vegetables, whole grains, nuts, and beans, your body can’t digest the fiber while it’s in the upper parts of your GI tract. It passes through to your lower gut, where healthy bacteria ferment it. That produces short-chain fatty acids, which send signals throughout your body, including ones related to appetite and feeling full.
Phenols: Phenolic compounds are antioxidants that give plant-based foods their color — when you talk about eating the rainbow, you’re talking about phenols. The microbes in your gut feed on them, too. “My goal for a meal is five distinct colors on the plate,” Ms. Chapmon said. “That rounds out the bases for the different polyphenols.”
Fermented foods: You can get a different kind of health benefit by eating food that’s already fermented — like sauerkraut, kimchi, kefir, yogurt, miso, tempeh, and kombucha. Fermentation can make the phenols in foods more accessible to your body. Plus, each mouthful introduces good bacteria into your body, some of which make it down to your gut. The bacteria that are already there feed on these new strains, which helps to increase the diversity of your microbiome.
Healthy fats: Here, it’s not so much about feeding the good bacteria in your microbiome. Dr. Damman says that omega-3 fatty acids, found in fatty fish, canola oil, some nuts, and other foods, decrease inflammation in the lining of your gut. Plus, healthy fat sources like extra-virgin olive oil and avocados are full of phenols.
Eating for gut health isn’t a magic bullet in terms of weight loss. But the benefits of a healthy gut go far beyond shedding a few pounds.
“I think we need to strive for health, not weight loss.” Dr. Krajmalnik-Brown said. “Keep your gut healthy and your microbes healthy, and that should eventually lead to a healthy weight. You’ll make your microbes happy, and your microbes do a lot for your health.”
A version of this article appeared on WebMD.com.
Injectable weight loss drugs like Wegovy, Saxenda, and Zepbound have been getting all the glory lately, but they’re not for everyone. If the inconvenience or cost of weight-loss drugs isn’t for you, another approach may be boosting your gut microbiome.
So how does one do that, and how does it work?
“There are a lot of different factors naturally in weight gain and weight loss, so the gut microbiome is certainly not the only thing,” said Chris Damman, MD, a gastroenterologist at the University of Washington. He studies how food and the microbiome affect your health. “With that caveat, it probably is playing an important role.”
Trillions of Microbes
The idea that your gut is home to an enormous range of tiny organisms — microbes — has existed for more than 100 years, but only in the 21st century have scientists had the ability to delve into specifics.
We now know you want a robust assortment of microbes in your gut, especially in the lower gut, your colon. They feast on fiber from the food you eat and turn it into substances your body needs. Those substances send signals all over your body.
If you don’t have enough microbes or have too many of the wrong kinds, it influences those signals, which can lead to health problems.
Thanks to these efforts, we know a lot about the interactions between your gut and the rest of your body, but we don’t know exactly how many things happen — whether some teeny critters within your microbiome cause the issues or vice versa.
“That’s the problem with so much of the microbiome stuff,” said Elizabeth Hohmann, MD, a physician investigator at the Massachusetts General Research Institute. “Olympic athletes have a better gut microbiome than most people. Well, sure they do — because they’re paying attention to their diet, they’re getting enough rest. Correlation does not causation make.”
The American Diet Messes With Your Gut
If you’re a typical American, you eat a lot of ultra-processed foods — manufactured with a long ingredients list that includes additives or preservatives. According to one study, those foods make up 73% of our food supply. That can have a serious impact on gut health.
“When you process a food and mill it, it turns a whole food into tiny particles,” Dr. Damman said. “That makes the food highly digestible. But if you eat a stalk of broccoli, a large amount of that broccoli in the form of fiber and other things will make its way to your lower gut, where it will feed microbes.”
With heavily processed foods, on the other hand, most of it gets digested before it can reach your lower gut, which leaves your microbes without the energy they need to survive.
Rosa Krajmalnik-Brown, PhD, is director of the Biodesign Center for Health Through Microbiomes at Arizona State University. Her lab has done research into how microbes use the undigested food that reaches your gut. She describes the problem with processed foods this way:
“Think about a Coke. When you drink it, all the sugar goes to your bloodstream, and the microbes in your gut don’t even know you’ve had it. Instead of drinking a Coke, if you eat an apple or something with fiber, some will go to you and some to the microbes. You’re feeding them, giving them energy.”
Weight and Your Gut Microbiome
The link between gut health and body weight has received a lot of attention. Research has shown, for example, that people with obesity have less diversity in their gut microbiome, and certain specific bacteria have been linked to obesity. In animal studies, transplanting gut microbes from obese mice to “germ-free” mice led those GF mice to gain weight. This suggests excess weight is, in fact, caused by certain microbes, but to date there’s scant evidence that the same is true with humans.
Dr. Krajmalnik-Brown’s group did an experiment in which they had people follow two different diets for 23 days each, with a break in between. Both provided similar amounts of calories and macronutrients each day but via different foods. The study’s typical Western menu featured processed foods — think grape juice, sandwiches made with deli turkey and white bread, and spaghetti with jarred sauce and ground beef. The other menu, what researchers called a “microbiome enhancer diet,” included foods like whole fruit, veggie sandwiches on multigrain buns, and steak with a side of whole wheat spaghetti.
While the study wasn’t designed for weight loss, an interesting thing happened when researchers analyzed participants’ bowel movements.
“We found that when you feed subjects a diet designed to provide more energy to the microbes and not to the [body], our subjects lost a little weight,” Dr. Krajmalnik-Brown said. “It looks like by feeding your microbes, it seems to make people healthier and potentially even lose a little.”
Another possible mechanism involves the same hormone that powers those injectable weight loss drugs. The lower part of your gut makes hormones that tell the entire gut to slow down and also help orchestrate metabolism and appetite. Among them is GLP-1. The drugs use a synthetic version, semaglutide or tirzepatide, to trigger the same effect.
According to Dr. Damman, you can stimulate your gut to make those helpful hormones with the food you eat — by giving your microbes the right fuel.
Eat to Feed Your Microbes
The foods you eat can affect your gut microbiome and so your weight. But don’t go looking for that one perfect ingredient, experts warn.
“Oftentimes we get this micro-focus, is this a good food or a bad food?” warned Katie Chapmon, a registered dietitian whose practice focuses on gut health. “You just want to make sure your microbiome is robust and healthy, so it communicates that your body is running, you’ve got it.”
Instead, try to give your body more of the kinds of food research has shown can feed your microbiome, many of which are plant-based. “Those are the things that are largely taken out during processing,” Dr. Damman said. He calls them the “Four Fs”:
Fiber: When you eat fiber-rich foods like fruits, vegetables, whole grains, nuts, and beans, your body can’t digest the fiber while it’s in the upper parts of your GI tract. It passes through to your lower gut, where healthy bacteria ferment it. That produces short-chain fatty acids, which send signals throughout your body, including ones related to appetite and feeling full.
Phenols: Phenolic compounds are antioxidants that give plant-based foods their color — when you talk about eating the rainbow, you’re talking about phenols. The microbes in your gut feed on them, too. “My goal for a meal is five distinct colors on the plate,” Ms. Chapmon said. “That rounds out the bases for the different polyphenols.”
Fermented foods: You can get a different kind of health benefit by eating food that’s already fermented — like sauerkraut, kimchi, kefir, yogurt, miso, tempeh, and kombucha. Fermentation can make the phenols in foods more accessible to your body. Plus, each mouthful introduces good bacteria into your body, some of which make it down to your gut. The bacteria that are already there feed on these new strains, which helps to increase the diversity of your microbiome.
Healthy fats: Here, it’s not so much about feeding the good bacteria in your microbiome. Dr. Damman says that omega-3 fatty acids, found in fatty fish, canola oil, some nuts, and other foods, decrease inflammation in the lining of your gut. Plus, healthy fat sources like extra-virgin olive oil and avocados are full of phenols.
Eating for gut health isn’t a magic bullet in terms of weight loss. But the benefits of a healthy gut go far beyond shedding a few pounds.
“I think we need to strive for health, not weight loss.” Dr. Krajmalnik-Brown said. “Keep your gut healthy and your microbes healthy, and that should eventually lead to a healthy weight. You’ll make your microbes happy, and your microbes do a lot for your health.”
A version of this article appeared on WebMD.com.
Is It Possible to Change a Slow Metabolism?
Many patients with obesity blame weight gain on their metabolism. The reality is that metabolism can be blamed for weight regain after people try to lose weight! As we age, our metabolism does slow down; sometimes we think it stops working.
What happens to our metabolism when we try to lose weight? Let’s first discuss what metabolism is.
What Is Metabolism?
Metabolism refers to the chemical reactions in the body’s cells that convert food into energy for sustaining life, cellular processes, and as storage for a rainy day.
Total energy expenditure (TEE) is broken down into resting energy expenditure (REE), thermic effect of food (TEF), and nonresting expenditure (NREE) or physical activity, and is made up of: TEE = 60% REE + 10% TEF + 30% NREE.
An elegant study performed by Dr. Rudy Leibel explored the effects of weight loss or weight gain on metabolism in 23 lean and 18 patients with obesity who were placed in a metabolic chamber. Weight loss of 10% or 20% body weight led to a decrease in TEE roughly equal to about 300 kcal/d, and an increase in body weight of 10% caused an increase in TEE of about 500 kcal/d. These changes led to the patient reverting to the prior weight (before weight loss or gain). In other words, Dr. Leibel postulated a feedback mechanism for the effect of fat mass decrease or increase on energy metabolism. The feedback mechanism or signal from fat was subsequently found to be leptin.
In a later study, Dr. Leibel and colleagues investigated the effects of body fat mass change on TEE and found that a 10% reduction in weight caused a decrease of TEE by 21%, comprising a decrease in NREE of 37.5% and a decrease in REE of 11.6%.
Therefore, the biggest change in TEE comes from NREE or exercise energy expenditure. The 35% variance in NEE change was accounted for by a decrease in muscle work efficiency in generating 10 watts or low levels of work such as walking.
In other words, when persons with obesity or lean persons lose weight, the efficiency of muscle at low levels of work increases such that one burns less energy when walking than one normally would. This helps conserve energy and tends to cause the body to go back to the higher weight.
So, How Can One Change Metabolism?
Let’s say one did lose weight and wants to counteract this TEE loss and increased muscle efficiency at low levels of work.
To counteract this effect, one should increase muscle work beyond low level so that more energy is expended. Another way would be to increase muscle mass so that there is more muscle that can do work.
This is exactly how metabolism can be altered or increased. What can be changed most readily, and what we have the most power over in our bodies, is the NREE.
To do this, muscles need anabolic power — the power to heal and build muscle mass. Anabolic power comes from eating healthy protein sources such as lean chicken, fish, beef, and eggs as well as dry beans, tofu, and dairy products.. It seems that older adults (> 60 years) need more protein than younger adults to build muscle mass, due to the body’s natural aging process which leads to sarcopenia. How much more? Studies show between 1.2 and 1.5 g/kg of body weight per day, whereas younger persons need 0.80 g/kg.
Developing sarcopenia with age involves muscle losing the ability to use protein and amino acids to rebuild injured tissue.
Let’s put this in perspective for treating obesity.
Obesity is brought on by the body’s defense of a higher body weight by interaction with the environment of highly processed foods that work on the reward pathway, leading to weight gain and resistance to satiety. Weight loss via diet, exercise, and medications works, but this weight loss is also accompanied by a decrease in TEE.
Weight loss is primarily fat mass loss, but depending on the degree of protein intake and muscle resistance training, 20%-50% of the total weight loss is muscle mass loss. Therefore, higher-protein diets and resistance exercise can be useful in preserving muscle mass and counteracting the decrease in TEE, maintaining energy expenditure. In older patients, an additional factor is the muscle’s lack of ability to use protein as an anabolic agent to protect muscle mass and thus the need for higher protein loads to do this.
All in all, can doctors help patients boost their metabolism, especially as they lose weight and maintain that loss? Yes — through protein intake and resistance exercise training.
Here are some tips to help your patients get cardio and resistance exercise into their routine.
First find out whether your patient prefers a social exercise interaction or solo training. If social, then the gym or classes such as cycling or boot camps at those gyms may work for them, especially if they can go with a friend. If solo is better, than a gym in the home might work. Peloton bikes are expensive but the interaction is all on the website!
A personal trainer may help motivate the patient if they know someone is waiting for them.
Let’s hit the gym!
Another note: There are agents in the obesity treatment pipeline that purport to change body composition while helping patients lose weight. Some of these agents are myostatin antagonists and antibodies that inhibit the activity of myostatin to break down muscle. These agents have been found to build muscle mass, but whether the quality of the muscle mass leads to an increase in muscle strength or functionality remains controversial. The next frontier in obesity treatment will be about decreasing fat mass and increasing muscle mass while making sure that increased muscle mass leads to improved functionality.
In the meantime, aside from new agents on the horizon, the best and healthiest way to keep metabolism on the up and up is to eat healthy lean proteins and exercise. How much exercise? The recommendation is 30-60 minutes of moderate to vigorous physical activity at least 5 days per week; plus 20 minutes of resistance exercise training 2-3 days per week for upper- and lower-extremity and core strength.
Again, let’s hit the gym!
Dr. Apovian is in the department of medicine, and codirector, Center for Weight Management and Wellness, Section of Endocrinology, Diabetes, and Hypertension, at Brigham and Women’s Hospital, Harvard Medical School, Boston. She disclosed ties with Altimmune, Cowen and Company, Currax Pharmaceuticals, EPG Communication Holdings, Gelesis, Srl, L-Nutra, and NeuroBo Pharmaceuticals, and Novo Nordisk. She received research grant from the National Institutes of Health, Patient-Centered Outcomes Research Institute, and GI Dynamics.
A version of this article appeared on Medscape.com.
Many patients with obesity blame weight gain on their metabolism. The reality is that metabolism can be blamed for weight regain after people try to lose weight! As we age, our metabolism does slow down; sometimes we think it stops working.
What happens to our metabolism when we try to lose weight? Let’s first discuss what metabolism is.
What Is Metabolism?
Metabolism refers to the chemical reactions in the body’s cells that convert food into energy for sustaining life, cellular processes, and as storage for a rainy day.
Total energy expenditure (TEE) is broken down into resting energy expenditure (REE), thermic effect of food (TEF), and nonresting expenditure (NREE) or physical activity, and is made up of: TEE = 60% REE + 10% TEF + 30% NREE.
An elegant study performed by Dr. Rudy Leibel explored the effects of weight loss or weight gain on metabolism in 23 lean and 18 patients with obesity who were placed in a metabolic chamber. Weight loss of 10% or 20% body weight led to a decrease in TEE roughly equal to about 300 kcal/d, and an increase in body weight of 10% caused an increase in TEE of about 500 kcal/d. These changes led to the patient reverting to the prior weight (before weight loss or gain). In other words, Dr. Leibel postulated a feedback mechanism for the effect of fat mass decrease or increase on energy metabolism. The feedback mechanism or signal from fat was subsequently found to be leptin.
In a later study, Dr. Leibel and colleagues investigated the effects of body fat mass change on TEE and found that a 10% reduction in weight caused a decrease of TEE by 21%, comprising a decrease in NREE of 37.5% and a decrease in REE of 11.6%.
Therefore, the biggest change in TEE comes from NREE or exercise energy expenditure. The 35% variance in NEE change was accounted for by a decrease in muscle work efficiency in generating 10 watts or low levels of work such as walking.
In other words, when persons with obesity or lean persons lose weight, the efficiency of muscle at low levels of work increases such that one burns less energy when walking than one normally would. This helps conserve energy and tends to cause the body to go back to the higher weight.
So, How Can One Change Metabolism?
Let’s say one did lose weight and wants to counteract this TEE loss and increased muscle efficiency at low levels of work.
To counteract this effect, one should increase muscle work beyond low level so that more energy is expended. Another way would be to increase muscle mass so that there is more muscle that can do work.
This is exactly how metabolism can be altered or increased. What can be changed most readily, and what we have the most power over in our bodies, is the NREE.
To do this, muscles need anabolic power — the power to heal and build muscle mass. Anabolic power comes from eating healthy protein sources such as lean chicken, fish, beef, and eggs as well as dry beans, tofu, and dairy products.. It seems that older adults (> 60 years) need more protein than younger adults to build muscle mass, due to the body’s natural aging process which leads to sarcopenia. How much more? Studies show between 1.2 and 1.5 g/kg of body weight per day, whereas younger persons need 0.80 g/kg.
Developing sarcopenia with age involves muscle losing the ability to use protein and amino acids to rebuild injured tissue.
Let’s put this in perspective for treating obesity.
Obesity is brought on by the body’s defense of a higher body weight by interaction with the environment of highly processed foods that work on the reward pathway, leading to weight gain and resistance to satiety. Weight loss via diet, exercise, and medications works, but this weight loss is also accompanied by a decrease in TEE.
Weight loss is primarily fat mass loss, but depending on the degree of protein intake and muscle resistance training, 20%-50% of the total weight loss is muscle mass loss. Therefore, higher-protein diets and resistance exercise can be useful in preserving muscle mass and counteracting the decrease in TEE, maintaining energy expenditure. In older patients, an additional factor is the muscle’s lack of ability to use protein as an anabolic agent to protect muscle mass and thus the need for higher protein loads to do this.
All in all, can doctors help patients boost their metabolism, especially as they lose weight and maintain that loss? Yes — through protein intake and resistance exercise training.
Here are some tips to help your patients get cardio and resistance exercise into their routine.
First find out whether your patient prefers a social exercise interaction or solo training. If social, then the gym or classes such as cycling or boot camps at those gyms may work for them, especially if they can go with a friend. If solo is better, than a gym in the home might work. Peloton bikes are expensive but the interaction is all on the website!
A personal trainer may help motivate the patient if they know someone is waiting for them.
Let’s hit the gym!
Another note: There are agents in the obesity treatment pipeline that purport to change body composition while helping patients lose weight. Some of these agents are myostatin antagonists and antibodies that inhibit the activity of myostatin to break down muscle. These agents have been found to build muscle mass, but whether the quality of the muscle mass leads to an increase in muscle strength or functionality remains controversial. The next frontier in obesity treatment will be about decreasing fat mass and increasing muscle mass while making sure that increased muscle mass leads to improved functionality.
In the meantime, aside from new agents on the horizon, the best and healthiest way to keep metabolism on the up and up is to eat healthy lean proteins and exercise. How much exercise? The recommendation is 30-60 minutes of moderate to vigorous physical activity at least 5 days per week; plus 20 minutes of resistance exercise training 2-3 days per week for upper- and lower-extremity and core strength.
Again, let’s hit the gym!
Dr. Apovian is in the department of medicine, and codirector, Center for Weight Management and Wellness, Section of Endocrinology, Diabetes, and Hypertension, at Brigham and Women’s Hospital, Harvard Medical School, Boston. She disclosed ties with Altimmune, Cowen and Company, Currax Pharmaceuticals, EPG Communication Holdings, Gelesis, Srl, L-Nutra, and NeuroBo Pharmaceuticals, and Novo Nordisk. She received research grant from the National Institutes of Health, Patient-Centered Outcomes Research Institute, and GI Dynamics.
A version of this article appeared on Medscape.com.
Many patients with obesity blame weight gain on their metabolism. The reality is that metabolism can be blamed for weight regain after people try to lose weight! As we age, our metabolism does slow down; sometimes we think it stops working.
What happens to our metabolism when we try to lose weight? Let’s first discuss what metabolism is.
What Is Metabolism?
Metabolism refers to the chemical reactions in the body’s cells that convert food into energy for sustaining life, cellular processes, and as storage for a rainy day.
Total energy expenditure (TEE) is broken down into resting energy expenditure (REE), thermic effect of food (TEF), and nonresting expenditure (NREE) or physical activity, and is made up of: TEE = 60% REE + 10% TEF + 30% NREE.
An elegant study performed by Dr. Rudy Leibel explored the effects of weight loss or weight gain on metabolism in 23 lean and 18 patients with obesity who were placed in a metabolic chamber. Weight loss of 10% or 20% body weight led to a decrease in TEE roughly equal to about 300 kcal/d, and an increase in body weight of 10% caused an increase in TEE of about 500 kcal/d. These changes led to the patient reverting to the prior weight (before weight loss or gain). In other words, Dr. Leibel postulated a feedback mechanism for the effect of fat mass decrease or increase on energy metabolism. The feedback mechanism or signal from fat was subsequently found to be leptin.
In a later study, Dr. Leibel and colleagues investigated the effects of body fat mass change on TEE and found that a 10% reduction in weight caused a decrease of TEE by 21%, comprising a decrease in NREE of 37.5% and a decrease in REE of 11.6%.
Therefore, the biggest change in TEE comes from NREE or exercise energy expenditure. The 35% variance in NEE change was accounted for by a decrease in muscle work efficiency in generating 10 watts or low levels of work such as walking.
In other words, when persons with obesity or lean persons lose weight, the efficiency of muscle at low levels of work increases such that one burns less energy when walking than one normally would. This helps conserve energy and tends to cause the body to go back to the higher weight.
So, How Can One Change Metabolism?
Let’s say one did lose weight and wants to counteract this TEE loss and increased muscle efficiency at low levels of work.
To counteract this effect, one should increase muscle work beyond low level so that more energy is expended. Another way would be to increase muscle mass so that there is more muscle that can do work.
This is exactly how metabolism can be altered or increased. What can be changed most readily, and what we have the most power over in our bodies, is the NREE.
To do this, muscles need anabolic power — the power to heal and build muscle mass. Anabolic power comes from eating healthy protein sources such as lean chicken, fish, beef, and eggs as well as dry beans, tofu, and dairy products.. It seems that older adults (> 60 years) need more protein than younger adults to build muscle mass, due to the body’s natural aging process which leads to sarcopenia. How much more? Studies show between 1.2 and 1.5 g/kg of body weight per day, whereas younger persons need 0.80 g/kg.
Developing sarcopenia with age involves muscle losing the ability to use protein and amino acids to rebuild injured tissue.
Let’s put this in perspective for treating obesity.
Obesity is brought on by the body’s defense of a higher body weight by interaction with the environment of highly processed foods that work on the reward pathway, leading to weight gain and resistance to satiety. Weight loss via diet, exercise, and medications works, but this weight loss is also accompanied by a decrease in TEE.
Weight loss is primarily fat mass loss, but depending on the degree of protein intake and muscle resistance training, 20%-50% of the total weight loss is muscle mass loss. Therefore, higher-protein diets and resistance exercise can be useful in preserving muscle mass and counteracting the decrease in TEE, maintaining energy expenditure. In older patients, an additional factor is the muscle’s lack of ability to use protein as an anabolic agent to protect muscle mass and thus the need for higher protein loads to do this.
All in all, can doctors help patients boost their metabolism, especially as they lose weight and maintain that loss? Yes — through protein intake and resistance exercise training.
Here are some tips to help your patients get cardio and resistance exercise into their routine.
First find out whether your patient prefers a social exercise interaction or solo training. If social, then the gym or classes such as cycling or boot camps at those gyms may work for them, especially if they can go with a friend. If solo is better, than a gym in the home might work. Peloton bikes are expensive but the interaction is all on the website!
A personal trainer may help motivate the patient if they know someone is waiting for them.
Let’s hit the gym!
Another note: There are agents in the obesity treatment pipeline that purport to change body composition while helping patients lose weight. Some of these agents are myostatin antagonists and antibodies that inhibit the activity of myostatin to break down muscle. These agents have been found to build muscle mass, but whether the quality of the muscle mass leads to an increase in muscle strength or functionality remains controversial. The next frontier in obesity treatment will be about decreasing fat mass and increasing muscle mass while making sure that increased muscle mass leads to improved functionality.
In the meantime, aside from new agents on the horizon, the best and healthiest way to keep metabolism on the up and up is to eat healthy lean proteins and exercise. How much exercise? The recommendation is 30-60 minutes of moderate to vigorous physical activity at least 5 days per week; plus 20 minutes of resistance exercise training 2-3 days per week for upper- and lower-extremity and core strength.
Again, let’s hit the gym!
Dr. Apovian is in the department of medicine, and codirector, Center for Weight Management and Wellness, Section of Endocrinology, Diabetes, and Hypertension, at Brigham and Women’s Hospital, Harvard Medical School, Boston. She disclosed ties with Altimmune, Cowen and Company, Currax Pharmaceuticals, EPG Communication Holdings, Gelesis, Srl, L-Nutra, and NeuroBo Pharmaceuticals, and Novo Nordisk. She received research grant from the National Institutes of Health, Patient-Centered Outcomes Research Institute, and GI Dynamics.
A version of this article appeared on Medscape.com.
Eat Earlier and More Often to Prevent Obesity
TOPLINE:
(BMI) and reduced obesity risk.
METHODOLOGY:
- According to recent research in the field of “chrononutrition,” which refers to the circadian pattern of eating behaviors, the timing of eating can affect an individual’s health and obesity.
- This exploratory, population-based study looked at the association between the timing of the largest meal of the day and the number of meals per day with BMI and obesity in 2050 nonpregnant adults in Brazil (ages 18-65 years; 15% with BMI ≥ 30; 73% women).
- In an online survey, participants reported their weight and height for BMI calculation and filled in questionnaires related to meal timing and frequency as well as diet quality and lifestyle traits.
- The 24-hour clock time (hh:mm) averages for the first eating event, lunch, and evening eating event were 8:27, 12:47, and 20:57, respectively, among all the participants.
- The median time of the largest meal was 12:38 and was the dividing line to classify people as early-eaters or late-eaters. Overall, lunch was the largest meal for 75% of people, and 75% ate more than three meals a day.
TAKEAWAY:
- Compared with participants who had up to three meals a day, those who reported more than three meals a day had a 0.48 lower BMI (P = .04) and lower odds of obesity (odds ratio [OR], 0.68; P = .005).
- Eating the largest meal later was associated with higher BMI values (0.07 for each additional hour; P = .03) and higher odds of obesity (OR, 1.04; P = .01).
- The group that reported dinner as the largest meal of the day had a 0.85 higher BMI (P = .02) and greater odds of obesity (OR, 1.67; P = .004) than the group that did not have dinner as the largest meal.
- On the other hand, having lunch as the main meal appeared to serve as a protective factor with lower odds of obesity (OR, 0.71; P = .01).
IN PRACTICE:
“Late-eaters (individuals who ate their largest meal after 12:38) exhibited several obesogenic and unhealthy behaviors (such as lower diet quality, shorter sleep duration, sedentary lifestyle, and prolonged screen time) that could potentially contribute to long-term weight gain and obesity,” the authors wrote.
SOURCE:
Giovana Longo-Silva, Faculty of Nutrition, Federal University of Alagoas, Maceió, Alagoas, Brazil, led this study, which was published online in Clinical Nutrition ESPEN.
LIMITATIONS:
The study used self-reported questionnaires, which are susceptible to underreporting. The participants included a greater number of highly educated women. The study used food scoring to evaluate the overall quality of each person’s dietary intake and may have missed variations in the distribution of nutrients in meals and in the total amount of energy and nutrients consumed, which could affect the BMI of participants. Despite adjustments for sociodemographic, diet-related, and lifestyle traits, a cross-sectional study cannot distinguish between cause and effect.
DISCLOSURES:
This work was supported by Fundação de Amparo à Pesquisa do Estado de Alagoas. The authors declared no conflicts of interest.
A version of this article appeared on Medscape.com.
TOPLINE:
(BMI) and reduced obesity risk.
METHODOLOGY:
- According to recent research in the field of “chrononutrition,” which refers to the circadian pattern of eating behaviors, the timing of eating can affect an individual’s health and obesity.
- This exploratory, population-based study looked at the association between the timing of the largest meal of the day and the number of meals per day with BMI and obesity in 2050 nonpregnant adults in Brazil (ages 18-65 years; 15% with BMI ≥ 30; 73% women).
- In an online survey, participants reported their weight and height for BMI calculation and filled in questionnaires related to meal timing and frequency as well as diet quality and lifestyle traits.
- The 24-hour clock time (hh:mm) averages for the first eating event, lunch, and evening eating event were 8:27, 12:47, and 20:57, respectively, among all the participants.
- The median time of the largest meal was 12:38 and was the dividing line to classify people as early-eaters or late-eaters. Overall, lunch was the largest meal for 75% of people, and 75% ate more than three meals a day.
TAKEAWAY:
- Compared with participants who had up to three meals a day, those who reported more than three meals a day had a 0.48 lower BMI (P = .04) and lower odds of obesity (odds ratio [OR], 0.68; P = .005).
- Eating the largest meal later was associated with higher BMI values (0.07 for each additional hour; P = .03) and higher odds of obesity (OR, 1.04; P = .01).
- The group that reported dinner as the largest meal of the day had a 0.85 higher BMI (P = .02) and greater odds of obesity (OR, 1.67; P = .004) than the group that did not have dinner as the largest meal.
- On the other hand, having lunch as the main meal appeared to serve as a protective factor with lower odds of obesity (OR, 0.71; P = .01).
IN PRACTICE:
“Late-eaters (individuals who ate their largest meal after 12:38) exhibited several obesogenic and unhealthy behaviors (such as lower diet quality, shorter sleep duration, sedentary lifestyle, and prolonged screen time) that could potentially contribute to long-term weight gain and obesity,” the authors wrote.
SOURCE:
Giovana Longo-Silva, Faculty of Nutrition, Federal University of Alagoas, Maceió, Alagoas, Brazil, led this study, which was published online in Clinical Nutrition ESPEN.
LIMITATIONS:
The study used self-reported questionnaires, which are susceptible to underreporting. The participants included a greater number of highly educated women. The study used food scoring to evaluate the overall quality of each person’s dietary intake and may have missed variations in the distribution of nutrients in meals and in the total amount of energy and nutrients consumed, which could affect the BMI of participants. Despite adjustments for sociodemographic, diet-related, and lifestyle traits, a cross-sectional study cannot distinguish between cause and effect.
DISCLOSURES:
This work was supported by Fundação de Amparo à Pesquisa do Estado de Alagoas. The authors declared no conflicts of interest.
A version of this article appeared on Medscape.com.
TOPLINE:
(BMI) and reduced obesity risk.
METHODOLOGY:
- According to recent research in the field of “chrononutrition,” which refers to the circadian pattern of eating behaviors, the timing of eating can affect an individual’s health and obesity.
- This exploratory, population-based study looked at the association between the timing of the largest meal of the day and the number of meals per day with BMI and obesity in 2050 nonpregnant adults in Brazil (ages 18-65 years; 15% with BMI ≥ 30; 73% women).
- In an online survey, participants reported their weight and height for BMI calculation and filled in questionnaires related to meal timing and frequency as well as diet quality and lifestyle traits.
- The 24-hour clock time (hh:mm) averages for the first eating event, lunch, and evening eating event were 8:27, 12:47, and 20:57, respectively, among all the participants.
- The median time of the largest meal was 12:38 and was the dividing line to classify people as early-eaters or late-eaters. Overall, lunch was the largest meal for 75% of people, and 75% ate more than three meals a day.
TAKEAWAY:
- Compared with participants who had up to three meals a day, those who reported more than three meals a day had a 0.48 lower BMI (P = .04) and lower odds of obesity (odds ratio [OR], 0.68; P = .005).
- Eating the largest meal later was associated with higher BMI values (0.07 for each additional hour; P = .03) and higher odds of obesity (OR, 1.04; P = .01).
- The group that reported dinner as the largest meal of the day had a 0.85 higher BMI (P = .02) and greater odds of obesity (OR, 1.67; P = .004) than the group that did not have dinner as the largest meal.
- On the other hand, having lunch as the main meal appeared to serve as a protective factor with lower odds of obesity (OR, 0.71; P = .01).
IN PRACTICE:
“Late-eaters (individuals who ate their largest meal after 12:38) exhibited several obesogenic and unhealthy behaviors (such as lower diet quality, shorter sleep duration, sedentary lifestyle, and prolonged screen time) that could potentially contribute to long-term weight gain and obesity,” the authors wrote.
SOURCE:
Giovana Longo-Silva, Faculty of Nutrition, Federal University of Alagoas, Maceió, Alagoas, Brazil, led this study, which was published online in Clinical Nutrition ESPEN.
LIMITATIONS:
The study used self-reported questionnaires, which are susceptible to underreporting. The participants included a greater number of highly educated women. The study used food scoring to evaluate the overall quality of each person’s dietary intake and may have missed variations in the distribution of nutrients in meals and in the total amount of energy and nutrients consumed, which could affect the BMI of participants. Despite adjustments for sociodemographic, diet-related, and lifestyle traits, a cross-sectional study cannot distinguish between cause and effect.
DISCLOSURES:
This work was supported by Fundação de Amparo à Pesquisa do Estado de Alagoas. The authors declared no conflicts of interest.
A version of this article appeared on Medscape.com.
Bariatric Surgery Yields Significant Cognitive Benefits
Bariatric surgery is associated with long-term improvements in cognition and brain structure in addition to general health benefits and expected weight loss, a large study found.
Among 133 adults with severe obesity who underwent bariatric surgery, roughly two in five showed > 20% improvement in global cognitive function at 24 months following the surgery.
“Notably, the temporal cortex exhibited not only higher cortical thickness but also higher vascular efficiency after surgery,” reported Amanda Kiliaan, PhD, Radboud University Medical Center, Nijmegen, the Netherlands, and colleagues.
“These results highlight beneficial vascular responses occurring in conjunction with bariatric surgery,” the researchers wrote.
They also suggested that weight-loss surgery may represent a treatment option for patients with obesity and dementia.
The study was published online on February 9, 2024, in JAMA Network Open.
Obesity is associated with an increased risk of developing dementia. Bariatric surgery-induced weight loss has been associated with improvements in brain function and structure in some small cohort studies with short follow-up periods. However, long-term neurological outcomes associated with bariatric surgery are unclear.
To investigate, Dr. Kiliaan and colleagues studied 133 adults with severe obesity (mean age, 46 years; 84% women) who underwent Roux-en-Y gastric bypass. The researchers collected relevant data from laboratory tests, cognitive tests, and MRI brain scans before surgery and at 6 and 24 months after surgery.
Overall, mean body weight, body mass index, waist circumference, and blood pressure were significantly lower at 6 and 24 months after surgery. At 24 months, significantly fewer patients were taking antihypertensive medication (17% vs 36% before surgery).
Improvements in inflammatory markers, depressive symptoms, and physical activity were also evident after surgery.
Cognitive Improvements
Several cognitive domains showed significant improvement at 6 and 24 months after bariatric surgery. Based on the 20% change index, improvements in working memory, episodic memory, and verbal fluency were seen in 11%, 32%, and 24% of participants, respectively.
Forty percent of patients showed improvement in their able to shift their attention, and 43% showed improvements in global cognition after surgery.
Several changes in brain parameters were also noted. Despite lower cerebral blood flow (CBF) in several regions, volumes of hippocampus, nucleus accumbens, frontal cortex, white matter, and white matter hyperintensity remained stable after surgery.
The temporal cortex showed a greater thickness (mean, 2.724 mm vs 2.761 mm; P = .007) and lower spatial coefficient of variation (sCOV; median, 4.41% vs 3.97%; P = .02) after surgery.
Overall, the results suggest that cognitive improvements “begin shortly after bariatric surgery and are long lasting,” the authors wrote.
Various factors may be involved including remission of comorbidities, higher physical activity, lower depressive symptoms, and lower inflammatory factors, they suggest. Stabilization of volume, CBF, and sCOV in brain regions, coupled with gains in cortical thickness and vascular efficiency in the temporal cortex could also play a role.
‘Remarkable’ Results
“Taken together, the research intimates bariatric surgery’s potential protective effects against dementia manifest through both weight-related brain changes and reducing cardiovascular risk factors,” Shaheen Lakhan, MD, a neurologist and researcher based in Miami, who wasn’t involved in the study, told this news organization.
“These remarkable neurological transformations intimate this surgery represents a pivotal opportunity to combat the parallel public health crises of obesity and dementia threatening society,” he said.
“In demonstrating a durable cognitive and brain boost out years beyond surgery, patients now have an emphatic answer — these aren’t short-lived benefits but rather profound improvements propelling them positively for the rest of life,” he added.
This opens up questions on whether the new class of obesity medications targeting glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide pathways, that can achieve weight loss approaching that of bariatric surgery, could have similar benefits.
The use of GLP-1 drugs have also shown neuroprotective effects such as improvement in motor and cognitive deficits, reduction of neuroinflammation, prevention of neuronal loss, and possibly slowing of neurodegeneration across animal models of Parkinson’s disease, Alzheimer’s disease, and stroke, said Dr. Lakhan. However, the exact mechanisms and ability to cross the blood-brain barrier require further confirmation, especially in humans.
Large, long-term, randomized controlled trials looking into potential effects of semaglutide on early Alzheimer›s disease, including the EVOKE Plus trial, are currently underway, he noted.
“These game-changing obesity drugs may hand us medicine’s holy grail — a pill to rival surgery’s brain benefits without the scalpel, allowing patients a more accessible path to protecting their brain,” Dr. Lakhan said.
The study had no funding from industry. Dr. Kiliaan and Dr. Lakhan had no relevant disclosures.
A version of this article first appeared on Medscape.com.
Bariatric surgery is associated with long-term improvements in cognition and brain structure in addition to general health benefits and expected weight loss, a large study found.
Among 133 adults with severe obesity who underwent bariatric surgery, roughly two in five showed > 20% improvement in global cognitive function at 24 months following the surgery.
“Notably, the temporal cortex exhibited not only higher cortical thickness but also higher vascular efficiency after surgery,” reported Amanda Kiliaan, PhD, Radboud University Medical Center, Nijmegen, the Netherlands, and colleagues.
“These results highlight beneficial vascular responses occurring in conjunction with bariatric surgery,” the researchers wrote.
They also suggested that weight-loss surgery may represent a treatment option for patients with obesity and dementia.
The study was published online on February 9, 2024, in JAMA Network Open.
Obesity is associated with an increased risk of developing dementia. Bariatric surgery-induced weight loss has been associated with improvements in brain function and structure in some small cohort studies with short follow-up periods. However, long-term neurological outcomes associated with bariatric surgery are unclear.
To investigate, Dr. Kiliaan and colleagues studied 133 adults with severe obesity (mean age, 46 years; 84% women) who underwent Roux-en-Y gastric bypass. The researchers collected relevant data from laboratory tests, cognitive tests, and MRI brain scans before surgery and at 6 and 24 months after surgery.
Overall, mean body weight, body mass index, waist circumference, and blood pressure were significantly lower at 6 and 24 months after surgery. At 24 months, significantly fewer patients were taking antihypertensive medication (17% vs 36% before surgery).
Improvements in inflammatory markers, depressive symptoms, and physical activity were also evident after surgery.
Cognitive Improvements
Several cognitive domains showed significant improvement at 6 and 24 months after bariatric surgery. Based on the 20% change index, improvements in working memory, episodic memory, and verbal fluency were seen in 11%, 32%, and 24% of participants, respectively.
Forty percent of patients showed improvement in their able to shift their attention, and 43% showed improvements in global cognition after surgery.
Several changes in brain parameters were also noted. Despite lower cerebral blood flow (CBF) in several regions, volumes of hippocampus, nucleus accumbens, frontal cortex, white matter, and white matter hyperintensity remained stable after surgery.
The temporal cortex showed a greater thickness (mean, 2.724 mm vs 2.761 mm; P = .007) and lower spatial coefficient of variation (sCOV; median, 4.41% vs 3.97%; P = .02) after surgery.
Overall, the results suggest that cognitive improvements “begin shortly after bariatric surgery and are long lasting,” the authors wrote.
Various factors may be involved including remission of comorbidities, higher physical activity, lower depressive symptoms, and lower inflammatory factors, they suggest. Stabilization of volume, CBF, and sCOV in brain regions, coupled with gains in cortical thickness and vascular efficiency in the temporal cortex could also play a role.
‘Remarkable’ Results
“Taken together, the research intimates bariatric surgery’s potential protective effects against dementia manifest through both weight-related brain changes and reducing cardiovascular risk factors,” Shaheen Lakhan, MD, a neurologist and researcher based in Miami, who wasn’t involved in the study, told this news organization.
“These remarkable neurological transformations intimate this surgery represents a pivotal opportunity to combat the parallel public health crises of obesity and dementia threatening society,” he said.
“In demonstrating a durable cognitive and brain boost out years beyond surgery, patients now have an emphatic answer — these aren’t short-lived benefits but rather profound improvements propelling them positively for the rest of life,” he added.
This opens up questions on whether the new class of obesity medications targeting glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide pathways, that can achieve weight loss approaching that of bariatric surgery, could have similar benefits.
The use of GLP-1 drugs have also shown neuroprotective effects such as improvement in motor and cognitive deficits, reduction of neuroinflammation, prevention of neuronal loss, and possibly slowing of neurodegeneration across animal models of Parkinson’s disease, Alzheimer’s disease, and stroke, said Dr. Lakhan. However, the exact mechanisms and ability to cross the blood-brain barrier require further confirmation, especially in humans.
Large, long-term, randomized controlled trials looking into potential effects of semaglutide on early Alzheimer›s disease, including the EVOKE Plus trial, are currently underway, he noted.
“These game-changing obesity drugs may hand us medicine’s holy grail — a pill to rival surgery’s brain benefits without the scalpel, allowing patients a more accessible path to protecting their brain,” Dr. Lakhan said.
The study had no funding from industry. Dr. Kiliaan and Dr. Lakhan had no relevant disclosures.
A version of this article first appeared on Medscape.com.
Bariatric surgery is associated with long-term improvements in cognition and brain structure in addition to general health benefits and expected weight loss, a large study found.
Among 133 adults with severe obesity who underwent bariatric surgery, roughly two in five showed > 20% improvement in global cognitive function at 24 months following the surgery.
“Notably, the temporal cortex exhibited not only higher cortical thickness but also higher vascular efficiency after surgery,” reported Amanda Kiliaan, PhD, Radboud University Medical Center, Nijmegen, the Netherlands, and colleagues.
“These results highlight beneficial vascular responses occurring in conjunction with bariatric surgery,” the researchers wrote.
They also suggested that weight-loss surgery may represent a treatment option for patients with obesity and dementia.
The study was published online on February 9, 2024, in JAMA Network Open.
Obesity is associated with an increased risk of developing dementia. Bariatric surgery-induced weight loss has been associated with improvements in brain function and structure in some small cohort studies with short follow-up periods. However, long-term neurological outcomes associated with bariatric surgery are unclear.
To investigate, Dr. Kiliaan and colleagues studied 133 adults with severe obesity (mean age, 46 years; 84% women) who underwent Roux-en-Y gastric bypass. The researchers collected relevant data from laboratory tests, cognitive tests, and MRI brain scans before surgery and at 6 and 24 months after surgery.
Overall, mean body weight, body mass index, waist circumference, and blood pressure were significantly lower at 6 and 24 months after surgery. At 24 months, significantly fewer patients were taking antihypertensive medication (17% vs 36% before surgery).
Improvements in inflammatory markers, depressive symptoms, and physical activity were also evident after surgery.
Cognitive Improvements
Several cognitive domains showed significant improvement at 6 and 24 months after bariatric surgery. Based on the 20% change index, improvements in working memory, episodic memory, and verbal fluency were seen in 11%, 32%, and 24% of participants, respectively.
Forty percent of patients showed improvement in their able to shift their attention, and 43% showed improvements in global cognition after surgery.
Several changes in brain parameters were also noted. Despite lower cerebral blood flow (CBF) in several regions, volumes of hippocampus, nucleus accumbens, frontal cortex, white matter, and white matter hyperintensity remained stable after surgery.
The temporal cortex showed a greater thickness (mean, 2.724 mm vs 2.761 mm; P = .007) and lower spatial coefficient of variation (sCOV; median, 4.41% vs 3.97%; P = .02) after surgery.
Overall, the results suggest that cognitive improvements “begin shortly after bariatric surgery and are long lasting,” the authors wrote.
Various factors may be involved including remission of comorbidities, higher physical activity, lower depressive symptoms, and lower inflammatory factors, they suggest. Stabilization of volume, CBF, and sCOV in brain regions, coupled with gains in cortical thickness and vascular efficiency in the temporal cortex could also play a role.
‘Remarkable’ Results
“Taken together, the research intimates bariatric surgery’s potential protective effects against dementia manifest through both weight-related brain changes and reducing cardiovascular risk factors,” Shaheen Lakhan, MD, a neurologist and researcher based in Miami, who wasn’t involved in the study, told this news organization.
“These remarkable neurological transformations intimate this surgery represents a pivotal opportunity to combat the parallel public health crises of obesity and dementia threatening society,” he said.
“In demonstrating a durable cognitive and brain boost out years beyond surgery, patients now have an emphatic answer — these aren’t short-lived benefits but rather profound improvements propelling them positively for the rest of life,” he added.
This opens up questions on whether the new class of obesity medications targeting glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide pathways, that can achieve weight loss approaching that of bariatric surgery, could have similar benefits.
The use of GLP-1 drugs have also shown neuroprotective effects such as improvement in motor and cognitive deficits, reduction of neuroinflammation, prevention of neuronal loss, and possibly slowing of neurodegeneration across animal models of Parkinson’s disease, Alzheimer’s disease, and stroke, said Dr. Lakhan. However, the exact mechanisms and ability to cross the blood-brain barrier require further confirmation, especially in humans.
Large, long-term, randomized controlled trials looking into potential effects of semaglutide on early Alzheimer›s disease, including the EVOKE Plus trial, are currently underway, he noted.
“These game-changing obesity drugs may hand us medicine’s holy grail — a pill to rival surgery’s brain benefits without the scalpel, allowing patients a more accessible path to protecting their brain,” Dr. Lakhan said.
The study had no funding from industry. Dr. Kiliaan and Dr. Lakhan had no relevant disclosures.
A version of this article first appeared on Medscape.com.
Weight Management Therapies Work, But Utilization Low
TOPLINE:
A cohort study of primary care patients with obesity found significant associations between weight management treatments (WMTs) and ≥ 5% weight loss for individuals.
Yet, low WMT utilization hindered population-level benefit.
METHODOLOGY:
This retrospective, population-based cross-sectional cohort study included 149,959 primary care patients from a Michigan academic health system between October 2015 and March 2020.
TAKEAWAY:
- From 2017 to 2019, the average unadjusted body mass index (BMI) increased from 29.34 kg/m2 to 29.61 kg/m2 and the prevalence of obesity from 39.2% to 40.7%.
- Among 31,284 patients with obesity in 2017, 25.9% (6665) achieved ≥ 5% weight loss at 2 years.
- Among 37,245 with obesity in either 2017 or 2019 and sufficient follow-up, 1-year WMT utilization increased from 5.3% in 2017 to 7.1% in 2019 (difference, 1.7%; 95% CI, 1.3%-2.2%), including nutritional counseling (6.3%), weight loss medication prescriptions (2.6%), and bariatric surgery (1.0%).
- In two groups of n = 5090 with and without WMT exposure who were propensity score–matched on covariates including BMI, sex, and age, the probabilities of ≥ 5% weight loss at 1 year were 15.6% without WMTs, 23.1% for nutrition counseling, 54.6% for meal replacement, 27.8% for weight loss medication, and 93% for bariatric surgery, with all approaches significant compared to no WMTs.
IN PRACTICE:
“Health systems and insurers should consider novel strategies to enhance preference-sensitive use of WMT to optimize achievement of 5% or greater weight loss among individuals and populations with obesity.”
“While we included glucagon-like peptide 1 receptor agonists for type 2 diabetes, including semaglutide 1.0 mg, in our analyses, the study period predated the [US Food and Drug Administration]-approval of semaglutide 2.4 mg for weight management. Future work should explore the potential for semaglutide 2.4 mg and other medications with substantial weight loss effectiveness to reduce weight at the population level.”
SOURCE:
This study was conducted by James Henderson, PhD, of the Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, and colleagues and was published online in JAMA Network Open .
LIMITATIONS:
Single health system. Electronic health record data may be subject to weight and WMT measurement error, lack of adherence data, and any information about outside WMT access. Retrospective, observational study, subject to bias. Study period occurred before FDA approval of semaglutide for weight management, and thus, the findings may understate current use and effectiveness of weight loss medications.
DISCLOSURES:
The study was supported by grants from the National Institutes of Health and National Institute of Diabetes and Digestive and Kidney Diseases, Michigan Center for Diabetes Translational Research, Michigan Nutrition Obesity Research Center, and the Elizabeth Weiser Caswell Diabetes Institute at the University of Michigan. Dr. Henderson had no further disclosures, but some of the coauthors had industry ties.
A version of this article appeared on Medscape.com.
TOPLINE:
A cohort study of primary care patients with obesity found significant associations between weight management treatments (WMTs) and ≥ 5% weight loss for individuals.
Yet, low WMT utilization hindered population-level benefit.
METHODOLOGY:
This retrospective, population-based cross-sectional cohort study included 149,959 primary care patients from a Michigan academic health system between October 2015 and March 2020.
TAKEAWAY:
- From 2017 to 2019, the average unadjusted body mass index (BMI) increased from 29.34 kg/m2 to 29.61 kg/m2 and the prevalence of obesity from 39.2% to 40.7%.
- Among 31,284 patients with obesity in 2017, 25.9% (6665) achieved ≥ 5% weight loss at 2 years.
- Among 37,245 with obesity in either 2017 or 2019 and sufficient follow-up, 1-year WMT utilization increased from 5.3% in 2017 to 7.1% in 2019 (difference, 1.7%; 95% CI, 1.3%-2.2%), including nutritional counseling (6.3%), weight loss medication prescriptions (2.6%), and bariatric surgery (1.0%).
- In two groups of n = 5090 with and without WMT exposure who were propensity score–matched on covariates including BMI, sex, and age, the probabilities of ≥ 5% weight loss at 1 year were 15.6% without WMTs, 23.1% for nutrition counseling, 54.6% for meal replacement, 27.8% for weight loss medication, and 93% for bariatric surgery, with all approaches significant compared to no WMTs.
IN PRACTICE:
“Health systems and insurers should consider novel strategies to enhance preference-sensitive use of WMT to optimize achievement of 5% or greater weight loss among individuals and populations with obesity.”
“While we included glucagon-like peptide 1 receptor agonists for type 2 diabetes, including semaglutide 1.0 mg, in our analyses, the study period predated the [US Food and Drug Administration]-approval of semaglutide 2.4 mg for weight management. Future work should explore the potential for semaglutide 2.4 mg and other medications with substantial weight loss effectiveness to reduce weight at the population level.”
SOURCE:
This study was conducted by James Henderson, PhD, of the Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, and colleagues and was published online in JAMA Network Open .
LIMITATIONS:
Single health system. Electronic health record data may be subject to weight and WMT measurement error, lack of adherence data, and any information about outside WMT access. Retrospective, observational study, subject to bias. Study period occurred before FDA approval of semaglutide for weight management, and thus, the findings may understate current use and effectiveness of weight loss medications.
DISCLOSURES:
The study was supported by grants from the National Institutes of Health and National Institute of Diabetes and Digestive and Kidney Diseases, Michigan Center for Diabetes Translational Research, Michigan Nutrition Obesity Research Center, and the Elizabeth Weiser Caswell Diabetes Institute at the University of Michigan. Dr. Henderson had no further disclosures, but some of the coauthors had industry ties.
A version of this article appeared on Medscape.com.
TOPLINE:
A cohort study of primary care patients with obesity found significant associations between weight management treatments (WMTs) and ≥ 5% weight loss for individuals.
Yet, low WMT utilization hindered population-level benefit.
METHODOLOGY:
This retrospective, population-based cross-sectional cohort study included 149,959 primary care patients from a Michigan academic health system between October 2015 and March 2020.
TAKEAWAY:
- From 2017 to 2019, the average unadjusted body mass index (BMI) increased from 29.34 kg/m2 to 29.61 kg/m2 and the prevalence of obesity from 39.2% to 40.7%.
- Among 31,284 patients with obesity in 2017, 25.9% (6665) achieved ≥ 5% weight loss at 2 years.
- Among 37,245 with obesity in either 2017 or 2019 and sufficient follow-up, 1-year WMT utilization increased from 5.3% in 2017 to 7.1% in 2019 (difference, 1.7%; 95% CI, 1.3%-2.2%), including nutritional counseling (6.3%), weight loss medication prescriptions (2.6%), and bariatric surgery (1.0%).
- In two groups of n = 5090 with and without WMT exposure who were propensity score–matched on covariates including BMI, sex, and age, the probabilities of ≥ 5% weight loss at 1 year were 15.6% without WMTs, 23.1% for nutrition counseling, 54.6% for meal replacement, 27.8% for weight loss medication, and 93% for bariatric surgery, with all approaches significant compared to no WMTs.
IN PRACTICE:
“Health systems and insurers should consider novel strategies to enhance preference-sensitive use of WMT to optimize achievement of 5% or greater weight loss among individuals and populations with obesity.”
“While we included glucagon-like peptide 1 receptor agonists for type 2 diabetes, including semaglutide 1.0 mg, in our analyses, the study period predated the [US Food and Drug Administration]-approval of semaglutide 2.4 mg for weight management. Future work should explore the potential for semaglutide 2.4 mg and other medications with substantial weight loss effectiveness to reduce weight at the population level.”
SOURCE:
This study was conducted by James Henderson, PhD, of the Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, and colleagues and was published online in JAMA Network Open .
LIMITATIONS:
Single health system. Electronic health record data may be subject to weight and WMT measurement error, lack of adherence data, and any information about outside WMT access. Retrospective, observational study, subject to bias. Study period occurred before FDA approval of semaglutide for weight management, and thus, the findings may understate current use and effectiveness of weight loss medications.
DISCLOSURES:
The study was supported by grants from the National Institutes of Health and National Institute of Diabetes and Digestive and Kidney Diseases, Michigan Center for Diabetes Translational Research, Michigan Nutrition Obesity Research Center, and the Elizabeth Weiser Caswell Diabetes Institute at the University of Michigan. Dr. Henderson had no further disclosures, but some of the coauthors had industry ties.
A version of this article appeared on Medscape.com.
Obesity’s Effect on Neonatal Outcomes Is Dose Dependent
TOPLINE:
Higher body mass index (BMI) at the start of pregnancy is associated with increased risk for adverse maternal outcomes, including preeclampsia, and neonatal complications, such as respiratory distress syndrome (RDS), in a dose-dependent manner, new research shows.
METHODOLOGY:
- Researchers conducted a retrospective study of 58,497 singleton pregnancies delivered at an urban hospital between 2013 and 2021.
- They focused on pregnancies delivered between 24 and 42 weeks of gestation, for which information about BMI at the first prenatal visit was available.
- 21.1% of mothers had class I , 9.3% had class II obesity, and 6% had class III obesity.
TAKEAWAY:
- Obesity was associated with a dose-dependent increase in cesarean deliveries (27% of deliveries without obesity vs 46% of deliveries with class III obesity).
- Severe preeclampsia occurred in 8% of mothers without obesity and in 19% of mothers with class III obesity.
- Infants born to mothers with class III obesity were more likely than were infants born to mothers without obesity to have RDS, with a relative risk (RR) of 2.66.
- With class II obesity, the RR was 1.77. With class I obesity, the RR was 1.3.
- Obesity also was associated with increased risk for grade III-IV (RR), 4.58 for class III obesity) and (RR, 3.76).
IN PRACTICE:
“Infants born to patients with higher classes of obesity have significant associated morbidity including a 2 to 4 times increased risk of neonatal acidosis, grades III-IV intraventricular hemorrhage, sepsis, and RDS,” the researchers reported.
SOURCE:
Sara I. Jones, MD, with University of Texas Southwestern Medical Center in Dallas, presented the study on February 14 at the 2024 Pregnancy Meeting of the Society for Maternal-Fetal Medicine, in National Harbor, Maryland.
DISCLOSURES:
The researchers had no conflicts of interest to disclose.
A version of this article appeared on Medscape.com.
TOPLINE:
Higher body mass index (BMI) at the start of pregnancy is associated with increased risk for adverse maternal outcomes, including preeclampsia, and neonatal complications, such as respiratory distress syndrome (RDS), in a dose-dependent manner, new research shows.
METHODOLOGY:
- Researchers conducted a retrospective study of 58,497 singleton pregnancies delivered at an urban hospital between 2013 and 2021.
- They focused on pregnancies delivered between 24 and 42 weeks of gestation, for which information about BMI at the first prenatal visit was available.
- 21.1% of mothers had class I , 9.3% had class II obesity, and 6% had class III obesity.
TAKEAWAY:
- Obesity was associated with a dose-dependent increase in cesarean deliveries (27% of deliveries without obesity vs 46% of deliveries with class III obesity).
- Severe preeclampsia occurred in 8% of mothers without obesity and in 19% of mothers with class III obesity.
- Infants born to mothers with class III obesity were more likely than were infants born to mothers without obesity to have RDS, with a relative risk (RR) of 2.66.
- With class II obesity, the RR was 1.77. With class I obesity, the RR was 1.3.
- Obesity also was associated with increased risk for grade III-IV (RR), 4.58 for class III obesity) and (RR, 3.76).
IN PRACTICE:
“Infants born to patients with higher classes of obesity have significant associated morbidity including a 2 to 4 times increased risk of neonatal acidosis, grades III-IV intraventricular hemorrhage, sepsis, and RDS,” the researchers reported.
SOURCE:
Sara I. Jones, MD, with University of Texas Southwestern Medical Center in Dallas, presented the study on February 14 at the 2024 Pregnancy Meeting of the Society for Maternal-Fetal Medicine, in National Harbor, Maryland.
DISCLOSURES:
The researchers had no conflicts of interest to disclose.
A version of this article appeared on Medscape.com.
TOPLINE:
Higher body mass index (BMI) at the start of pregnancy is associated with increased risk for adverse maternal outcomes, including preeclampsia, and neonatal complications, such as respiratory distress syndrome (RDS), in a dose-dependent manner, new research shows.
METHODOLOGY:
- Researchers conducted a retrospective study of 58,497 singleton pregnancies delivered at an urban hospital between 2013 and 2021.
- They focused on pregnancies delivered between 24 and 42 weeks of gestation, for which information about BMI at the first prenatal visit was available.
- 21.1% of mothers had class I , 9.3% had class II obesity, and 6% had class III obesity.
TAKEAWAY:
- Obesity was associated with a dose-dependent increase in cesarean deliveries (27% of deliveries without obesity vs 46% of deliveries with class III obesity).
- Severe preeclampsia occurred in 8% of mothers without obesity and in 19% of mothers with class III obesity.
- Infants born to mothers with class III obesity were more likely than were infants born to mothers without obesity to have RDS, with a relative risk (RR) of 2.66.
- With class II obesity, the RR was 1.77. With class I obesity, the RR was 1.3.
- Obesity also was associated with increased risk for grade III-IV (RR), 4.58 for class III obesity) and (RR, 3.76).
IN PRACTICE:
“Infants born to patients with higher classes of obesity have significant associated morbidity including a 2 to 4 times increased risk of neonatal acidosis, grades III-IV intraventricular hemorrhage, sepsis, and RDS,” the researchers reported.
SOURCE:
Sara I. Jones, MD, with University of Texas Southwestern Medical Center in Dallas, presented the study on February 14 at the 2024 Pregnancy Meeting of the Society for Maternal-Fetal Medicine, in National Harbor, Maryland.
DISCLOSURES:
The researchers had no conflicts of interest to disclose.
A version of this article appeared on Medscape.com.
Kimchi: Not Magically Protective Against Weight Gain
How much of societal diet-related scientific illiteracy can be blamed on the publication decisions of medical journals around food studies?
That was the question I pondered when reading “Association between kimchi consumption and obesity based on BMI and abdominal obesity in Korean adults: a cross-sectional analysis of the Health Examinees study,” recently published in BMJ Open. Although I will get to the study particulars momentarily, that it’s 2024 and journals are still publishing cross-sectional studies of the impact of a single food’s subjectively reported consumption on health outcomes is mind boggling.
You might wonder why I wasn’t mind boggled by the authors rather than the journal — but the authors’ interest in publishing a study on kimchi’s supposed impact on obesity is an easy thing to explain, in that the study was funded by the World Institute of Kimchi, where two of its four authors are employed.
You might also wonder why I wasn’t mind boggled by media running with this story — but the media’s job is to capture eyeballs, and who doesn’t love a good magic food story, doubly so for one involving obesity and one with a study backing it up?
Back to this World Institute of Kimchi project looking at kimchi intake on obesity rates. No doubt if I worked for the World Institute of Kimchi, I would want kimchi to be shown to be somehow magically protective against weight gain. So how might I go about exploring that?
Well, I could look to the data from the Health Examinees (HEXA) Study. The HEXA study was a cross-sectional look at South Koreans; included in their data collection was a 106-item food frequency questionnaire (FFQ).
That questionnaire looked at 106 food items — yep, you guessed it, explicitly including kimchi. Not included in this FFQ, though, were prepared foods, meaning that it was unable to measure seasonings, spices, or cooking oils. Also perhaps problematic is that no doubt most of us consume more than 106 total food items in our diets. Perhaps this is why the validation study of HEXA’s food item–based FFQ found that it had “relatively low validity” when compared against 12-day food diaries and why its creators themselves report it to be in their study’s conclusion only “reasonably acceptable” to apply to a population. But yes, kimchi!
So for the sake of this exercise, though, let’s assume that instead of only a reasonably acceptable FFQ with low validity, the FFQ was fantastic and its data robust. How great then is kimchi at preventing obesity? Certainly, the media report it’s pretty darn good. Here’s a smattering from the literal dozens of headlines of stories covering this paper:
Eating kimchi every day could help stave off weight gain, new study says — NBC News
Eating kimchi every day may prevent weight gain, research suggests — Sky News
Want to avoid piling on the pounds? Try kimchi for breakfast — The Telegraph
But when we turn to the paper itself, suddenly things aren’t so clear.
According to the paper, men who reported eating two to three servings of kimchi per day were found to have lower rates of obesity, whereas men who reported eating three to five servings of kimchi per day were not. But these are overlapping groups! Also found was that men consuming more than five servings of kimchi per day have higher rates of obesity. When taken together, these findings do not demonstrate a statistically significant trend of kimchi intake on obesity in men. Whereas in women, things are worse in that the more kimchi reportedly consumed, the more obesity, in a trend that did (just) reach statistical significance.
So even if we pretend the FFQs were robust enough to make conclusions about a single food’s impact on obesity, and we pretend there was a well-described, plausible mechanistic reason to believe same (there isn’t), and we pretend that this particular FFQ had better than “relatively low validity,” there is no conclusion here to be drawn about kimchi’s impact on obesity.
What we can conclude is that when it comes to publishing papers purporting to find the impact of single foods on obesity, journals will still happily publish them and their publication will lead to hyperbolic headlines and stories, which in turn reinforce the scientifically illiterate notion that the highly complex multifactorial problem of obesity boils down to simple food choices, which in turn keeps weight loss grifters everywhere in business while fueling societal weight bias.
Dr. Freedhoff is Associate Professor, Department of Family Medicine, University of Ottawa; Medical Director, Bariatric Medical Institute, Ottawa, Ontario, Canada. He disclosed ties with Bariatric Medical Institute, Constant Health, and Novo Nordisk.
A version of this article appeared on Medscape.com.
How much of societal diet-related scientific illiteracy can be blamed on the publication decisions of medical journals around food studies?
That was the question I pondered when reading “Association between kimchi consumption and obesity based on BMI and abdominal obesity in Korean adults: a cross-sectional analysis of the Health Examinees study,” recently published in BMJ Open. Although I will get to the study particulars momentarily, that it’s 2024 and journals are still publishing cross-sectional studies of the impact of a single food’s subjectively reported consumption on health outcomes is mind boggling.
You might wonder why I wasn’t mind boggled by the authors rather than the journal — but the authors’ interest in publishing a study on kimchi’s supposed impact on obesity is an easy thing to explain, in that the study was funded by the World Institute of Kimchi, where two of its four authors are employed.
You might also wonder why I wasn’t mind boggled by media running with this story — but the media’s job is to capture eyeballs, and who doesn’t love a good magic food story, doubly so for one involving obesity and one with a study backing it up?
Back to this World Institute of Kimchi project looking at kimchi intake on obesity rates. No doubt if I worked for the World Institute of Kimchi, I would want kimchi to be shown to be somehow magically protective against weight gain. So how might I go about exploring that?
Well, I could look to the data from the Health Examinees (HEXA) Study. The HEXA study was a cross-sectional look at South Koreans; included in their data collection was a 106-item food frequency questionnaire (FFQ).
That questionnaire looked at 106 food items — yep, you guessed it, explicitly including kimchi. Not included in this FFQ, though, were prepared foods, meaning that it was unable to measure seasonings, spices, or cooking oils. Also perhaps problematic is that no doubt most of us consume more than 106 total food items in our diets. Perhaps this is why the validation study of HEXA’s food item–based FFQ found that it had “relatively low validity” when compared against 12-day food diaries and why its creators themselves report it to be in their study’s conclusion only “reasonably acceptable” to apply to a population. But yes, kimchi!
So for the sake of this exercise, though, let’s assume that instead of only a reasonably acceptable FFQ with low validity, the FFQ was fantastic and its data robust. How great then is kimchi at preventing obesity? Certainly, the media report it’s pretty darn good. Here’s a smattering from the literal dozens of headlines of stories covering this paper:
Eating kimchi every day could help stave off weight gain, new study says — NBC News
Eating kimchi every day may prevent weight gain, research suggests — Sky News
Want to avoid piling on the pounds? Try kimchi for breakfast — The Telegraph
But when we turn to the paper itself, suddenly things aren’t so clear.
According to the paper, men who reported eating two to three servings of kimchi per day were found to have lower rates of obesity, whereas men who reported eating three to five servings of kimchi per day were not. But these are overlapping groups! Also found was that men consuming more than five servings of kimchi per day have higher rates of obesity. When taken together, these findings do not demonstrate a statistically significant trend of kimchi intake on obesity in men. Whereas in women, things are worse in that the more kimchi reportedly consumed, the more obesity, in a trend that did (just) reach statistical significance.
So even if we pretend the FFQs were robust enough to make conclusions about a single food’s impact on obesity, and we pretend there was a well-described, plausible mechanistic reason to believe same (there isn’t), and we pretend that this particular FFQ had better than “relatively low validity,” there is no conclusion here to be drawn about kimchi’s impact on obesity.
What we can conclude is that when it comes to publishing papers purporting to find the impact of single foods on obesity, journals will still happily publish them and their publication will lead to hyperbolic headlines and stories, which in turn reinforce the scientifically illiterate notion that the highly complex multifactorial problem of obesity boils down to simple food choices, which in turn keeps weight loss grifters everywhere in business while fueling societal weight bias.
Dr. Freedhoff is Associate Professor, Department of Family Medicine, University of Ottawa; Medical Director, Bariatric Medical Institute, Ottawa, Ontario, Canada. He disclosed ties with Bariatric Medical Institute, Constant Health, and Novo Nordisk.
A version of this article appeared on Medscape.com.
How much of societal diet-related scientific illiteracy can be blamed on the publication decisions of medical journals around food studies?
That was the question I pondered when reading “Association between kimchi consumption and obesity based on BMI and abdominal obesity in Korean adults: a cross-sectional analysis of the Health Examinees study,” recently published in BMJ Open. Although I will get to the study particulars momentarily, that it’s 2024 and journals are still publishing cross-sectional studies of the impact of a single food’s subjectively reported consumption on health outcomes is mind boggling.
You might wonder why I wasn’t mind boggled by the authors rather than the journal — but the authors’ interest in publishing a study on kimchi’s supposed impact on obesity is an easy thing to explain, in that the study was funded by the World Institute of Kimchi, where two of its four authors are employed.
You might also wonder why I wasn’t mind boggled by media running with this story — but the media’s job is to capture eyeballs, and who doesn’t love a good magic food story, doubly so for one involving obesity and one with a study backing it up?
Back to this World Institute of Kimchi project looking at kimchi intake on obesity rates. No doubt if I worked for the World Institute of Kimchi, I would want kimchi to be shown to be somehow magically protective against weight gain. So how might I go about exploring that?
Well, I could look to the data from the Health Examinees (HEXA) Study. The HEXA study was a cross-sectional look at South Koreans; included in their data collection was a 106-item food frequency questionnaire (FFQ).
That questionnaire looked at 106 food items — yep, you guessed it, explicitly including kimchi. Not included in this FFQ, though, were prepared foods, meaning that it was unable to measure seasonings, spices, or cooking oils. Also perhaps problematic is that no doubt most of us consume more than 106 total food items in our diets. Perhaps this is why the validation study of HEXA’s food item–based FFQ found that it had “relatively low validity” when compared against 12-day food diaries and why its creators themselves report it to be in their study’s conclusion only “reasonably acceptable” to apply to a population. But yes, kimchi!
So for the sake of this exercise, though, let’s assume that instead of only a reasonably acceptable FFQ with low validity, the FFQ was fantastic and its data robust. How great then is kimchi at preventing obesity? Certainly, the media report it’s pretty darn good. Here’s a smattering from the literal dozens of headlines of stories covering this paper:
Eating kimchi every day could help stave off weight gain, new study says — NBC News
Eating kimchi every day may prevent weight gain, research suggests — Sky News
Want to avoid piling on the pounds? Try kimchi for breakfast — The Telegraph
But when we turn to the paper itself, suddenly things aren’t so clear.
According to the paper, men who reported eating two to three servings of kimchi per day were found to have lower rates of obesity, whereas men who reported eating three to five servings of kimchi per day were not. But these are overlapping groups! Also found was that men consuming more than five servings of kimchi per day have higher rates of obesity. When taken together, these findings do not demonstrate a statistically significant trend of kimchi intake on obesity in men. Whereas in women, things are worse in that the more kimchi reportedly consumed, the more obesity, in a trend that did (just) reach statistical significance.
So even if we pretend the FFQs were robust enough to make conclusions about a single food’s impact on obesity, and we pretend there was a well-described, plausible mechanistic reason to believe same (there isn’t), and we pretend that this particular FFQ had better than “relatively low validity,” there is no conclusion here to be drawn about kimchi’s impact on obesity.
What we can conclude is that when it comes to publishing papers purporting to find the impact of single foods on obesity, journals will still happily publish them and their publication will lead to hyperbolic headlines and stories, which in turn reinforce the scientifically illiterate notion that the highly complex multifactorial problem of obesity boils down to simple food choices, which in turn keeps weight loss grifters everywhere in business while fueling societal weight bias.
Dr. Freedhoff is Associate Professor, Department of Family Medicine, University of Ottawa; Medical Director, Bariatric Medical Institute, Ottawa, Ontario, Canada. He disclosed ties with Bariatric Medical Institute, Constant Health, and Novo Nordisk.
A version of this article appeared on Medscape.com.