Latest news with #obesity
Health Line
a day ago
- Health
- Health Line
Is It Safe to Take a GLP-1 Medication with Digestive Health Conditions?
Consider safety when combining GLP-1 medications with preexisting digestive health conditions. GLP-1 medications are prescribed to lower blood sugar levels in people with type 2 diabetes. They're also prescribed for weight loss in people with obesity. GLP-1 medications belong to a class of drugs that include semaglutide, liraglutide, dulaglutide, and several others. Semaglutide is the active ingredient in Wegovy and Ozempic, two popular GLP-1 drugs. Liraglutide is the active ingredient in Saxenda, and dulaglutide is the active ingredient in Trulicity. GLP-1 medications may cause uncomfortable side effects and increase the risk of gastrointestinal conditions. Digestive health and GLP-1 medications GLP-1 medications work by mimicking the effects of the GLP-1 hormone, which is produced within the small intestine. Like the naturally occurring hormone your body makes, GLP-1 medications slow digestion (stomach emptying) and signal your brain that you feel full and can stop eating. They also trigger the release of insulin from the pancreas and inhibit the secretion of glucagon, a hormone that raises blood sugar levels. Several GLP-1 medications, including Wegovy, list many side effects, including gastrointestinal side effects, directly on their labels. These side effects may include: vomiting nausea diarrhea constipation bloating gas and belching heartburn stomach flu dehydration, especially in people with kidney failure More serious side effects may include: What the research says GLP-1 agonists are approved for people with type 2 diabetes to manage their blood sugar levels, and some are approved for weight loss. Let's take a look at the research and implications of people who have taken GLP-1 agonists along with various gastrointestinal conditions. A large 2023 study including people without diabetes who were using GLP-1 agonists for weight loss found that this class of medications may increase the risk of gastrointestinal conditions, such as gastroparesis. Researchers found the drugs did not increase the risk of biliary disease (conditions of the gallbladder or bile ducts) in participants. These adverse effects are thought to be rare but should be considered by people who wish to use GLP-1 medications for weight loss. A 2022 study involving people with Irritable Bowel Syndrome (IBS) found that ROSE 010, a GLP-1 receptor agonist, reduced IBS pain during flare-ups, primarily in female participants. When given in higher doses, however, nausea became more pronounced. A large 2024 study found that adults treated with semaglutide for diabetes mellitus are not at higher risk of diverticulitis and seem to have a lower risk of diverticulosis. Much more research is needed to uncover the potential benefits, as well as risks, of these medications. Tips for managing GLP-1 use with digestive conditions Talk with your healthcare professional about the benefits of GLP-1 medications versus their risks. Your age, underlying health conditions, and other factors, such as needle phobia, should be taken into account. In many instances, you and a healthcare professional may determine that the benefits outweigh the risks. Or, you may decide that the side effects are not worth the benefits, or that they make you too uncomfortable to continue taking these drugs. To manage digestive conditions and side effects while taking a GLP-1 agonist, follow these tips: follow the dosage instructions exactly as prescribed slowly increase your fiber intake, as recommended by your healthcare professional consider taking fiber supplements if constipation occurs drink plenty of water to remain hydrated eat small, frequent meals rather than large meals avoid eating too close to bedtime avoid spicy or fatty foods exercise regularly to aid with digestion
Medscape
a day ago
- Business
- Medscape
No, KETO-CTA Study Did Not Upend Causal Evidence on ASCVD
Few argue that eating too many carbohydrates is a key cause of the obesity crisis. The ideal solution would be to moderate carbohydrate intake to the amounts consumed by Sicilians. But some people have gone to the extreme of eliminating nearly all carbs. One result of eating only fat and protein is ketosis. Another may be a rise in atherogenic lipid particles, such as low-density lipoprotein cholesterol (LDL-C). Lean-Mass Hyperresponders Authors of the observational KETO-CTA study purport to show that a subgroup of people on keto diets who sustain serious increases in lipids may be protected from progression of atherosclerosis. This, despite nearly a half-century of evidence that higher LDL-C levels lead to coronary artery disease. They deemed this subgroup lean-mass hyperresponders(LMHRs). The idea stems from the observation that there may be heterogeneity in the LDL-C response to a keto diet. A meta-analysis (by some of the KETO-CTA authors) included 41 trials involving low-carbohydrate diets and found that rises in LDL-C turned largely on baseline BMI. Specifically, for trials including patients with a mean baseline BMI < 25, LDL-C increased by 41 mg/dL; for trials with a mean BMI of 25-35, LDL-C did not change; and for trials with a mean BMI ≥ 35, LDL-C decreased by 7 mg/dL. The association of baseline BMI with LDL-C was much stronger than the effect of dietary saturated fat. In the LMHR group, the rise in LDL-C can be striking, sometimes well north of 300 mg/dL. The obvious question is whether (or how much) this raises atherosclerotic risk. The best way to study this question would be long-term trials where people are randomly assigned and are adherent to specific diets. It would take years to sort out the effects because atherosclerosis is slowly progressive. Another way, perhaps the only realistic way, is to use surrogate markers of atherosclerosis, which now include imaging of the vessel itself. The KETO-CTA Study The KETO-CTA study, published in JACC: Advances , garnered lots of attention on social media. First, I will tell you the topline findings and then the critical appraisal. The authors aimed to study the association between plaque progression and its predicting factors in participants with an LMHR pattern. Plaque progression was measured on coronary CT imaging performed at baseline and repeated at 1 year. Images were blindly read, and software was required to quantify plaque characteristics. The authors recruited 100 individuals with the LMHR phenotype who had been on a ketogenic diet for at least 2 years to participate in the single-arm observational study. To qualify, they had to have a low BMI and a keto-induced LDL-C ≥ 190 mg/dL, HDL-C ≥ 60 mg/dL, triglycerides ≤ 80 mg/dL, and evidence of being metabolically healthy (normal CRP and A1c). The keto-induced criteria required that individuals had an LDL-C < 160 mg/dL before adopting the diet. They don't say how many individuals they screened to find these participants. Those included in the study had striking numbers. Despite an average BMI of 22, they had mean LDL-C levels of 254 mg/dL, HDL-C of 89 mg/dL, and triglycerides of 67 mg/dL. The average age was 55 years and most were men. They could not be on lipid-lowering therapy, which is remarkable for patients with very high LDL-C. Adherence to the keto diet was high and confirmed by beta-hydroxy-butyrate levels. Results Over the year, there were no substantial changes in ApoB or BMI, which you would expect because participants were on a stable keto diet. The presentation of the results was peculiar. The authors preregistered the study and declared the primary endpoint as the change in noncalcified plaque volume. But they did not formally present this endpoint. Instead, they gave the median change in percent atheroma volume, which was 0.8%. The primary endpoint was presented in a figure in which a horizontal line represented each individual. No quantification was given, but visual inspection of the graph revealed that most individuals sustained an increase in noncalcified plaque volume. The lack of clear presentation of the primary endpoint caused a stir online. This led the first author to present it in on X. The numerical pooled change in noncalcified plaque burden was an increase of 18.8 mm3. In the manuscript, they emphasized the correlations and lack of correlations. Neither the change in ApoB throughout the study nor the ApoB at the beginning of the study was associated with the change in noncalcified plaque volume. There was also no correlation between LDL-C and change in noncalcified plaque volume. The main finding was that the baseline coronary artery calcium score was positively associated with change in noncalcified plaque volume as was baseline plaque. They list four differences between the LMHR subgroup and people with elevated lipids from other metabolic risk factors: Difference 1: Their LDL-C and ApoB elevations are dynamic and result only from the metabolic response to carb restriction. Their LDL-C and ApoB elevations are dynamic and result only from the metabolic response to carb restriction. Difference 2: They are normal weight and metabolically healthy (ie, they don't have obesity, diabetes or insulin resistance). They are normal weight and metabolically healthy (ie, they don't have obesity, diabetes or insulin resistance). Difference 3: Their high LDL-C and ApoB are part of a lipid triad that includes high HDL-C and low triglycerides, representing a metabolic signature of a distinct physiologic state. Their high LDL-C and ApoB are part of a lipid triad that includes high HDL-C and low triglycerides, representing a metabolic signature of a distinct physiologic state. Difference 4: The degree of this phenotype appears inversely related to BMI ('leanness'), consistent with the idea that it is a metabolic response to carbohydrate restriction that is accentuated in leaner, more metabolically healthy persons. The authors go on to make highly provocative conclusions, such as: Conclusion 1: The LMHR population constitutes a unique and important natural experiment evaluating the lipid heart hypothesis in an unprecedented manner. The LMHR population constitutes a unique and important natural experiment evaluating the lipid heart hypothesis in an unprecedented manner. Conclusion 2: The data are consistent with the notion that elevated ApoB, even at extreme levels, does not drive atherosclerosis in a dose-dependent manner in this population of metabolically healthy individuals. The data are consistent with the notion that elevated ApoB, even at extreme levels, does not drive atherosclerosis in a dose-dependent manner in this population of metabolically healthy individuals. Conclusion 3: These insights can facilitate personalized treatment and risk-mitigation strategies based on modern, cost-effective cardiac imaging. For instance, LMHRs with CAC = 0 at baseline (n = 57) constitute a low-risk group for plaque progression, despite high LDL-C. These insights can facilitate personalized treatment and risk-mitigation strategies based on modern, cost-effective cardiac imaging. For instance, LMHRs with CAC = 0 at baseline (n = 57) constitute a low-risk group for plaque progression, despite high LDL-C. Conclusion 4: Because of the strong correlation of baseline coronary calcium with progression of noncalcified plaque, they coin the phrase plaque begets plaque. 6 Reasons the Keto-CTA Conclusions Are Problematic You don't have to be an expert in lipids, atherosclerosis, or imaging to oppose these conclusions. The study has limitations, but the main problem is the authors' outsized claims. I will outline six reasons why their conclusions are problematic: First, the primary endpoint of change in noncalcified plaque volume went up. The increase of 18.8 mm3 was 2.5 times higher than they predicted in their study protocol. If you believe that this endpoint is a great surrogate, the results are ominous. Second, imaging tests are almost always terrible surrogates. To assess risk, you need to measure cardiovascular events. Small, uncontrolled studies are fine, but you cannot claim clinical importance just because you weaved a nice story about high LDL-C in LMHRs being different from high LDL-C in other patients. Third, we have about 70 years of data supporting LDL-C being causal for atherosclerosis. Nearly every Bradford Hill criterion for causation is met for LDL-C and atherosclerosis. To claim an exception, you need more rigorous evidence than KETO-CTA. Fourth, assuming you believe the plaque images are precise, reproducible, and clinically relevant, KETO-CTA suffers from a lack of control. All they had to do is recruit a group of people eating another type of diet (eg Mediterranean diet) and make a comparison. Fifth, the authors don't tell us how many people they screened to find these 100 LMHRs. I get the sense they are a highly selected bunch. Sixth, the question of heart health from a specific diet will be difficult to sort out. Nutritional studies always are. A randomized trial in a prison might work, but cardiac event rates in young people, even with keto-induced-high LDL-C, will be infrequent. What's more, the LMHR group surely do other things that affect heart disease, like exercise, not smoking, etc. One final comment on the authors' messaging. It's been egregious and antiscientific. Their rhetoric and spin outdo some of the most hyped late-breaking trials. This was a small, noncontrolled observational study wherein the primary endpoint went the wrong way. It's nowhere near close to upending decades of causal evidence on the role of LDL-C and atherosclerosis. The journal editors and peer reviewers failed to modulate the outsized conclusions. I don't know what the solution is for this type of behavior, but I oppose it in the strongest terms.
The Sun
2 days ago
- Health
- The Sun
Key body measurement linked to 18% greater risk of bowel cancer – are you at risk?
WITH bowel cancer rates rising in younger adults around the world, experts are desperately searching for possible causes. Risk factors like diet, alcohol and smoking could be explanations, say experts. Now, researchers have found being overweight as a child, teenager and young adult is linked to higher risk of bowel cancer in later life. A higher birth weight was also associated with an increased chance of developing the disease, according to the new study. Experts in the Netherlands reviewed 37 studies on body weight in early life and the risk of colorectal cancer - also known as bowel cancer - in adults. Cancer is a complex disease which develops over several decades, so better understanding of its early origins is critical for more effective prevention efforts and understanding the research gaps The research, which is published in the International Journal of Cancer, found an increase in BMI of 5kg/m2 heightened the risk of bowel cancer by 12 per cent in people aged 18 to 25. In youngsters aged 10 to 19, an increased BMI was linked to a 5-18 per cent risk of developing the disease, while in children aged two to nine, BMI was linked to a higher risk of colon cancer. Meanwhile, each 1kg increase in birth weight was linked to a 9 per cent bowel cancer risk, the study found. Dr Dieuwertje Kok, associate professor of nutrition and cancer at Wageningen University & Research, said: "Although the relationship between adult body size and colorectal cancer risk is well-documented, the potential influence of measures of body size during early life is less understood. "The team was excited to review results from 37 publications that explored birth weight, as well as body mass index across different early life stages. "This study bridges the existing knowledge gap and enhances our understanding of how early life factors may affect colorectal cancer risk in adults." Popular drink is 'doubling' risk of bowel cancer in adults who have more than two per day Bowel cancer is the fourth most common cancer in the UK, with almost 44,000 new diagnoses every year. Dr Helen Croker, assistant director of research and policy at the World Cancer Research Fund, added: "Cancer is a complex disease which develops over several decades, so better understanding of its early origins is critical for more effective prevention efforts and understanding the research gaps. "The results of this study show that raised body mass index across childhood through young adulthood is an important risk factor for colorectal cancer." To help keep your child's BMI in check, focus on promoting a healthy, balanced lifestyle that includes a nutritious diet and regular physical activity. Prioritise fruits, vegetables, whole grains, lean protein, and dairy (or dairy alternatives). Reduce or eliminate sweets, sugary cereals, and sugary drinks. And encourage at least 60 minutes of physical activity daily for school-aged children. Diet Eat a balanced diet: Prioritise fruits, vegetables, and wholegrains, which are rich in fibre. Limit red and processed meat: Reduce your intake of these, and consider swapping for chicken or fish. Consider adding more calcium: Research suggests that an extra 300mg of calcium per day, from sources like milk or calcium-fortified plant milks, may be beneficial. Avoid excessive sugar and fat: Limit sweets, cakes, crisps, and fizzy drinks. Physical activity Be active regularly: Aim for at least 30 minutes of moderate-intensity exercise most days of the week. Lifestyle choices Maintain a healthy weight: Being overweight or obese increases bowel cancer risk. Limit alcohol intake: Excessive alcohol consumption is linked to increased risk. Quit smoking: Smoking is a known risk factor for various cancers, including bowel cancer. Bowel cancer screening Take part in screening programmes: The NHS Bowel Cancer Screening Programme offers screening for those over 50 in England and Wales and over 50 in Scotland.
Forbes
2 days ago
- Health
- Forbes
Having ADHD And Living In A Smaller City Might Increase Obesity Risk: Study
Attention deficit hyperactivity disorder (ADHD) is usually associated with the image of a child jumping off walls and being physically active. Still, a recent study found that ADHD-induced impulsivity can make people more likely to over-eat and have a higher body mass index — particularly if they live in a smaller city with lower access to mental health services and opportunities for physical activity. On the other hand, people with ADHD who live in larger cities are less likely to become obese due to better accessibility to mental health services. One of the study authors, Tian Gan, a Ph.D. student at the Tandon School of Engineering at New York University said in a press release: "Our research reveals a surprising urban advantage: as cities grow, both obesity and ADHD rates decrease proportionally. Meanwhile, mental health services become more accessible, helping combat physical inactivity—a key link between ADHD and obesity. This pattern suggests larger cities offer protective factors against these interconnected health challenges." Gan and colleagues analyzed data from 915 cities in the United States to investigate how impulsivity caused by ADHD could be contributing to a higher risk of obesity and how urban living conditions influence this correlation. 'Within each State, cities are different with respect to any of these features, confirming the inequalities in the United States in lifestyle, education, healthcare, and access to resources,' the authors noted in the study that was published in the journal PLoS Complex Systems. 'Our analysis highlights the role of physical activity as a feasible target for intervention, being sensitive to variations in college education, food insecurity, and access to mental health providers.' Since the last decade, researchers have hypothesized that people with ADHD might be less likely to be physically active and engage in the recommended levels of physical activity due to 'poor motor skills and executive function deficits.' Especially because ADHD causes executive dysfunction that impairs an individual's ability to follow exercise routines or adhere to stringent regimens required to exercise consistently. Prior studies conducted on Dutch and Korean children with ADHD found that living with this neurodevelopmental condition put them at a higher risk of being overweight and obese than their counterparts without ADHD. "Our analysis suggests that mental health care may contrast these tendencies, promoting awareness about health values of physical activity in city dwellers," the study authors highlighted. Because mental health treatments are mainly accessible in large cities, along with big city dwellers having higher levels of education and lower risks of food insecurity, they found that these benefits reduced the risk of over-eating and physical inactivity among ADHDers. "Our research suggests that supporting physical activity, especially in children with ADHD, could significantly improve long-term health outcomes. Surprisingly, we discovered ADHD influences obesity through dual pathways: reduced physical activity and independent biological mechanisms related to impulse control and eating behaviors—indicating that effective interventions need to address both aspects," explained Simone Macrì, a study author from the Centre for Behavioural Sciences and Mental Health at the Istituto Superiore di Sanità in Rome, Italy, in a press release.
Medscape
2 days ago
- Health
- Medscape
Can GLP-1s Protect Against Obesity-Related Cancers?
New data suggest that glucagon-like peptide 1 (GLP-1) receptor agonists, used to treat diabetes and obesity, may also help guard against obesity-related cancers. In a large observational study, new GLP-1 agonist users with obesity and diabetes had a significantly lower risk for 14 obesity-related cancers than similar individuals who received dipeptidyl peptidase-4 (DPP-4) inhibitors, which are weight-neutral. This study provides a 'reassuring safety signal' showing that GLP-1 drugs are linked to a modest drop in obesity-related cancer risk, and not a higher risk for these cancers, said lead investigator Lucas Mavromatis, medical student at NYU Grossman School of Medicine in New York City, during a press conference at American Society of Clinical Oncology (ASCO) 2025 annual meeting. However, there were some nuances to the findings. The protective effect of GLP-1 agonists was only significant for colon and rectal cancers and for women, Mavromatis reported. And although GLP-1 users had an 8% lower risk of dying from any cause, the survival benefit was also only significant for women. Still, the overall 'message to patients is GLP-1 receptor treatments remain a strong option for patients with diabetes and obesity and may have an additional, small favorable benefit in cancer,' Mavromatis explained at the press briefing. 'Intriguing Hypothesis' Obesity is linked to an increased risk of developing more than a dozen cancer types, including esophageal, colon, rectal, stomach, liver, gallbladder, pancreatic, kidney, postmenopausal breast, ovarian, endometrial and thyroid, as well as multiple myeloma and meningiomas. About 12% of Americans have been prescribed a GLP-1 medication to treat diabetes and/or obesity. However, little is known about how these drugs affect cancer risk. To investigate, Mavromatis and colleagues used the Optum healthcare database to identify 170,030 adults with obesity and type 2 diabetes from 43 health systems in the United States. Between 2013 and 2023, half started a GLP-1 agonist and half started a DPP-4 inhibitor, with propensity score matching used to balance characteristics of the two cohorts. Participants were a mean age of 56.8 years, with an average body mass index of 38.5; more than 70% were White individuals and more than 14% were Black individuals. During a mean follow-up of 3.9 years, 2501 new obesity-related cancers were identified in the GLP-1 group and 2671 in the DPP-4 group — representing a 7% overall reduced risk for any obesity-related cancer in the GLP-1 group (hazard ratio [HR], 0.93). When analyzing each of the 14 obesity-related cancers separately, the protective link between GLP-1 use and cancer was primarily driven by colon and rectal cancers. GLP-1 users had a 16% lower risk for colon cancer (HR, 0.84) and a 28% lower risk for rectal cancer (HR, 0.72). 'No other cancers had statistically significant associations with GLP-1 use,' Mavromatis told briefing attendees. But 'importantly, no cancers had statistically significant adverse associations with GLP-1 use,' he added. Experts have expressed some concern about a possible link between GLP-1 use and pancreatic cancer given that pancreatitis is a known side effect of GLP-1 use. However, 'this is not borne out by epidemiological data,' Mavromatis said. 'Additionally, we were not able to specifically assess medullary thyroid cancer, which is on the warning label for several GLP-1 medications, but we did see a reassuring lack of association between GLP-1 use and thyroid cancer as a whole,' he added. During follow-up, there were 2783 deaths in the GLP-1 group and 2961 deaths in the DPP-4 group — translating to an 8% lower risk for death due to any cause among GLP-1 users (HR, 0.92; P = .001). Mavromatis and colleagues observed sex differences as well. Women taking a GLP-1 had an 8% lower risk for obesity-related cancers (HR, 0.92; P = .01) and a 20% lower risk for death from any cause (HR, 0.80; P < .001) compared with women taking a DPP-4 inhibitor. Among men, researchers found no statistically significant difference between GLP-1 and DPP-4 use for obesity-related cancer risk (HR, 0.95; P = .29) or all-cause mortality (HR, 1.04; P = .34). Overall, Mavromatis said, it's important to note that the absolute risk reduction seen in the study is 'small and the number of patients that would need to be given one of these medications to prevent an obesity-related cancer, based on our data, would be very large.' Mavromatis also noted that the length of follow-up was short, and the study assessed primarily older and weaker GLP-1 agonists compared with newer agents on the market. Therefore, longer-term studies with newer GLP-1s are needed to confirm the effects seen as well as safety. In a statement, ASCO President Robin Zon, MD, said this trial raises the 'intriguing hypothesis' that the increasingly popular GLP-1 medications might offer some benefit in reducing the risk of developing cancer. Zon said she sees many patients with obesity, and given the clear link between cancer and obesity, defining the clinical role of GLP-1 medications in cancer prevention is 'important.' This study 'leads us in the direction' of a potential protective effect of GLP-1s on cancer, but 'there are a lot of questions that are generated by this particular study, especially as we move forward and we think about prevention of cancers,' Zon told the briefing.
