Medical Bulletin 05/December/2025

One major worry has been whether creatine increases cancer risk due to compounds called heterocyclic amines (HCAs), which form when creatine reacts with amino acids and sugars during high-heat cooking. While HCAs can be mutagenic at very high levels in lab models, the amounts in cooked meat and creatine supplements are significantly lower.

In fact, human studies have found virtually no increase in harmful HCA production from creatine supplementation. Interestingly, some research even suggests creatine may slow tumor growth and boost cancer-fighting immune cells, although results vary by cancer type and model.

Kidney health concerns arose decades ago, often from isolated cases involving people with pre-existing renal disease or other risk factors. However, a large body of strong human evidence now shows no harmful effects of creatine on kidney function in healthy individuals, even at doses up to 20 grams daily for years.

Creatine may raise serum creatinine—a marker of kidney stress—but other measures confirm stable kidney filtration. For those with significant kidney problems, caution and close monitoring remain advisable.

Claims that creatine causes dehydration or muscle cramps during exercise are largely unsupported; controlled trials show no negative impact on hydration, thermoregulation, or cramping. Gastrointestinal side effects, like bloating or diarrhea, can occur, especially at high single doses, but splitting intake or taking moderate doses usually prevents these issues.

Creatine’s safety in pregnancy remains unproven—animal studies suggest benefits, but human data are lacking, so supplementation is not currently recommended during pregnancy.

Overall, this review affirms that creatine monohydrate is one of the safest, most effective supplements when used properly and stresses choosing high-quality, third-party tested products to avoid contamination risks.

REFERENCE: Longobardi, I., Solis, M.Y., Roschel, H., Gualano, B. (2025). A short review of the most common safety concerns regarding creatine ingestion. Frontiers in Nutrition 12. DOI: 10.3389/fnut.2025.1682746. https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2025.1682746/full

Study reveals fructose consumption may silently increase inflammation levels

Fructose, the sugar found in many sweetened drinks and processed foods, may do more harm than just add calories. Researchers at the University of Vienna, led by Ina Bergheim, discovered that even short-term fructose consumption causes immune cells called monocytes to become more sensitive to bacterial toxins, increasing inflammation in the body.

Their findings, published in Redox Biology, shed new light on how diet influences immune defenses and infection risk.

The team conducted two randomized studies with healthy adults, comparing the immune response after drinking fructose-sweetened beverages versus glucose-sweetened ones. They also isolated monocytes and ran cell culture tests to understand the biological mechanisms behind this sensitivity. Results showed that fructose—but not glucose—raised levels of Toll-like receptor 2 (TLR2) on monocytes.

TLR2 plays a crucial role in detecting bacterial toxins, and its increase made immune cells far more reactive to a toxin called lipoteichoic acid. This led to elevated release of inflammatory messengers like interleukin-6, interleukin-1β, and tumor necrosis factor-alpha—signals that can cause tissue damage if overproduced.

These findings reveal for the first time that fructose consumption primes the immune system in a way that might backfire by escalating harmful inflammation during infections. The researchers caution that even healthy people can experience this immune priming from brief periods of high fructose intake.

Broader implications concern people with metabolic disorders such as type 2 diabetes and fatty liver disease, who are already prone to inflammation and infection. Long-term fructose intake likely worsens these risks, and further research is needed to confirm these effects and explore preventive dietary strategies.

Overall, this study highlights a hidden danger in common dietary sugars: fructose not only affects metabolism but actively changes immune responses, potentially making infections worse. Reducing intake of sugary drinks and processed sweets emerges as a vital step toward healthier immune function and lowering infection risks for all.

REFERENCE: Raphaela Staltner, Katja Csarmann, Amelie Geyer, Anika Nier, Anja Baumann, Ina Bergheim. Fructose intake enhances lipoteichoic acid-mediated immune response in monocytes of healthy humans. Redox Biology, 2025; 85: 103729 DOI: 10.1016/j.redox.2025.103729

Study shows maternal fatty food aroma exposure increases offspring obesity risk

The development of obesity in children may begin before birth, influenced by factors as subtle as the smell of fatty foods experienced during pregnancy.

Researchers at the Max Planck Institute for Metabolism Research discovered that exposure to the scent of fatty foods, such as bacon, in pregnant mice—even when their diet was low in fat—can prime their offspring for a higher risk of obesity and insulin resistance later in life.

Their work, published in Nature Metabolism reveals how prenatal and early postnatal environments can shape long-term metabolic health.

In this study, pregnant mice were fed a healthy diet infused with the aroma of fatty foods. Despite the mothers’ unchanged metabolism, their offspring displayed heightened sensitivity to high-fat diets, gaining more weight and showing signs of impaired insulin signaling compared to controls.

Analysis of the offspring’s brains identified changes in critical regions involved in reward and hunger, notably the dopaminergic system linked to motivation and AgRP neurons controlling appetite and metabolism. These neural adaptations resembled those found in genetically obese mice, suggesting the scent exposure alone rewired brain circuits tied to energy balance.

Further experiments demonstrated that fetuses and newborn mice encounter these odors both in the womb and through breast milk. Remarkably, artificially stimulating the brain pathways activated by fatty food smells during early life was enough to trigger obesity in adulthood, indicating a powerful early-life programming effect.

This research shifts the focus from maternal obesity alone to the sensory environment shaping fetal development. While overweight mothers increase obesity risk in children, even lean mothers consuming diets with fatty aromas might unknowingly influence their offspring's future weight. Notably, only ingestion of these odor-containing diets—not mere exposure to smells—led to these changes.

Flavoring agents used in processed foods often include similar compounds found to replicate these effects, raising concerns about widespread additive use during pregnancy and lactation. The findings highlight the urgent need for further investigation into how maternal diet and aroma exposure may contribute to the global obesity epidemic and how modifying these exposures could promote healthier metabolic outcomes from the start of life.

This groundbreaking study expands our understanding of early obesity risk, emphasizing that a mother's dietary experience and its sensory signals profoundly shape her child’s lifelong health trajectory.

REFERENCE: Casanueva Reimon, L., et al. (2025). Fat sensory cues in early life program central response to food and obesity. Nature Metabolism. DOI: 10.1038/s42255-025-01405-8. https://www.nature.com/articles/s42255-025-01405-8