Latest news with #obesity
WebMD
14 hours ago
- Health
- WebMD
Obesity's Cancer Link Is Worse Than You Think
July 31, 2025 — Cancer deaths are dropping overall, but not the ones linked to obesity. That's what mounting evidence now shows. A sweeping new report on U.S. cancer trends, published in April, revealed that cancers linked to obesity are becoming more common. Another study, presented in July at the Endocrine Society Annual Meeting in San Francisco, found that deaths from obesity-related cancers have more than tripled over the past two decades. These include esophageal, colon and rectal, breast (postmenopausal), uterine, gallbladder, upper stomach, kidney, liver, ovarian, pancreatic, thyroid, meningioma (brain), and multiple myeloma — 13 types in all, now accounting for 40% of new cancer diagnoses in the U.S. Women, older adults, Native Americans, and Black Americans are especially vulnerable. Second only to smoking, obesity ranks as one of the leading preventable causes of cancer. Yet even as the public's awareness of smoking's risks has dramatically increased, experts warn we've underestimated just how much excess weight — and the complex biology behind it — can fuel the disease. What exactly drives this link is not fully understood, but experts are homing in on some strong possibilities. It could be estrogen, fat cells, the microbiome, insulin resistance, or all of the above. One thing is sure: The public health threat of obesity is only increasing. So what does this mean for cancer prevention, and how can you protect yourself? A Risk for Women Behind the drop in overall cancer rates are significant declines in the number of smokers — and smoking-related cancers. Between 1965 and 2015, the smoking rate fell from 42% of the population to 15%, putting a major dent in rates of lung cancer, which is still the deadliest form. Meanwhile, obesity rates have gone the other way, rising from 13% in 1960 to more than 40% today. Estimates reveal a crucial gender difference. While overall cancer diagnoses in men are down —decreasing from 2001 through 2013, and plateauing after that — the same is not true for women, according to the April report, jointly published by top health organizations like the CDC, the National Cancer Institute, the American Cancer Society. Cancer diagnoses among women increased every year from 2003 to 2021. That includes upticks among women in every major racial and ethnic group since 2017, even while cancer rates have remained stable among men in those groups. According to the American Cancer Society, women under 50 are now 82% more likely to be diagnosed with cancer than are men of the same age — up from a 51% difference in 2002. 'One of my most common referrals is cancer doctors,' said Ethan Lazarus, MD, an obesity medicine specialist in Colorado, who is often recruited by oncologists to help patients in remission, commonly from breast cancer, lose weight. Evidence has repeatedly shown that higher amounts of fat tissue increase the risk of cancer recurrence. Weight loss is linked to improvements in cancer survival, particularly with breast and colon cancer. Women tend to have higher rates of obesity than men — and higher rates of severe obesity, in particular — which may partly explain why they're more affected by obesity-related cancers. Also worth highlighting is that several of the obesity-related cancers are female-specific or far more common in women. But that doesn't explain the bigger question: Why does obesity raise the risk of cancer in women — or in anyone? When Fat Makes You Sick 'The truth is, no one really knows why obesity causes cancer,' said Scott Summers, PhD, co-executive director of the Diabetes and Metabolism Research Center at the University of Utah Health. But Summers' research group believes fat cells are a big part of the problem. 'Fat cells are weird, and they can be nasty,' he said. Obesity experts have coined a term for the tipping point when fat cells start to affect your health: adiposopathy — 'adipos' meaning fat, and 'pathy' meaning disease, Lazarus said. For one, they may drive cancer simply by proximity. Almost all of the obesity-related cancers occur in or next to parts of the body where fat tissue is more concentrated, like the abdomen and breast, according to a 2023 review in Frontiers in Endocrinology. And research in mice shows that breast cancer is more aggressive when surrounded by more fat tissue. One leading theory is that fat tissue is 'hormonally active,' especially after menopause — meaning it releases hormones like estrogen that can cause certain cancers like breast or endometrial to grow, said Priya Jaisinghani, MD, an obesity medicine specialist in New York City. In fact, postmenopausal breast cancer is the most common obesity-associated cancer in women. The Role of Inflammation and Insulin Inflammation is another suspect. As fat cells accumulate and grow — or as a person gains weight — those tissues stimulate an immune response. 'There are a few ways that happens,' Summers said. 'One is immune cells infiltrate fat tissue because they are clearing out dying fat cells.' This immune activation produces a chronic, low-grade inflammation, which raises the risk of DNA damage and cellular mutations — potentially priming the body for cancer. Chronic inflammation may also contribute to insulin malfunctions, which can promote cancer. People with obesity often have insulin resistance, meaning their cells don't respond properly to normal levels of insulin, the hormone secreted by the pancreas to regulate blood sugar. When that happens, the pancreas releases more insulin to try to keep blood sugar under control, elevating blood levels of insulin, which can stimulate tissue growth, including cancer tissue, Summers said. What's Happening in the Gut Summers's team at U Health has also uncovered a potential driver in the gut: a type of fat-storage molecule called sphingolipids, which build up in the body during obesity. 'We think they do a lot of damage in obesity, and they're a sign the other pathways for [fat] storage are full,' Summers said. In mouse studies, removing sphingolipids eliminated obesity-related diseases like kidney disease, fatty liver disease, diabetes, and heart failure. One study showed that sphingolipids drive up the rapid production of stem cells in the intestine — an unexpected finding that suggests the fat molecules could trigger excessive cell proliferation in the colon, increasing the risk for colon cancer, Summers said. This is critically important given the unexplained, global rise in colon cancer among people under 50. Data shows persistent obesity increases the risk of colon cancer by as much as 57%. Big Problem With Bias Forty-two percent of Americans now live with obesity, and that number is projected to hit 50% by 2030. That leaves us with two options for cancer prevention, Lazarus said. 'Do we want to go after all the cancers [individually] or recognize obesity as a serious health threat?' Jaisinghani agreed. Preventing obesity-related cancers starts with equitable access to obesity care, 'regular physical activity, balanced and nutritious eating, and early treatment of metabolic conditions like insulin resistance or prediabetes,' she said. 'And prevention shouldn't be a privilege,' or it can't just be for those who can afford it. Only about 10% of people with obesity receive medical treatment, compared with 85% of patients with diabetes, Lazarus said. Many people, doctors included, still see obesity as a lifestyle issue instead of a medical one. 'Most don't get any care, much less comprehensive.' Early cancer symptoms are often overlooked and blamed on excess body weight, and machines used for screening, such as MRIs and mammography machines, don't always fit properly. For these reasons, obesity often goes untreated, and cancers in people with obesity go undetected. Experts say it's a public health crisis that, like smoking and lung cancer, calls for a public health approach. 'It's policy-level interventions that shape the environments in which people live, work, and make decisions about their health,' Jaisinghani said. But you can take steps to protect yourself too. Know that if you have health concerns with obesity, that is a medical issue and seeking treatment is completely appropriate. Consider seeing an obesity medicine specialist. This subspecialty is rapidly expanding, and doctors with this training can help you avoid bias and inadequate care. You can find one by searching the Obesity Medicine Association's provider directory.
Yahoo
18 hours ago
- Business
- Yahoo
Viking Therapeutics, Inc. (VKTX) Nears Obesity Drug Breakthrough with Phase 3 VK2735 Trial
We recently compiled a list of Viking Therapeutics, Inc. stands third on our list. Viking Therapeutics, Inc. (NASDAQ:VKTX) is a clinical-stage biopharma company developing treatments for metabolic and endocrine disorders, including obesity, NASH, and rare diseases like X-linked adrenoleukodystrophy (X-ALD). Its lead candidate, VK2735—a dual GLP-1/GIP receptor agonist- is now in Phase 3 VANQUISH trials for obesity and obesity with type 2 diabetes, following strong Phase 1 and 2 results demonstrating significant weight loss and safety, making it one of the best growth stocks in the biotech sector. Viking Therapeutics, Inc. (NASDAQ:VKTX) has also completed enrollment in a Phase 2 trial for an oral version of VK2735, with top-line results expected in the second half of 2025. If successful, the oral formulation could offer a more convenient alternative to injectable obesity drugs. The company is further expanding its pipeline with a novel amylin agonist program aimed at metabolic disorders, expecting to file an IND by Q4 2025. Additionally, VK2809, a thyroid hormone receptor beta agonist for NASH, has shown positive Phase 2b results. The business is also advancing VK0214 for X-ALD and other programs targeting lipid metabolism. A scientist in the lab, researching the development of biopharmaceutical monoclonal antibody drugs. With a robust pipeline and $808 million in cash (as of June 2025), Viking Therapeutics, Inc. (NASDAQ:VKTX) is well-positioned to fund upcoming milestones. The Phase 3 VK2735 trials and pending oral trial results are key near-term catalysts. While we acknowledge the potential of GOOGL as an investment, we believe certain AI stocks offer greater upside potential and carry less downside risk. If you're looking for an extremely undervalued AI stock that also stands to benefit significantly from Trump-era tariffs and the onshoring trend, see our free report on the best short-term AI stock. READ NEXT: The Best and Worst Dow Stocks for the Next 12 Months and 10 Unstoppable Stocks That Could Double Your Money. Disclosure: None. Sign in to access your portfolio
Yahoo
21 hours ago
- Health
- Yahoo
Radella Pharmaceuticals Announces New Obesity Trial Data Showing Statistically Significant Weight Loss and Broader Cardiometabolic Benefits
First‑in‑class, PTP1B‑modulating peptide reduced body weight, improved insulin sensitivity and lowered LDL cholesterol without tolerability issues NEW YORK, July 31, 2025 /PRNewswire/ -- Radella Pharmaceuticals, LLC, a clinical-stage biopharmaceutical company developing innovative therapies for cardiometabolic disorders, today announced that its Phase 1b clinical trial of MD-18 targeting obesity and type 2 diabetes met its objectives, achieving statistically significant weight loss and broader cardiometabolic improvements in healthy volunteers, with a clean safety and tolerability profile. The first-in-class peptide utilizes a dual-pronged approach to increase insulin sensitivity and increase energy expenditure by reactivating leptin signaling, a pathway often impaired in obesity, through precise modulation of the enzyme PTP1B. The company believes MD-18 prompts the body to use more of the calories it has already stored, enabling weight loss while preserving lean muscle mass. This differs from glucagon-like peptide-1 receptor agonists (GLP-1 RAs), which primarily induce weight loss through appetite suppression, and are associated with lean mass loss and tolerability issues. "These data validate MD-18 as a next-generation approach to cardiovascular and metabolic health," said Daniel Cohen, Founder and Chief Executive Officer of Radella. "Participants lost weight and waist circumference, and saw improvements in cholesterol and insulin measures. These findings indicate that MD-18 may offer pan-cardiometabolic benefits for common obesity co-morbidities, including heart disease and diabetes." Study Design and Results The double‑blind, placebo‑controlled multiple ascending dose (MAD) Phase 1b trial enrolled healthy volunteers [n=36] with an average body‑mass index (BMI) of 28.8 +2.5 in the MD-18 arm. Participants received either placebo or escalating weekly doses of MD‑18 for four weeks without titration. The study was conducted in the early phase clinical trial facility in Sheba Medical Center, Israel. Topline results from the initial six cohorts in the Phase 1b trial include: Significant weight loss of up to 2.7% in otherwise healthy volunteers in 28 days of treatment. These results were seen in primarily non-obese subjects and were accompanied by a 2.2% decrease in waist circumference with weekly administration. The data suggest greater weight loss would be observed in obese individuals. Data are consistent with lean mass preservation. As expected with the drug's novel mechanism of action and nonclinical data indicating the ability to preserve lean mass, the data are in line with expectations for a next-generation cardiometabolic therapeutic. Unlike other therapies that optimize weight loss primarily via anorexic effect, MD-18 holds the potential to achieve sustainable adipose tissue loss while preserving muscle mass. Significant reductions in key cardiovascular biomarkers. In healthy subjects with elevated LDL cholesterol levels, MD-18 demonstrated a statistically significant decrease in LDL cholesterol vs. placebo. Further, MD-18 demonstrated a statistically significant decrease in alanine aminotransferase (ALT) levels vs. placebo, suggesting the potential to reduce liver fat content. No safety signals and best-in-class tolerability profile. All drug related adverse events (AEs) were mild (Grade 1) and most AEs, including gastrointestinal events, were similar between MD-18 and placebo. How MD-18 differs from GLP-1 therapies Current GLP-1 therapies promote weight loss primarily via appetite reduction, and a recent meta-analysis showed that approximately 25% of weight lost with these drugs is lean muscle mass1. These medications are also associated with side effects such as nausea and other gastrointestinal issues. According to a 2025 study in JAMA Network Open, nearly two-thirds of adults without type 2 diabetes and nearly half of those with diabetes discontinued GLP-1 therapy within one year, primarily due to tolerability concerns2. In contrast, MD-18's approach aims to restore metabolic signaling through targeted PTP1B modulation. In both preclinical models and clinical trials, MD-18 has demonstrated improved insulin sensitivity, lower cholesterol, and reduced ALT levels, a marker of liver health. These are important biomarkers, as more than two in five American adults with obesity also have other chronic conditions, including high blood pressure, heart disease, and diabetes, according to the CDC3. "We believe MD-18 is better positioned to maintain weight loss long term," said Amir Tirosh, MD, PhD, Chief Medical Officer at Radella. "The cardiometabolic signals we're seeing, which include not just weight loss but also improved lipids, insulin and liver enzymes, point to a therapy that treats the whole patient, not just the numbers on the scale. In addition, with MD-18 we may be able to finally enter an era of highly effective combination therapy in obesity, in which MD-18 may also be used with GLP-1 therapies." PTP1B and Leptin as a Target PTP1B is well understood to modulate insulin sensitivity and energy expenditure via the leptin pathway. Leptin plays a crucial role in regulating body weight, but in people with obesity, resistance to the hormone leads to lower energy expenditure and increased fat storage. Early attempts to restore leptin sensitivity or deliver leptin directly in humans failed, producing unintended effects such as hypoglycemia, immune dysfunction, and other toxicities, often due to drugs that indiscriminately blocked enzymes throughout the body. Radella's approach is different: MD-18 is a small peptide that disrupts with high specificity a key protein-protein interaction in the leptin signaling pathway, avoiding the off-target effects seen with earlier therapeutic approaches targeting PTP1B. Next Steps Based on these topline results from the six cohorts in the MAD portion of the Phase 1b study, Radella will initiate two additional cohorts in the intent-to-treat population, including obese patients without type 2 diabetes and overweight and obese patients with type 2 diabetes. In each cohort patients will receive either placebo or once weekly injections of MD-18 for 12 weeks. The company expects to report topline data from these cohorts in Q1 2026. About Radella Pharmaceuticals Radella Pharmaceuticals, LLC, headquartered in New York, NY, with operations in Aberdeen, Scotland and Tel Aviv, Israel, is a privately backed, clinical-stage biopharmaceutical company developing transformative therapies in cardiometabolic disease and beyond. Singularly focused on delivering curative solutions to patients and bettering human health, the company has successfully advanced its lead asset, MD-18, into clinical trials, developing a pipeline of follow-on assets targeting unmet needs in other large therapeutic areas, including neurodegenerative and fatty liver disease. MD-18 is a first-in-class peptide that targets multiple pathways involved in obesity and related metabolic conditions. MD-18 demonstrates a breakthrough in targeting protein-tyrosine phosphatase 1B (PTP1B), a historically challenging therapeutic target that plays a crucial role in metabolic regulation. MD-18's unique mechanism of action, which targets both insulin sensitivity and energy expenditure through PTP1B regulation and the leptin pathway, represents a potentially transformative approach for patients with cardiometabolic disease and its adjacencies. For more information on Radella's clinical program and current trials, visit Contacts Company ContactPhilip LehmanRadella Pharmaceuticals, Operating Officer & Head of Business Developmentplehman@ Media ContactRyan FlinnIn Like Flinn Communicationsryan@ Citations 1 Effect of glucagon-like peptide-1 receptor agonists and co-agonists on body composition: Systematic review and network meta-analysis Karakasis, Paschalis et al. Metabolism - Clinical and Experimental, Volume 164, 156113. Rodriguez PJ, Zhang V, Gratzl S, et al. Discontinuation and Reinitiation of Dual-Labeled GLP-1 Receptor Agonists Among US Adults With Overweight or Obesity. JAMA Netw Open. 2025;8(1):e2457349. doi:10.1001/jamanetworkopen.2024.57349. CDC Website, Adult Obesity Facts. View original content to download multimedia: SOURCE Radella Pharmaceuticals Error in retrieving data Sign in to access your portfolio Error in retrieving data Error in retrieving data Error in retrieving data Error in retrieving data
Medscape
a day ago
- Health
- Medscape
Metabolic Disease: When Biology Advances, but Care Lags
Metabolic diseases, including type 2 diabetes (T2D), obesity, and metabolic syndrome, are a growing threat to global public health. More than 537 million adults currently live with T2D, and this number continues to rise, especially in developing countries where sedentary lifestyles and poor diets are driving the surge. These conditions impose a substantial economic burden on health systems worldwide, particularly in resource-limited areas. These disorders disrupt energy metabolism and alter the mechanisms for generating, storing, and utilizing energy. T2D is characterized by insulin resistance and chronic hyperglycemia. Obesity exacerbates insulin resistance and triggers persistent low-grade inflammation, leading to compounded metabolic dysfunctions. Currently, 39% of adults are overweight, and 13% are classified as obese. Metabolic syndromes include abdominal obesity, hypertension, dyslipidemia, and insulin resistance, together with a significantly increased risk for cardiovascular disease and T2D. This rising prevalence is driven by population aging and unhealthy lifestyles. Nonalcoholic fatty liver disease, also known as metabolic dysfunction-associated steatotic liver disease (MASLD), is a common complication of metabolic syndrome and is among the top causes of chronic liver disease globally. Coexisting T2D, obesity, and metabolic syndrome sharply increase the risk for myocardial infarction, stroke, kidney failure, and neuropathy. This cluster leads to severe health consequences and increased costs, reinforcing the need for integrated preventive and therapeutic strategies. Therapeutic Approaches Current treatments for metabolic diseases, particularly T2D, include metformin; SGLT2 inhibitors such as empagliflozin, canagliflozin, and dapagliflozin; and GLP‑1 agonists, for example, liraglutide, semaglutide, and dulaglutide. Metformin remains the first-line therapy due to its proven efficacy, low cost, and tolerability. SGLT2 inhibitors lower blood glucose levels by increasing urinary glucose excretion and offer added benefits for weight and cardiovascular health but may increase the risk for urinary and genital infections. GLP‑1 agonists improve glycemic control and support weight loss and cardiovascular protection, although they often cause gastrointestinal side effects. Emerging therapies include dual GLP‑1/glucose-dependent insulinotropic polypeptide (GIP) agonists such as tirzepatide and triple agonists targeting GLP‑1, GIP, and glucagon, which aim to enhance efficacy, improve weight loss, and reduce dosing frequency to support better treatment adherence. Research Highlights Recent findings have reshaped the understanding and management of metabolic diseases by targeting the underlying biological mechanisms. Mitochondrial dysfunction in adipose tissue is a key contributor to insulin resistance in patients with T2D. Thus, enhancing mitochondrial biogenesis and function may offer an effective therapeutic strategy for treating these diseases. Disruption of circadian rhythms impairs energy metabolism and worsens obesity, T2D, and metabolic syndrome, supporting the use of chronotherapy by aligning meals, light exposure, and medication timing with the body's natural rhythms. A 2024 report, 'Heart Disease and Stroke Statistics,' provides comprehensive data on cardiovascular health and its link with metabolic diseases. This report underscores the importance of therapies that address both glucose regulation and subclinical vascular damage associated with metabolic conditions. A review in Frontiers in Medicine identified insulin resistance as a central factor in metabolic diseases and explored gut microbiome-based therapies for MASLD, including probiotics, prebiotics, targeted antibiotics, and fecal transplantation. Patient phenotype-based treatment was proposed to improve outcomes in T2D, aiming to tailor therapies based on individual metabolic profiles. Advances in imaging and biomarkers have been highlighted for the early detection of metabolic disorders, enabling timely intervention before the development of clinical symptoms. Therapeutic Innovations Gene therapy and gut-liver axis modulation improve insulin sensitivity and reduce liver fat in MASLD models, although safety and durability remain challenging. Dual and triple agonists targeting GLP‑1, GIP, and glucagon receptors improve glycemic control, weight loss, and cardiovascular health. These therapies may also alter gene expression through epigenetic mechanisms, thereby supporting personalized treatment approaches. Early metabolic changes are linked to vascular damage, supporting early intervention in at-risk patients. mRNA therapies delivered via lipid nanoparticles improve glucose control with fewer side effects in diabetes models. Triple agonists show superior metabolic control, weight loss, and cardiovascular benefits, with better adherence and tolerability. Future Challenges Despite recent advances in the treatment of metabolic diseases, several barriers have hindered the widespread adoption of new therapies. A recent analysis highlighted the need for long-term clinical trials to validate therapies that target mitochondrial function in humans. Similarly, the implementation of personalized chronotherapy based on circadian rhythms remains technically and clinically challenging. In cardiovascular care, early vascular damage in young individuals at metabolic risk often goes undetected, delaying preventive intervention. Microbiome-based treatments for MASLD also face limitations due to individual variability and the lack of standardized protocols. Environmental factors, such as diet and stress, can amplify gene expression linked to metabolic disorders, underscoring the need for multisectoral prevention strategies. Phenotypic classification of T2D could support personalized care, but its implementation requires resources and infrastructure that are not widely available. Advanced metabolic imaging and molecular diagnostics are still inaccessible with many limited resources, restricting early detection and personalized treatment. The long-term use of GLP-1 agonists may be limited by gastrointestinal side effects in some patients, highlighting the need for more precise therapeutic selection. Triple GLP-1/GIP/glucagon agonists show strong potential but are costly and lack data in diverse populations, limiting global rollout. High costs, investment needs for gene and mRNA therapies, gaps in medical training, and public awareness are significant barriers. Addressing these challenges requires sustainable care models and innovative financing policies. Furthermore, the ongoing training of medical personnel and public education campaigns are key to ensuring effective prevention, early diagnosis, and equitable application of recent therapeutic advances. Conclusions Advances in the understanding of mitochondrial dysfunction, circadian rhythms, and the gut microbiome are transforming the management of metabolic diseases into clinical practice. Gene therapy and mRNA-based treatments show promise for T2D, obesity, and MASLD; however, further research is required to confirm their safety, effectiveness, and long-term outcomes. Standard treatments, such as metformin, SGLT2 inhibitors, and GLP-1 agonists, remain widely used, whereas newer dual and triple agonists offer additional benefits for glycemic control, weight loss, and cardiovascular protection. Personalized medicine based on phenotypic and molecular data may improve treatment outcomes but faces logistical, technological, and economic barriers. Limited access to advanced therapies in low- and middle-income countries highlights the global equity gap, which necessitates innovative public funding and sustainable care models. Strengthening diagnostic capacity, medical education, and public awareness are key to improving prevention, early diagnosis, and treatment. A coordinated global effort involving healthcare professionals, policymakers, researchers, and communities is essential to ensure that new therapies lead to meaningful and equitable improvements in public health.
Medscape
a day ago
- Health
- Medscape
Eating Earlier May Help Genes Keep Weight in Check
TOPLINE: Among adults with overweight or obesity in a standardized weight-loss program, later meal intake was linked to a higher BMI, slower weight loss, and poorer long-term maintenance. However, this association was observed only in those with a high genetic predisposition to obesity. METHODOLOGY: Meal timing is increasingly recognized as a key factor in obesity and weight management, but responses vary significantly by individual. Researchers conducted a cross-sectional and prospective observational study to explore how meal timing relates to obesity, weight-loss rate, and long‐term weight‐loss maintenance, and whether the polygenic risk score for BMI (PRS-BMI) influences these outcomes. They analyzed 1195 adults with overweight or obesity (mean age, 41.07 years; 80.8% women; mean baseline BMI, 31.32) who participated in a standardized, multimodal weight-loss intervention, of whom 456 were assessed for long-term outcomes. Participants' meal timing was unrestricted, allowing their natural eating patterns to be observed. The midpoint between the weekly averages of first and last daily meals was calculated to determine meal timing; PRS‐BMI was calculated and grouped into tertiles, with higher tertiles reflecting greater genetic susceptibility to obesity. TAKEAWAY: Each 1-hour delay in the midpoint of meal intake was associated with a 0.952 increase in BMI at baseline (P = .0002), a 2.2% increase in long-term body weight (P = .042), and a 0.046 kg/wk slower weight-loss rate (P = .013). Each one SD increase in the PRS-BMI was associated with a 1.763 higher BMI (P = 2.728E-30). A significant interaction was found between meal timing and PRS-BMI (P = .008). In those with the highest genetic susceptibility to obesity, each 1-hour delay in the midpoint of meal timing was linked to a 2.208-unit increase in BMI, whereas no significant effect was observed in those with lower genetic susceptibility. IN PRACTICE: 'This study adds to the evidence that early meal timing may attenuate the impact of genetic obesity susceptibility. These results advocate for the inclusion of chronobiological principles in personalized obesity prevention and treatment strategies,' experts wrote in an accompanying commentary. SOURCE: This study was led by Rocío De la Peña-Armada, Complutense University of Madrid, Madrid, and María Rodríguez-Martín, University of Murcia, Murcia, both in Spain. It was published online in Obesity. LIMITATIONS: The study findings may not be generalizable beyond adults with overweight or obesity. Meal timing and dietary intake were self-reported, potentially introducing recall bias. As an observational study, causal relationships could not be established. DISCLOSURES: This study was supported by the Spanish Ministry of Science, Innovation and Universities; Seneca Foundation; and National Institute of Diabetes and Digestive and Kidney Diseases. One author serves on the Board of Directors of the Sleep Research Society and has received consulting fees from the University of Alabama, Tuscaloosa, Alabama, outside the submitted work. Another author is a cofounder of Magnet Biomedicine, also unrelated to the current work. This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
