Can nondrug remedies relieve gastrointestinal (GI) issues such as heartburn, bloating, constipation, and diarrhea? Patients are requesting these solutions, and some doctors are complying, according to this roundup of potentially helpful natural treatments.
The story presents advice from clinicians on nondrug strategies that seem to work for their patients. A few of the remedies — such as a diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols; kiwifruits for constipation; and fermented foods for gastroesophageal reflux disease — have some research behind them suggesting efficacy.
Readers were interested in the story, but a number of commentators wanted more robust evidence, whereas a few shared their own advice. Luis Pina, MD, a surgeon in Pennsylvania, simply commented, “Show me the data!” Similarly, Oscar Cuzzani, MD, an ophthalmologist in Canada, wrote, “I was expecting more RCT [randomized controlled trial] data and well-founded research.”
But Patty Buzzelli, an advanced practice nurse in the state of Washington, wrote, “A ‘cleanse’ especially for parasites with some ivermectin/fenben would be a good thing for anyone with gut problems.”
Experts cited in this story reinforce the role of lifestyle changes as “foundational” to any weight-loss intervention, including drugs and bariatric surgery, while acknowledging that diet and nutrition changes may not be enough on their own and that weight regain is common with any intervention.
The story was based on presentations at the International Conference on Nutrition in Medicine, sponsored by the Physicians Committee for Responsible Medicine. The presenters provided research and compared three approaches to sustained weight loss: lifestyle (nutrition and exercise), drugs, and bariatric surgery. Included were clinical guidelines from various organizations and data on the durability of weight loss, side effects, discontinuation rates, and drivers of weight gain with the different approaches.
Because there are no head-to-head comparisons, no firm conclusions could be drawn regarding which is best.
The story was popular with readers. Commentators pointed to strategies such as intermittent fasting and psychotherapy, which were not included in the presentations, and factors such as antidepressants and genetic vulnerabilities, which were not included in the discussion of weight drivers. They also expressed varying views based on their professional and personal experiences. For example, Dr Carole Friend commented, “Love the evidence-based approach to most of the article, but why switch to opinion when discussing nutritional approaches and support dietary recommendations that continue to have NO evidence base?”
This story explores research on potential connections between eating according to natural microbial rhythms in the gut and metabolic health. The catch? All the work thus far has been done in mice.
Researchers from UC San Diego tracked microbial rhythms in mice to determine whether aligning eating times to active/wake phases — a strategy known as time-restricted feeding (TRF) — might improve metabolic health. Several experiments demonstrated that mice with unrestricted access to a high-fat diet showed signs of metabolic dysfunction due to disruptions in their circadian and microbial rhythms.
In contrast, in mice that consumed a high-fat diet within a TRF window, metabolic phenotyping demonstrated that the regimen protected them from harmful high-fat-induced effects, including adiposity, inflammation, and insulin resistance.
Of note, the team used metatranscriptomics, a novel technique that captures real-time microbial activity by profiling RNA transcripts, to observe dynamic microbial changes.
The details of the work are intriguing, and the work seems promising. However, as a commentator not involved in the study noted, translating the findings in mice to humans is “highly speculative.” Furthermore, many animal models are more sensitive to time-restricted eating and caloric restriction than humans.
Reader commentators also were hesitant to draw any clinical conclusions. For example, Durwood Dugger, a health business administrator in Florida, wrote, “As someone who [has] done hundreds of animal nutrition studies, the biggest problem with this study is trying to compare it to the human diet and digestion processes.”
Dr Larry Bloom, a psychologist in Florida, pointed to issues around causality, “Perhaps I am missing something, but the differences observed in the mice for TRF vs unrestricted feeding are not necessarily causally related at all to their microbiota but may simply be the result of either TRF in general or the circadian rhythms of the TRF mice.”
Most clinicians are aware of the nausea and vomiting that may occur when patients take GLP-1s for weight loss. But a presentation at the American Association of Clinical Endocrinology Annual Meeting 2025 pinpointed some lesser-known effects.
The story addresses some of these underappreciated issues, including bone loss along with lean mass loss, especially among those who take the drugs but don’t exercise; fatigue to the point that individuals lose their appetites and can’t eat even when advised to do so; and abdominal pain that, for some patients, may be more severe than the more common side effects of nausea and vomiting.
The presenter noted that — regarding fatigue — patients may not be drinking enough water and should be counseled not only on proper nutrition when taking GLP-1s but also on the need for hydration.
Commentators appreciated the story and pointed to the importance of lifestyle changes and involving a multidisciplinary team to help patients with these issues. For example, Tammy Brown, an advanced practice nurse in Montana, commented, “Having a healthcare team of physicians, nutrition/dietitian specialists, and pharmacists monitoring GLP-1 weight loss patients is vital for the patient’s success.”
Robert Argo, MD, an internist in Mississippi, wrote, “No matter how many drugs we produce, permanent success will only accompany them with lifestyle changes. Interestingly, the lifestyle changes would probably do it by themselves for most of us. I can only imagine the amount of time, money, and brainpower that will be, and has already occurred, trying to find the magic drug, while all the time knowing that the key is lifestyle changes.”
How sweet it is — or isn’t? Researchers analyzed blood samples and brain scans to assess the possible effects of sucralose, sucrose, or a water control on brain mechanisms of appetite regulation and hunger ratings. The findings were complicated but of strong interest to readers.
For the randomized controlled trial, participants were separated into three groups: obese (n = 23), overweight (n = 24), and healthy weight (n = 28). They all came into the study with similar noncaloric sweetener use.
On three separate visits, researchers collected baseline brain scans and blood samples, and participants rated how hungry they were. Participants then consumed 300 mL of water, a sugar-sweetened drink, or a drink sweetened with sucralose. Researchers collected follow-up brain scans, blood samples, and hunger ratings several times during the subsequent 2 hours.
Among the findings from various analyses: Sucrose, but not sucralose, had a hunger-dampening effect while also raising peripheral glucose levels, corresponding to reduced medial hypothalamic blood flow; acute consumption of sucralose vs sucrose stimulated hypothalamic blood flow and greater hunger responses; among individuals with healthy weight, sucralose produced greater activation of the hypothalamus than sucrose, whereas individuals with obesity showed a greater response in the lateral hypothalamic to sucralose relative to water.
Sucralose also showed evidence of increased signaling between the hypothalamus and the brain areas involved in motivation and decision-making, suggesting that the sweetener could affect cravings or eating behavior.
Susan Swithers, PhD, Purdue University, West Lafayette, Indiana, an independent commentator on the study, concluded, “These results add to our understanding of the ways in which high-intensity sweeteners like sucralose are not inert,” she said. “They produce effects in the brain different from those produced by sugars or by water, and ultimately, these differences could contribute to metabolic dysregulation.”
Should vitamin D testing or targeted treatment be part of routine GI disease management? Yes, wrote David A. Johnson, MD, a regular contributor to Medscape Medical News and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia.
Although the latest guidelines from the Endocrine Society recommend against routine vitamin D supplementation, they do not specifically address its use in populations with, or at risk for, GI diseases, Johnson wrote. Hence, his recommendation that clinicians consider testing or empiric treatment as part of their GI management and risk-reduction strategies.
Johnson explained the biological effects of vitamin D on the gut and touched on data linking low vitamin D with GI diseases such as inflammatory bowel disease, diverticulitis, colon cancer, and liver disease. He also noted studies suggesting that vitamin D supplementation can improve the diversity and stability of the fecal microbiome.
Of note, he wrote, there are two main dietary forms of vitamin D: D2, which is primarily found in plants and fungi, and D3, which is animal derived. Although both contribute to overall vitamin D levels, “D3 is significantly more effective in raising serum levels,” and testing for the biologically active form of vitamin D — 1,25-dihydroxyvitamin D — is recommended to more accurately identify a deficiency.
The story was popular with readers, and commentators had a few specific questions, demonstrating a desire for more information on this topic.
This Medbrief describes ongoing work on a blood-based assay that identified pancreatic ductal adenocarcinoma (PDAC) at all stages and improved early-stage detection of early-stage disease when combined with carbohydrate antigen 19-9 (CA 19-9).
The assay, dubbed PAC-MANN-1, identified PDAC with 98% specificity and 73% sensitivity and accurately distinguished patients with chronic pancreatitis or pancreatic neoplasias from those with PDAC, according to the Oregon Health & Science University, Portland, Oregon, research team. In contrast, the use of CA 19-9 alone showed a 45% sensitivity for detecting PDAC.
However, the assay is not ready for prime time. The authors wrote it was not designed as a point-of-care device; it has only been tested in venous blood draws; and its potential application in the real world — for example, home, pharmacies, and underserved settings — will need an alternate design.
For now, the assay “has promise to serve as the foundation for a sensitive, inexpensive, low serum volume and scalable early detection of PDAC assay that can be used regularly in high-risk patient populations or the general population with less access to medical tests,” they wrote.
Readers were interested in the new assay, and a few commented on conflicts of interest and patent rights.
This exploration of common medications’ deleterious effects on the microbiome drew great interest. The story pointed to the long list of drugs that can directly alter the gut microbiota, including antibiotics, antivirals, antifungals, anthelmintics, proton pump inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs), laxatives, oral antidiabetics, antidepressants, antipsychotics, statins, chemotherapeutics, and immunosuppressants.
The story elaborated on the specific effects in each category, according to various experts. For example, “NSAIDs can modify the function and composition of the intestinal microbiota, favor the growth of pathogenic species, and reduce the diversity of preexisting bacteria by reducing the presence of beneficial commensal bacteria, such as Lactobacillus and Bifidobacterium,” said coloproctologist Maria Júlia Segantini, MD, from the University of São Paulo in São Paulo, Brazil.
Laxatives can accelerate intestinal transit, impairing the quality of the microbiota and altering bile acid, she said. Statins may alter the composition of the gut microbiota, affecting its diversity.
“There are still no protocols aimed at preserving the microbiota during pharmacological treatment,” she noted. “Future research should identify biomarkers of drug-induced dysbiosis and potentially adapt live biotherapeutics to counteract it.”
Commenting on the story, Dr Michael Forman, a general practitioner in Florida, wrote, “Finally! This has to be one of the most underdeveloped areas of primary care medicine.” Karen Khal, an advanced practice nurse in Nevada, quipped, “The moral of the story is, don’t take medications that you don’t clearly need.”
This story, excerpted from an online commentary by David A. Johnson, MD, a regular contributor to Medscape Medical News and chief of gastroenterology at Eastern Virginia Medical School, reviews advances in bowel prep that aim to improve quality.
New consensus recommendations from the US Multi-Society Task Force on Colorectal Cancer around colonoscopy preparation bring a clear message: “Quality matters,” Johnson wrote. In line with that message, the new threshold for the rate of adequate bowel preparation for both individual endoscopists and endoscopy units is now > 90%.
The new recommendations also specify that quality in colonoscopy refers to adenoma detection and sessile serrated lesion detection, along with the associated documentation, Johnson explained.
“Achieving that level of quality is not just about writing a prescription for the prep and instructing your patients to follow through with it,” he wrote. “Rather, it means providing guidance around diet modification and medication management and explaining the importance of the prep and how it is integral to colonoscopy performance. It’s a shared responsibility. You, as well as your staff, need to take the time to discuss it with your patients.”
Other changes in the recommendations include the use of adjunctive simethicone to improve tolerance and modifications to steps to take after a previous inadequate prep.
Among the few comments, Dr Chuck Pool detailed his personal difficult and “worrisome” experience with bowel prep, and Donald Condliffe wrote, “Just had a colonoscopy at [a large medical center], and there was no human personal guidance at all. Just a few pages of downloaded instructions, and that was it.”
This Medbrief reports on a study suggesting that weekly poultry consumption > 300 g was associated with a greater risk for all-cause mortality and more than double the risk for death from GI cancers compared with weekly consumption < 100 g. The study was based on data analyses of close to 5000 participants in two Italian cohort studies who were followed for an average of 19 years.
The researchers found that individuals who died from GI cancers ate more poultry than those who died from other causes. They suggested that white meat may not be a healthy protein choice — although they acknowledged that cooking methods might play a role in the findings.
Commentators proposed other factors that could be at play, including fat-soluble contaminants or hormones from feed, how the chicken was processed, and vaccination of animals in the food supply.
Most commentators were skeptical of the findings.
Brian Wilson, a mental health provider in the UK, commented, “highly processed chicken, reared in a factory, fried to a crisp in refined oils, coated with breadcrumbs, and eaten with fried potatoes, possibly?”
In a similar vein, Robert quipped, “And we are still left with the mystery of why the chicken crossed the road!” to which Wilson replied, “To get away from the KFC [Kentucky Fried Chicken]!”
Marilynn Larkin, MA, is an award-winning medical writer and editor whose work has appeared in numerous publications, including Medscape Medical News and its sister publication MDedge, The Lancet (where she was a contributing editor), and Reuters Health.