Category: 8. Health

July 9 (UPI) — A healthy plant-based diet might protect people from inflammatory bowel diseases, a new study says.

People noshing healthy plant-based foods had a 14% lower risk of Crohn’s disease and an 8% lower risk of ulcerative colitis, researchers found.

On the other hand, an unhealthy diet containing more animal fats and vegetable oils was associated with a 15% increased risk of Crohn’s disease, results show.

“Our research indicates that a healthy plant-based diet may protect against inflammatory bowel disease, with its anti-inflammatory properties playing a key role,” senior researcher Dr. Zhe Shen of the Zhejiang University School of Medicine in China said in a news release.

For the study, researchers tracked more than 143,000 people participating in the UK Biobank, a large-scale health research project among residents of the United Kingdom. As part of the project, patients filled out diet questionnaires.

During an average 14.5 years of follow-up, more than 1,000 people developed inflammatory bowel disease, researchers found.

Researchers graded participants’ diet based on their intake of healthy plant foods, unhealthy plant foods, and animal products.

Analysis showed that higher intake of fruits and vegetables accounted for part of the lower risk for Crohn’s disease, researchers said.

Blood tests from participants indicate that the anti-inflammatory properties of plant-based foods might explain this protection, researchers said.

“These findings underscore the beneficial association between healthy plant-based diets and reduced risk of ulcerative colitis and Crohn’s disease,” researchers concluded. “They provide important insights for the development of dietary guidelines aimed at preventing IBD.”

The new study appears in the journal Molecular Nutrition & Food Research.

More information

The Mayo Clinic has more on inflammatory bowel disease.

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A study of more than 70,000 US pregnancies suggests a commonly used antibiotic for urinary tract infections (UTIs) may be tied to increased risk of congenital malformations when taken during the first trimester of pregnancy.

The study, published today in JAMA Network Open, found that exposure to trimethoprim-sulfamethoxazole (TMP-SMX) during the first trimester was associated with increased risk of any malformation, severe cardiac and other cardiac malformations, and cleft lip and palate compared with beta-lactam antibiotics. No increased risk of congenital malformations was observed with nitrofurantoin, which is also commonly used to treat UTIs.

The study partly substantiates the concerns of the American College of Obstetricians and Gynecologists (ACOG), which has suggested that TMP-SMX and nitrofurantoin be avoided during the first trimester when possible because of uncertainty about the risk of congenital malformations, though studies to date have produced mixed results. Despite the ACOG recommendation, the two antibiotics still account for more than half of first-trimester UTI prescriptions, according to the study authors. 

One of the more common infections during pregnancy

For the study, a team of researchers from Vanderbilt University Medical Center, Washington University School of Medicine in St. Louis, and the University of Washington used the Merative MarketScan Commercial Database to identify a cohort of pregnant women who received first-trimester antibiotics (TMP-SMX, nitrofurantoin, fluoroquinolones, and beta-lactams) for uncomplicated UTIs and their live-born infants. 

UTIs are one of the more common infections that occur during pregnancy, affecting roughly 8% of pregnancies.

“Existing evidence on the risk of malformations associated with first-trimester antibiotic therapy for UTI is limited,” the researchers wrote. “To our knowledge, our study is the first large-scale examination restricted to pregnant individuals with UTI.”

The primary outcome of the study was congenital malformations (any and by organ system) identified up to a year after birth. To assess associations with increased risk of congenital malformations, the study used beta-lactams as the active comparator because beta-lactams are widely accepted as safe during pregnancy.

Higher risk of any malformation

Of the 71,604 pregnancies that met the inclusion criteria, 42,402 (59.2%) had first-trimester exposure to nitrofurantoin, 3,494 (4.9%) to TMP-SMX, 3,663 (5.1%) to fluoroquinolones, and 22,045 (30.8%) to beta-lactams. The median age of pregnant individuals was 30, and patient characteristics were similar across agents. The median gestational age differed by antibiotic (nitrofurantoin, 62 days; TMP-SMX, 26 days; fluoroquinolones, 18 days; beta-lactams, 63 days).

A total of 1,518 infants had malformations, including 729 with cardiac malformations. The unadjusted absolute risk of any malformation was 26.9 per 1,000 infants for TMP-SMX, 23.5/1,000 infants for fluoroquinolones, 21.2/1,000 infants for nitrofurantoin, and 19.8/1,000 infants for beta-lactams. 

After adjustments were made for potential confounders—including demographic characteristics, comorbidities, concomitant medications, and measures of healthcare use—TMP-SMX-exposed pregnancies had a 35% higher risk of any malformation compared with those exposed to beta-lactams (risk ratio [RR], 1.35; 95% confidence interval [CI], 1.04 to 1.75). The number needed to harm was 1 additional malformation for every 145 TMP-SMX-exposed pregnancy. The risks for infants exposed to nitrofurantoin (RR, 1.12; 95% CI, 1.00 to 1.26) and fluoroquinolones (RR, 1.18; 95% CI, 0.87 to 1.60) were similar to those exposed to beta-lactams.

In the analysis of organ-specific malformations, TMP-SMX was associated with increased risk of severe cardiac malformations (RR, 2.09; 95% CI, 1.09 to 3.99) and other cardiac malformations (RR, 1.52; 95% CI, 1.02 to 2.25) on a relative scale compared with beta-lactams. The risk of cleft lip and palate was more than triple (RR, 3.23; 95% CI, 1.44 to 7.22) among TMP-SMX-exposed pregnancies. 

The results were generally consistent in sensitivity analyses.

“Our results support the current ACOG recommendation for caution in using TMP-SMX during the first trimester but do not support current recommendations to limit nitrofurantoin use,” the authors concluded.

Researchers at MIT say they designed an implantable reservoir that releases glucagon when blood sugar levels get too low in people with diabetes.

For those with type 1 diabetes, hypoglycemia (low blood sugar) remains a life-threatening possibility. The researchers say they developed an implantable device that remains under the skin to combat this. When blood sugar levels get too low, they trigger the device to release glucagon. The approach could help in cases where hypoglycemia occurs during sleep or for diabetic children unable to administer injections on their own.

Currently, most patients with type 1 diabetes use daily insulin injections to prevent blood sugar levels from getting too high. Some patients carry preloaded glucagon syringes to combat hypoglycemia, but there are hurdles, according to a post on the MIT website.

“This is a small, emergency-event device that can be placed under the skin, where it is ready to act if the patient’s blood sugar drops too low,” says Daniel Anderson, a professor in MIT’s Department of Chemical Engineering, a member of MIT’s Koch Institute for Integrative Cancer Research and Institute for Medical Engineering and Science (IMES), and the senior author of the study. “Our goal was to build a device that is always ready to protect patients from low blood sugar. We think this can also help relieve the fear of hypoglycemia that many patients, and their parents, suffer from.”

Siddharth Krishnan, a former MIT research scientist who is now an assistant professor of electrical engineering at Stanford University, is the lead author of the study, which appeared today in Nature Biomedical Engineering. 

The researchers sought to design an emergency device that can be triggered either by the person using it or automatically by a sensor. Coming in at the size of a U.S. quarter, the device contains a small drug reservoir made of a 3D-printed polymer. The researchers seal the reservoir with a shape memory alloy that can change its shape when heated. They used a nickel-titanium allow programmed to curl from a fat slab into a U-shape when heated to 40 degrees celsius.

According to MIT, glucagon often breaks down quickly, preventing long-term storage in the body. The researchers addressed this by creating a powdered version of the drug that remains stable longer and stays in the reservoir until released. Each device can carry either one or four doses of glucagon and has an antenna tuned to respond to a specific frequency in the radiofrequency range. That allows remote triggering to turn on a small electrical current and heat the alloy. When the temperature reaches 40 degrees, the slab bends and releases the contents of the reservoir.

Because the device can receive wireless signals, a wearable glucose monitor could also trigger the glucagon release. This isn’t dissimilar to existing automated insulin delivery systems that communicate with sensors, although none on the U.S. market are fully implantable.

“One of the key features of this type of digital drug delivery system is that you can have it talk to sensors,” said Krishnan. “In this case, the continuous glucose-monitoring technology that a lot of patients use is something that would be easy for these types of devices to interface with.”

The researchers implanted the device in diabetic mice to trigger glucagon release. Within less than 10 minutes of activating the release, blood sugar levels tailed off to bring the mice into the normal range and avoid hypoglycemia. With the mice, researchers kept the devices implanted for up to four weeks but aim to evaluate if they can extend that time up to at least a year.

“The idea is you would have enough doses that can provide this therapeutic rescue event over a significant period of time. We don’t know exactly what that is — maybe a year, maybe a few years, and we’re currently working on establishing what the optimal lifetime is. But then after that, it would need to be replaced,” Krishnan says.

Additionally, the researchers say that implantable devices can often have scar tissue develop around them and interfere. In the study, they saw that even when this happened, they could still trigger the drug release. They plan to conduct additional animal studies and begin clinical trials within the next three years.

The researchers also tested powdered epinephrine with the device. They found that within 10 minutes of drug release, epinephrine levels in the bloodstream became elevated and heart rate increased.

“It’s really exciting to see our team accomplish this, which I hope will someday help diabetic patients and could more broadly provide a new paradigm for delivering any emergency medicine,” says Robert Langer, the David H. Koch Institute Professor at MIT and an author of the paper.

pregnancy may increase the risk of type 1 diabetes in offspring, according to findings from a large prospective cohort study in Denmark published in the Journal of Epidemiology & Community Health.^1,2

Researchers evaluated data from 67,701 mother-child pairs enrolled in the Danish National Birth Cohort (DNBC) between 1996 and 2002. The study excluded mothers with pre-existing diabetes or implausible dietary reports. Maternal diet was assessed at approximately 25 weeks of gestation using a comprehensive 360-item food frequency questionnaire. An empirical dietary inflammatory index (EDII) score was calculated to quantify the inflammatory potential of each participant’s diet, with higher scores indicating a more pro-inflammatory dietary pattern.

Over an average follow-up period of 17.6 years, 281 children (0.42%) were diagnosed with type 1 diabetes. The investigators observed a statistically significant association between maternal EDII score and the risk of type 1 diabetes in offspring. Each 1 standard deviation increase in the EDII score was associated with a 16% increased hazard (adjusted HR, 1.16; 95% CI, 1.02–1.32) of type 1 diabetes diagnosis during childhood or adolescence.

“A low-grade inflammatory state secondary to an altered immune cell profile, which triggers pro-inflammatory pathways, is increasingly acknowledged as a critical early-life factor influencing offspring health,” the authors wrote.

The EDII score was derived using reduced rank regression and weighted based on associations between specific food group intake and circulating C-reactive protein (CRP) concentrations, using data from a similar Nordic cohort. Diets high in red or processed meats, low-fat dairy, pizza, French fries, margarine, and savory snacks were associated with higher EDII scores. Conversely, higher intake of alliums, tomatoes, whole grains, fruits, vegetables, tea, and dark meat fish contributed to lower (anti-inflammatory) EDII scores.

Higher EDII scores were also associated with other maternal characteristics such as younger age, higher body mass index (BMI), smoking beyond 12 weeks of pregnancy, lower alcohol consumption, shorter breastfeeding duration, and lower socioeconomic status. However, total energy intake did not significantly differ across EDII quintiles.

Importantly, the observed association between a pro-inflammatory diet and type 1 diabetes remained robust after adjusting for multiple potential confounders, including maternal age, BMI, smoking status, socioeconomic status, breastfeeding duration, and energy intake. Additional analyses indicated that gluten intake during pregnancy was also independently associated with elevated type 1 diabetes risk in offspring (HR per 10 g/day increase, 1.36; 95% CI, 1.09–1.71). In contrast, continued smoking during pregnancy was associated with a reduced risk (HR, 0.47; 95% CI, 0.31–0.72).

“Of particular note is the fact that three factors during mid-pregnancy, a pro-inflammatory dietary pattern, gluten, and smoking, seemed to independently predict the child’s risk of type 1 diabetes,” the authors stated. “This suggests that mid-pregnancy may be a critical period during which the fetus is particularly susceptible to maternal lifestyle influences in relation to the individual’s later risk for developing type 1 diabetes during childhood or adolescence.”

While the findings support the role of fetal programming in the development of autoimmune disease, the authors acknowledge limitations. As an observational study, causality cannot be established. Additionally, the child’s own diet postnatally was not assessed, and residual confounding from unmeasured factors remains possible.

Nevertheless, the study adds to a growing body of evidence linking maternal dietary exposures during pregnancy to long-term metabolic and immune outcomes in children. The authors concluded that further studies are warranted to replicate these findings and elucidate underlying biological mechanisms.

This article was originally published by our sister publication Contemporary OB/GYN.

References:

1. BMJ Group. ‘Inflammatory’ diet during pregnancy may raise child’s diabetes type 1 risk. Eurekalert. July 1, 2025. Accessed July 9, 2025. https://www.eurekalert.org/news-releases/1089224?

2. Rohina Noorzae, Bjerregaard AA, Thorhallur Ingi Halldorsson, et al. Association between a pro-inflammatory dietary pattern during pregnancy and type 1 diabetes risk in offspring: prospective cohort study. Journal of Epidemiology & Community Health. Published online July 1, 2025:jech-223320. doi:https://doi.org/10.1136/jech-2024-223320

Fourteen metabolites appeared to have a causal relationship with idiopathic pulmonary fibrosis (IPF) in a recent study.¹ The research represents the first time the association between these metabolites and the disease has been reported.

The investigators explained the metabolites they identified could be potential biomarkers of IPF and help lead to better understanding of how the disease develops. The study was published in The Clinical Respiratory Journal.

Understanding the pathogenesis of IPF is a critical public health problem in part because there is no cure for the disease and in part because diagnosis of IPF is burdensome, the authors noted.

“The diagnosis of IPF is based on a lung biopsy that indicates typical features and excludes other interstitial lung diseases in a multidisciplinary setup,” they wrote. The invasive, risky nature of lung biopsies creates a significant incentive to find biomarkers that might make it easier to diagnose the disease at an earlier stage.

Genomics and metabolomics have sparked an opportunity to do just that, the authors explained. Recent genome-wide association studies (GWAS) have identified metabolite-based associations with numerous disorders. They pointed to a Finnish study from 2022 which involved GWAS for more than 6000 men and led to the identification of hundreds of new association signals that may help scientists better understand the mechanisms behind diseases and disease-related traits.²

The investigators leveraged this technology to see whether they could better understand potential causal links between metabolites in patients’ blood and IPF. They obtained GWAS data for serum metabolites from an existing database and then used 2-sample Mendelian randomization (MR) to identify potential causal relationships between the metabolites and IPF.¹

Using inverse variance weighted (IVW) analysis, the investigators found 23 serum metabolites that were significantly associated with IPF. The list contained amino acids, carbohydrates, energy, lipids, peptides, xenobiotics, and 9 with chemical compositions that have not yet been distinguished.

The investigators next conducted a sensitivity analysis, which showed that 2 of the identified metabolites—the lipids epiandrosterone sulfate and n-butyl oleate—met the criteria for having a “robust” causal relationship with IPF. The other 12 metabolites can be considered to have “potential” causal associations with IPF.

“​​The results showed that higher levels of n-butyl oleate are causally associated with an increased risk of IPF and that higher levels of epiandrosterone sulfate play a protective role in the development of IPF,” the authors wrote.

The authors said their findings are an example of the ways in which the “swift development” of metabolomics is helping to clarify the pathophysiologic mechanisms underlying diseases like IPF.

“Our findings suggest that these metabolites can be regarded as useful biomarkers for IPF screening in clinical practice as well as presenting a reference direction for mechanism explorations in future cohorts and experimental research,” they wrote.

Still, the authors also noted certain limitations to their research. They said the patient population from which the GWAS database was derived was entirely of European descent. Therefore, they said the findings may not translate to other populations. In addition, they said the identification of 9 metabolites with unknown biological composition represents an important caveat to their findings, since it is not known how they might contribute to the disease’s pathogenesis.

References

1. Shi Y, Chen S, Zhou Z, Huang M, Li Y, Jing X. Causal effects between genetically determined human serum metabolite levels on the risk of idiopathic pulmonary fibrosis: a mendelian randomization study. Clin Respir J. 2025;19(6):e70087. doi:10.1111/crj.70087
2. Yin X, Chan LS, Bose D, et al. Genome-wide association studies of metabolites in Finnish men identify disease-relevant loci. Nat Commun. 2022;13(1):1644. Published 2022 Mar 28. doi:10.1038/s41467-022-29143-5

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Patients with rheumatoid arthritis (RA) and concomitant cancer face complex treatment decisions and often seek more detailed information and collaborative communication with their care teams, according to findings from a qualitative study.¹

The study involved interviews with 20 patients who had both RA and cancer and were treated at University of Texas MD Anderson Cancer Center outpatient clinics. These interviews explored patients’ beliefs, treatment preferences, and informational needs regarding RA therapy. Researchers found that although most patients relied on their physicians for guidance, they expressed a strong desire for more personalized information, particularly regarding the impact of RA therapies on cancer outcomes. The findings were published in BMC Rheumatology.

Fifteen of the 20 participants were women, and the mean (SD) age was 59.9 (9.8) years. Cancer types varied, with 4 patients each having breast cancer, melanoma, or blood cancer; 1 patient each had lung, colon, prostate, uterine, ovarian, thyroid, oropharynx, or neuroendocrine cancer. At the time of the interviews, 11 patients had no evidence of cancer, whereas 6 had metastatic cancer and 3 had local. The median time since diagnosis was 11 years for RA and 3.5 for cancer; 18 patients reported active RA at the time of their cancer diagnosis.

Prior to receiving their cancer diagnosis, the majority of patients had used conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) to treat their RA, followed by biologic DMARDs, with a few patients receiving targeted synthetic DMARDs and glucocorticoids. Following their cancer diagnosis, however, fewer patients were still on DMARDs and only 7 remained on glucocorticoids. The biggest numerical difference was seen with csDMARDs, dropping from 15 to 9 patients still receiving the treatment.

Gaps in Decision-Making Conversations

Discussions with both rheumatologists and oncologists were central to decision-making. Most patients said their concerns—such as how RA treatment might affect their cancer or how cancer treatment might worsen RA symptoms—were addressed in clinical conversations. However, some noted gaps in clarity, particularly around drug interactions, risk statistics, and timing for restarting RA therapies after cancer treatment. For example, a participant said their provider described everything “down to the tee,” but others reported their RA being left untreated for 5 years due to cancer, not having a conversation with their oncologist about the crossover with RA, and confusion around treatment options.

“He wasn’t able to provide any statistics as far as, if there’s an increased risk or a frequency of lymphoma due to taking [etanercept] because I’ve already had cancer,” one participant said about their care provider. “There were no statistics available on that.”

Patient Beliefs About RA and Cancer

Although evidence linking RA medication use to cancer progression remains limited and inconsistent, patients expressed mixed beliefs about the relationship.² Half did not believe their RA treatment directly impacted their cancer progression or risk, or at least that it couldn’t happen to them.¹ “I think about it affecting my body,” a patient clarified. “I mean, I know that the medications that they use to treat the RA could cause cancer, but it’s highly doubtful that it caused the type of cancer that I have.”

“I don’t have any fears or concerns about that,” another patient said, expressing confidence in their care team. “My doctors—the oncologist and my rheumatologist—kept in close contact with one another, and so I felt very safe and secure.”

Yet the other half voiced fears about cancer recurrence, weakened immunity, and drug interactions, especially concerning tumor necrosis factor inhibitors like etanercept and adalimumab, as well as steroids. Still, most patients said they would be willing to continue or start RA therapy even if its impact on cancer was uncertain. “I’m more concerned about the arthritis than I am the cancer,” one participant said. “I care about quality of life.”

Patients Value Collaboration

The decision-making process was largely collaborative, according to the study. Most patients said they shared treatment decisions with their physicians, and those who were not involved in the process said they would have liked a greater voice. Factors contributing to treatment decisions included prior experiences with RA medications, test results, risk-benefit conversations with providers, and—less common—information from websites or educational materials.

When asked about preferred ways to receive information, nearly all patients said they valued direct conversations with their rheumatologists and oncologists. Many also appreciated having written materials, videos, or visuals and were interested in peer testimonials, whereas others wanted to see numerical or probabilistic data on treatment risks.

“We discussed the steroid shots to help with the joint swelling and pain—and the muscle soreness, but I wanted to talk with my cancer doctor before I gave the rheumatologist an answer about using the steroids,” a patient shared. Another said it helped for their doctors to use plain language when explaining the science, and that “some doctors will just use doctors’ terms, but they actually broke it down,” calling it “medical science for dummies.”

The authors emphasized the need for consensus guidance that addresses the concerns of patients with RA and cancer. Recommendations developed by rheumatology and oncology societies together may help fill this gap.

References

1. Ruiz JI, Madramootoo ST, Lopez-Olivo MA, Singh N, Suarez-Almazor ME. Beliefs, preferences, and informational needs of patients with rheumatoid arthritis and concomitant cancer: a qualitative study. BMC Rheumatol. 2025;9(1):79. doi:10.1186/s41927-025-00526-7
2. Davio K. Biologics associated with lower overall risk of malignancy in patients with early RA. AJMC^®. January 2, 2018. Accessed July 9, 2025. https://www.ajmc.com/view/biologics-associated-with-lower-overall-risk-of-malignancy-in-patients-with-early-ra