The need for such an approach arises because animals sharing a diagnosis or receiving the same recommendation may respond differently. A dog enrolled in a weight-management program, for example, may lose weight at a different rate from another dog given a controlled diet. Such variation can reflect genetics, age, body composition, activity, health status, feeding behavior, gut microbes and owner adherence. Population-level nutrient recommendations remain necessary for formulating complete and balanced diets, but they cannot capture every difference in energy requirements, nutrient use, metabolic phenotype or dietary tolerance. Precision nutrition is therefore presented as an extension of clinical nutrition, not a new diet category, and its defining feature is a measurable feedback loop linking initial characterization, intervention and subsequent reassessment.

Clinical phenotyping remains the core of that loop. Body weight, body-condition and muscle-condition scores, fecal quality, urinary signs, disease history and previous dietary responses are established, repeatable measures that veterinarians can connect directly to feeding decisions. A detailed dietary history adds information about food composition, portion size, moisture, treats, water intake, feeding frequency and owner adherence, although recall and record accuracy can limit precision. Laboratory data can characterize metabolic and organ status, but their value depends on the clinical question: serum phosphate, for example, directly informs dietary management in chronic kidney disease. Host characteristics such as species, breed, body size, life stage, reproductive status and activity add biological context, yet none is sufficient on its own to prescribe a diet.

Emerging technologies broaden the possible evidence base but face substantial barriers to routine use. Genomes, transcriptomes, proteomes, metabolomes, lipidomes and microbiome profiles can illuminate appetite regulation, inherited risk, host–microbiome interactions and diet-responsive metabolic changes. However, most molecular candidates have not been prospectively validated as predictors of dietary response. Microbiome results are especially sensitive to sampling method, recent diet, medication exposure, sequencing platform, bioinformatic pipeline and reference database, making a dysbiosis index or microbial signature unsuitable as a stand-alone prescription. Likewise, machine-learning models face small samples, heterogeneous study designs, limited longitudinal data and inadequate external validation. Smart feeders, connected scales and activity monitors may improve home monitoring, but device accuracy, data completeness and owner engagement determine whether their signals are dependable.

Obesity demonstrates how established measures can drive a response-guided cycle. Weight-management plans begin with controlled energy restriction, accurate accounting for treats, increased physical activity where appropriate and long-term follow-up. Body weight, body condition, muscle condition, food intake, activity and the weight-loss trajectory then determine whether the current allowance or satiety strategy should change. High-protein and high-fiber formulations have reduced voluntary food intake and improved satiety in dogs, while fermentable fibers may support satiety and microbial fermentation. Genetic findings involving POMC, MC4R and DENND1B indicate variation in appetite and energy-homeostasis pathways, but genotype-specific dietary effects have not been demonstrated. Probiotic and targeted microbial strategies remain investigational, including findings from mouse models that have not established efficacy in obese dogs or cats.

Chronic enteropathy shows why response classification can be more informative than a single diet label. In clinically stable dogs with chronic inflammatory enteropathy, dietary treatment trials are recommended first, and reported food responsiveness ranges from 38% to 89%. Hydrolyzed or novel-protein diets are considered when adverse reactions to dietary proteins are suspected; fiber-enriched diets are more relevant to large-bowel or fiber-responsive phenotypes; and low-fat diets may suit selected dogs with protein-losing enteropathy or intestinal lymphangiectasia. During a trial, stool quality, appetite, body weight, adherence and disease activity—using the CIBDAI or CCECAI in dogs—determine whether the intervention is working. Microbial dysbiosis, bile acids, short-chain fatty acids and candidate barrier markers may illuminate mechanisms or change during remission, but they remain supportive rather than prescriptive.

Kidney disease offers a similarly direct example through biochemical feedback. As renal function declines, phosphate regulation becomes increasingly difficult, and dietary phosphorus restriction is adjusted according to serum phosphate, concurrent calcium and CKD stage. Cats that develop ionized hypercalcemia during marked restriction can have that restriction attenuated while phosphorus control is maintained, demonstrating how a measured biochemical response can determine the next dietary step. Protein and energy intake should likewise be individualized to preserve appetite, body weight and lean mass. Experimental observations involving phosphorus source, calcium-to-phosphorus ratio, microbial metabolites and multi-omics responses identify plausible ways to characterize heterogeneity, but these findings do not yet replace stage-based recommendations or direct clinical monitoring.

Urolithiasis illustrates why one “urinary diet” cannot fit every urinary problem. Management depends on stone composition, urine pH, urine specific gravity, culture results, relative supersaturation where available, imaging and recurrence history. Sterile struvite stones in cats may be dissolved with magnesium-restricted, moderately acidifying diets that promote urine dilution, whereas infection-associated struvite requires control of the causative bacteria because diet alone is unlikely to dissolve the stones. Calcium oxalate stones cannot be dissolved nutritionally and are managed mainly through recurrence prevention, including increased urine volume and avoidance of excessive acidification. High-moisture feeding can increase feline urine volume and lower specific gravity and relative supersaturation for calcium oxalate and struvite. Microbiome and metabolomic studies may eventually refine risk assessment, but microbial interventions targeting crystal formation remain experimental.

Translation into practice will depend on evidence that new tools add value beyond conventional assessment. Diagnostic biomarkers classify disease or phenotype, predictive biomarkers estimate who is likely to respond, and monitoring biomarkers track change, relapse and the need for adjustment. Companion-animal research is closest to implementation through monitoring measures rather than molecular prediction: weight and condition scores for obesity, clinical activity and fecal outcomes for canine enteropathy, and urinary chemistry and stone characteristics for urolithiasis. Future studies will require standardized collections of host, dietary, clinical, sampling and longitudinal-response data, as well as controlled feeding trials, larger cohorts, independent validation and interpretable models. Canine and feline organoids may help screen mechanisms and prioritize candidates, but they cannot replace in-vivo dietary trials. In the near term, smart feeders and activity monitors may add useful longitudinal data, while multi-omics and AI remain decision-support technologies awaiting prospective proof of clinical benefit.

Subject of Research: Response-guided precision nutrition for dietary management in dogs and cats

Article Title: Precision nutrition in companion animals: a response-based framework linking dietary strategies, metabolic function, and measurable clinical outcomes

Article References: Du, X., Zhang, H., Tian, W., Chen, J., Wen, M., & Fan, W. (2026). Precision nutrition in companion animals: a response-based framework linking dietary strategies, metabolic function, and measurable clinical outcomes. Frontiers in Veterinary Science, 13, Article 1914947. https://doi.org/10.3389/fvets.2026.1914947

Image Credits: AI Generated

DOI: 10.3389/fvets.2026.1914947

Keywords: precision nutrition, dogs, cats, dietary response, clinical nutrition, gut microbiome, metabolomics, chronic kidney disease, urolithiasis, obesity, artificial intelligence, Precision

Insulin resistance is a central metabolic abnormality associated with type 2 diabetes, obesity and gestational diabetes, yet the review presents it as a systemic condition shaped by interactions among diet, microbial function and the host proteome rather than by a single organ, nutrient or microbial species. Proteins are the primary functional units of cells, and their abundance, modification and secretion can differ from what gene-expression measurements alone predict. Proteomics therefore offers a more direct view of cellular activity, including changes in mitochondrial oxidation, inflammation, oxidative stress and insulin signaling that may be missed by transcriptomic surveys.

This distinction is central to the review’s proposal that functional pathways, rather than taxonomic composition alone, should guide efforts to understand metabolic health. Skeletal muscle is especially relevant because the review states that it accounts for approximately 80% of insulin-stimulated glucose disposal. Evidence drawn largely from preclinical models and early-stage human investigations associates insulin resistance with reduced abundance of mitochondrial oxidation proteins and altered phosphorylation of complexes associated with ATP synthase.

These changes could impair cellular energy metabolism and potentially weaken insulin-signaling pathways. Reviews of obesity also report higher levels of proteins linked to inflammation and oxidative stress, including complement C3 and catalase, while proteomic meta-analyses in gestational diabetes have identified 262 candidate biomarkers, with prominent links to complement and coagulation pathways. The findings identify candidate mechanisms and markers rather than establishing a clinical test or treatment.

At the microbial end, metaproteomics identifies the proteins actually expressed by a gut community. Whereas 16S ribosomal RNA sequencing mainly indicates which organisms are present and their broad metabolic potential, metaproteomics captures active reactions under particular conditions, including exposure to diet, inflammation or medication. In insulin resistance and type 2 diabetes, the reviewed literature points to increased microbial representation of enzymes involved in starch and pectin processing, including beta-glucosidase and pectate lyase.

This pattern is consistent with greater fermentation of carbohydrates that may not otherwise be absorbed by the host, although the review does not establish that these enzymes alone cause metabolic dysfunction. The distinction between microbial potential and measured activity is one reason the authors argue for a nutrition-centered metaproteomic framework. Differences in the abundance of bacterial proteins may also influence the production of short-chain fatty acids and other metabolites that communicate with host tissues.

Butyryl-CoA dehydrogenase, for example, has been differentially expressed in insulin-resistant states in the evidence summarized by the authors, raising the possibility of effects on pathways such as PI3K and Akt. Childhood obesity and insulin-resistance studies further link reduced abundance of Akkermansia muciniphila with lower levels of circulating host proteins, including IGFBP1 and GP6, that participate in metabolic and immune functions. The metaproteome can also track disruption of the intestinal barrier through host structural proteins such as mucin-2 and immunoglobulin polypeptides associated with inflammation and permeability.

These observations are relevant to host–microbiome communication, but the review treats many of the individual associations as preliminary. Host–microbiome protein communication provides a mechanistic bridge between diet and insulin action, although the strength of the evidence varies considerably across proposed links. Recent host-focused analyses have annotated commensal bacterial proteins with links to human immune, endocrine, apoptotic and cancer-related pathways.

In vitro work reviewed by the authors found that type III secretion effectors from human-gut Pseudomonadota could enter human cells and alter nuclear factor kappa B signaling and cytokine secretion. Such findings show that microbial proteins can modify host molecular networks, but the evidence remains largely mechanistic or preclinical. The clearest protein-level connections to insulin resistance discussed in the review run through innate immune sensing, gut-barrier integrity and short-chain-fatty-acid receptor signaling rather than through a large catalogue of individually named microbial–human protein pairs.

Evidence also points to a bidirectional relationship between insulin signaling and the gut environment. Preliminary animal findings suggest that acute insulin resistance can itself increase gut permeability, disturb the microbiota and weaken antimicrobial defenses, indicating that insulin signaling may act as a gatekeeper of intestinal barrier integrity. Short-chain fatty acids provide another route between diet, microbes and host metabolism: in mice, the receptor GPR43 senses these microbial products and regulates adipose-tissue insulin signaling.

Together, these observations suggest a signaling web rather than one linear route. Nutrients alter microbial metabolism, microbial metabolites engage host receptors, and the resulting signals may influence insulin action in the intestine, liver, adipose tissue and skeletal muscle. However, most relationships beyond the GPR43–short-chain-fatty-acid axis remain dependent on animal models, as the review notes.

The review’s broader analysis also identifies a potential functional signature of insulin-resistant dysbiosis. Reanalysis of ten fecal metaproteomic datasets from healthy people revealed a proposed core metaproteome containing 182 shared microbial functions and 83 metabolic pathways, suggesting that a functional layer can persist despite variation in community composition. In parallel, human multi-omics research has associated elevated fecal monosaccharides in insulin-resistant participants with microbial carbohydrate metabolism and host inflammatory cytokines.

The authors interpret these findings as a possible “energy surplus” state involving both the microbiome and the host, but the supplied evidence does not identify the design of the multi-omics study or establish the direction of the relationships. The associations therefore cannot demonstrate that microbial carbohydrate processing causes either elevated fecal monosaccharides or insulin resistance. Translation of these signals into nutrition practice is constrained by substantial technical and study-design limitations.

Diet, medication and microbial diversity influence gut and fecal samples, while differences in storage, protein extraction and peptide preparation can alter the recovery of microbial proteins. Host proteins often predominate in gastrointestinal specimens and can obscure low-abundance microbial enzymes linked to glucose metabolism, inflammation or insulin signaling. Taxonomic differences and uneven extraction across cellular compartments introduce further bias.

Incomplete reference databases also complicate identification of proteins from poorly characterized gut organisms, while divergent bioinformatics pipelines weaken reproducibility. Nutritional interventions additionally suffer from short follow-up, inconsistent dietary assessment and incomplete control of obesity, physical activity and medication use. These limitations make it difficult to determine whether a detected protein is a reproducible biomarker, a response to diet or an artifact of sample processing.

The authors consequently present a metagenome-informed, nutrition-centered metaproteomic framework as a research direction rather than an established clinical tool. Their priorities include longitudinal sampling before and after dietary interventions in human cohorts, direct validation of microbial protein–host receptor interactions in human tissues, and individual-level integration of metaproteomic, metagenomic and metabolomic data to model dietary response. Combining these measurements with host inflammatory markers may eventually help identify people whose microbial functions predict a metabolic response to a specified diet.

Until then, the reviewed evidence supports biological plausibility and promising analytical tools, not a validated test for insulin resistance, a proven dietary protocol or a demonstrated clinical benefit. The central implication is that personalized nutrition may need to account for active microbial pathways as well as organisms, diet and host biology, with rigorous longitudinal studies needed to determine when that approach can move from a conceptual framework into practice.

Subject of Research: Nutritional metaproteomics for understanding diet-linked microbial and host proteins in insulin resistance

Article Title: Nutritional modulation of microbiome proteomics in insulin resistance

Article References: Dener, B., Gülal, S. İ., Bulut, M., Hızlı-Güldemir, H., Raposa, B., & Aǧagündüz, D. (2026). Nutritional modulation of microbiome proteomics in insulin resistance. Frontiers in Nutrition, 13, Article 1913314. https://doi.org/10.3389/fnut.2026.1913314

Image Credits: AI Generated

DOI: 10.3389/fnut.2026.1913314

Keywords: insulin resistance, gut microbiome, metaproteomics, proteomics, nutrition, short-chain fatty acids, host–microbiome crosstalk, gut barrier, precision nutrition, microbial proteins, Nutritional, modulation

Parkinson’s disease is the second most common progressive neurodegenerative disorder worldwide, defined neuropathologically by the loss of dopaminergic neurons in the substantia nigra pars compacta and the widespread accumulation of alpha-synuclein-containing Lewy bodies. Its pharmacological backbone remains dopamine replacement therapy, anchored by levodopa—the metabolic precursor of dopamine that crosses the blood–brain barrier and is converted into the depleted transmitter within the striatum. Levodopa is still the undisputed gold standard for symptomatic control, outperforming dopamine receptor agonists, MAO-B inhibitors, COMT inhibitors, and newer non-dopaminergic agents such as the adenosine A2A receptor antagonist istradefylline in controlling bradykinetic motor features. Yet the drug’s long-term performance is notoriously fragile. Within five to ten years of continuous exposure, between 40 and 80 percent of patients develop disabling motor complications, including predictable wearing-off phenomena and levodopa-induced dyskinesias.

The review’s central technical insight is that levodopa’s fragility is baked into its pharmacokinetics. The drug has a short plasma half-life of roughly two hours, undergoes extensive peripheral metabolism, and—critically—shares a saturable transport system with dietary large neutral amino acids, or LNAAs. Levodopa relies on the L-type amino acid transporter 1, LAT1, to cross both the intestinal epithelium and the blood–brain barrier. When a protein-rich meal floods the circulation with LNAAs derived from dietary protein digestion, those amino acids competitively inhibit levodopa transport at both barriers. The result can be an abrupt termination of antiparkinsonian efficacy without any change in peripheral drug concentration: high-protein meals reduce central levodopa influx, precipitating sudden OFF states and delayed ON responses. This competitive dynamic has direct human evidence behind it. Randomized and crossover studies dating back decades have shown poorer motor response with high-protein intake and improvement with low-protein or protein-redistribution strategies in susceptible patients.

Protein competition is only one of several food-driven mechanisms the review dissects. Gastric emptying rate is the second major determinant of oral levodopa disposition. High caloric density and elevated lipid content prolong gastric emptying by inducing shallow peristalsis and enhancing antral retention, delaying the intestinal transfer of co-administered drugs. In patients receiving controlled-release levodopa/carbidopa, postprandial dosing delayed levodopa appearance and the time to peak plasma concentration, reduced the six-hour area under the curve, and delayed the onset of motor response compared with premeal administration. Meal timing therefore emerges as one of the better-supported behavioral determinants of oral levodopa response, alongside protein quantity and distribution across the day. The review also notes that non-protein constituents contribute variably: coffee, dietary fiber, and vitamin C have been observed to favorably support levodopa bioavailability, while specific botanical substances such as fresh banana juice markedly impair systemic exposure. Notably, macronutrient manipulations like the ketogenic diet show minimal effect on plasma levodopa kinetics, underscoring that competitive amino acid inhibition and gastric transit remain the predominant dietary determinants of levodopa efficacy.

Perhaps the most striking mechanism involves the gut microbiome itself. Gut bacteria expressing tyrosine decarboxylase can metabolize levodopa into peripheral dopamine before mucosal uptake, prematurely consuming the drug and drastically reducing brain delivery. The classic example is Enterococcus faecalis, whose enzymatic activity dictates local drug breakdown within the intestinal lumen. Westernized dietary patterns—characterized by excessive saturated fats, ultra-processed foods, and refined sugars—reshape gastrointestinal architecture and disrupt gut microbiota homeostasis, fostering a pro-inflammatory microbial environment that may promote bacterial levodopa metabolism. The review is careful to distinguish direct clinical evidence from mechanistic plausibility here: the proposed sequence linking Western diet-induced dysbiosis, increased bacterial levodopa degradation, and poorer therapeutic response remains largely indirect until prospective studies specifically measure medication response in Parkinson’s patients.

The microbiota–gut–brain axis, or MGBA, extends this story from drug disposition to disease progression itself. In Parkinson’s disease, pathological dietary habits trigger dysbiosis characterized by a loss of anti-inflammatory, short-chain fatty acid–producing taxa and an overgrowth of pro-inflammatory pathobionts. This microbial imbalance compromises gut mucosal barrier integrity and increases intestinal permeability, facilitating systemic dissemination of lipopolysaccharides that provoke chronic low-grade neuroinflammation, microglial activation, and blood–brain barrier dysfunction. Retrograde transport of preformed alpha-synuclein aggregates via the vagus nerve—a core neural pathway of the MGBA—directly connects gut dysregulation to progressive dopaminergic neuron loss, supporting a gut-first hypothesis in disease pathogenesis. Altered microbial metabolism also disrupts synthesis of neuroactive molecules such as gamma-aminobutyric acid, tryptophan derivatives, and secondary bile acids acting through farnesoid X receptor and TGR5 pathways, impairing central appetite and satiety signaling while exacerbating hypothalamic–pituitary–adrenal axis dysregulation.

Eating behaviors themselves add another layer of complexity. Dopaminergic therapy, particularly dopamine receptor agonists such as pramipexole and ropinirole, can precipitate impulse-control disorders that include compulsive binge eating. Large or protein-rich meals during such episodes delay gastric emptying and increase LNAA competition with levodopa, contributing to erratic absorption and unexpected motor fluctuations. Conversely, restrictive eating and unstructured calorie restriction may compromise nutritional adequacy and alter drug-metabolizing enzymes such as CYP3A4 and UDP-glucuronosyltransferases, reducing central drug efficacy even as they promote autophagy. Irregular meal timing—frequent unscheduled snacking and inconsistent daily meal times—causes fluctuating gastric pH, erratic gastric emptying, and altered splanchnic blood flow, leading to unpredictable plasma drug concentrations. The review emphasizes that medication–meal schedules should be individualized according to levodopa formulation, nutritional status, gastrointestinal function, and observed clinical response rather than applying a universal fasting strategy.

Regional dietary patterns receive a nuanced treatment that resists simple generalization. The Mediterranean diet and its MIND variant are associated with favorable neurological and metabolic outcomes—higher adherence has been linked to lower odds of Parkinson’s disease, later age at onset, and lower prodromal disease probability in longitudinal studies—yet direct evidence that these patterns improve the efficacy or pharmacokinetics of specific anti-Parkinsonian medications remains limited. Traditional East Asian dietary components show mechanistic promise: soy protein combined with time-restricted feeding suppresses MAO-B activity and preserves dopaminergic neurons in Parkinsonian models, while green tea polyphenols such as epigallocatechin-3-gallate act as multitarget agents capable of inhibiting MAO-B and preventing alpha-synuclein aggregation, though high concentrations can competitively inhibit intestinal uptake transporters such as OATP1A2 and OATP2B1. Fiber-rich traditional African dietary patterns support intestinal microbial diversity and mucosal function, and resistant starch intervention has been shown to selectively enrich beneficial taxa such as Faecalibacterium species while alleviating motor and non-motor symptoms in Parkinson’s cohorts. Legume- and maize-based Latin American diets provide high concentrations of plant proteins and LNAAs that influence systemic amino acid pools, though direct evidence that these patterns specifically alter levodopa pharmacokinetics is lacking.

The review’s most consequential argument concerns clinical translation. Despite decades of pharmacokinetic insight, the absence of precision nutrition frameworks, protein-redistribution diets, targeted chronotherapeutic meal scheduling, and multidisciplinary nutritional support substantially hinders effective translation of basic science into practice. Observational clinical data reveal that improper timing relative to meals occurs in up to 15.7 percent of general oral drug administrations. The authors advocate a paradigm shift toward precision nutrition therapy that integrates multiomics datasets—genomics, metabolomics, metagenomics—with artificial intelligence, machine learning, and smart wearable systems to predict individual metabolic responses to specific nutrient timing and food combinations. Practical interventions include administering levodopa 30 to 60 minutes before meals or two hours after, restricting protein during daytime and consuming it primarily at dinner, and establishing standardized daily meal schedules. Targeted microbiome restoration through prebiotics, probiotics, and fecal microbiota transplantation represents a promising non-invasive avenue to suppress neuroinflammation and stabilize drug pharmacokinetics. Ultimately, the review positions diet not as a peripheral lifestyle consideration but as an essential non-pharmacological pillar of Parkinson’s care—one that could stabilize drug absorption, minimize motor fluctuations, and potentially mitigate disease progression when aligned with individual drug absorption characteristics through data-driven, personalized protocols.

Subject of Research: health medicine

Article Title: Effects of eating behavior patterns and dietary habits on the therapeutic efficacy of Parkinson’s disease medications: from phenomena, mechanisms to clinical applications

Article References: Ye, J., Zhang, S. J., Guan, J., Shen, Z.-H., Wang, J., Yang, R., Huang, M., Li, Z.-M., Lin, Y., Gan, H., Wu, S., Wang, Y., & Yang, K. (2026). Effects of eating behavior patterns and dietary habits on the therapeutic efficacy of Parkinson’s disease medications: from phenomena, mechanisms to clinical applications. Frontiers in Nutrition, 13, Article 1969279. https://doi.org/10.3389/fnut.2026.1969279

Image Credits: AI Generated

DOI: 10.3389/fnut.2026.1969279

Keywords: Parkinson's disease, levodopa, nutrition, pharmacokinetics, gut microbiome, precision nutrition, LAT1 transporter, protein redistribution, Mediterranean diet, microbiota-gut-brain axis, Effects, eating

The changes that accompany microbial aging are not merely a passive reflection of growing older. Scientists increasingly view them as active drivers of health trajectories in later life. Alterations in the gut microbiome can influence cardiometabolic health, cognitive function, and immune responses, underscoring the microbiome’s critical role in healthy aging. Understanding these dynamics offers a promising avenue to enhance quality of life for older adults by identifying how the microbiome can be modulated through diet, prebiotics, and probiotics, as well as through physical activity, medications, and other modifiable lifestyle and environmental exposures.

One of the central concepts in this field is dysbiosis, the microbial imbalance that characterizes many age-related conditions. Research has linked dysbiosis to frailty, sarcopenia, neurodegenerative diseases, and cardiovascular issues, painting a picture in which a disturbed microbial ecosystem may accelerate or amplify the physiological declines of aging. The therapeutic implication is profound: developing microbiota-targeted therapeutics that restore microbial balance could ameliorate aging-related health declines, offering interventions that work with the body’s resident microbes rather than around them.

The exploration of gut-organ axes has further highlighted how deeply gut health is intertwined with systemic well-being. The gut-brain axis, in particular, has captured scientific and public attention because it suggests that the state of the intestinal microbiome can directly influence neurological well-being. Interventions aimed at the microbiome could therefore influence other aspects of health in older adults, potentially affecting cognitive aging, cognitive decline, and dementia. This systems-level perspective transforms the gut from an isolated digestive organ into a signaling hub whose microbial products reach distant tissues through metabolites, immune mediators, and neural pathways.

Looking ahead, researchers anticipate that the field may uncover new microbiome biomarkers of aging that can be used to predict health outcomes. Such biomarkers would carry real clinical weight only where they are replicated across independent longitudinal cohorts and tested in intervention studies, a rigorous standard that distinguishes robust predictors from statistical noise. Once validated, these biomarkers could enable personalized nutritional and therapeutic strategies tailored to individual microbiomic profiles, moving geriatric medicine toward precision approaches in which a patient’s microbial signature informs dietary recommendations, drug choices, and preventive care.

The technological backbone of this progress lies in advanced multi-omics methods. Integrating microbiome research with metagenomics, metatranscriptomics, metabolomics, and other multi-omics approaches could lead to groundbreaking insights into the complex interactions between gut microbiota and systemic aging processes. Metagenomics reveals which microbial genes are present in a community, metatranscriptomics shows which of those genes are actively expressed, and metabolomics captures the chemical conversation between microbes and host cells. Together, these layers of data can expose the mechanisms by which microbial metabolites and host-microbe interactions underlie aging phenotypes, from inflammation and insulin resistance to muscle wasting and cognitive change.

The scope of the collection reflects the breadth of microbiome science in geriatrics. Topics of interest include changes in gut, oral, respiratory, and skin microbiome populations in later life and their health outcomes; dysbiosis in aging populations; the gut-brain axis and cognitive decline; microbiome-targeted therapeutics for age-related diseases; and probiotics, prebiotics, synbiotics, postbiotics, and fecal microbiota transplantation in older adults. Diet, nutrition, and diet-microbiome interactions, including dietary patterns and precision nutrition approaches, feature prominently, as does the microbiome’s role in frailty, sarcopenia, physical function, and healthy aging trajectories.

Additional themes extend the field’s reach into cardiometabolic health and multimorbidity in later life, microbial metabolites and host-microbe mechanisms underlying aging phenotypes, and the effects of medications, polypharmacy, and environmental exposures as determinants of the aging microbiome. The collection also emphasizes the microbiome across geographically, culturally, and socioeconomically diverse aging populations, including long-term care and hospital settings, recognizing that microbial communities are shaped not only by biology but by where and how people live. Guest editors for the collection include Liliana Baptista of the University of Coimbra in Portugal, whose research investigates the role of the gut microbiome and gut-derived metabolites in modulating functional and metabolic outcomes under pathological conditions; Jiaqi Ni of Universitat Rovira i Virgili in Spain, whose work integrates nutritional epidemiology, microbiome science, multi-omics, and precision nutrition within large-scale population studies and landmark Mediterranean diet trials such as PREDIMED and PREDIMED-Plus; and Tsutomu Takeda of Juntendo University in Japan, whose interests span gut microbiota, disorders of gut-brain interaction, frailty, sarcopenia, and gastrointestinal health in older adults.

For clinicians and researchers, the message is that the microbiome has moved from the margins of geriatric science to its center. A disturbed microbial ecosystem is now implicated in conditions that define late-life disability, and the tools to study it have matured into technologies capable of resolving microbial function at the level of genes, transcripts, and metabolites. The next phase of the field will test whether microbial signatures can predict who will remain resilient and who will decline, and whether targeted interventions can bend those trajectories toward health.

For older adults and the people who care for them, the practical stakes are equally clear. Modifiable factors such as diet, physical activity, and medication use are already known to shape the aging microbiome, and validated microbial biomarkers could eventually allow clinicians to personalize nutritional and therapeutic strategies for each patient. As submissions to the collection make their way through the journal’s peer-review process, with reviewers and editors required to declare competing interests, the field is positioned to translate microbial science into strategies that preserve function, cognition, and metabolic health in the sixth decade of life and beyond.

Subject of Research: The role of microbiome changes in healthy aging and age-related disease

Article Title: Aging and the microbiome

Article References: Aging and the microbiome. Original publication (Bibliographic details unavailable.)

Image Credits: AI Generated

DOI: Not provided

Keywords: aging, microbiome, dysbiosis, gut-brain axis, frailty, sarcopenia, probiotics, precision nutrition, multi-omics, BMC Geriatrics, scientific research

Culinary medicine is defined in the review as an evidence-based field that combines the art of food and cooking with the science of medicine. Unlike general culinary education, which teaches food-preparation skills without necessarily connecting them to health outcomes, culinary medicine links hands-on cooking to explicit nutritional and clinical goals. Typical program components include practical food preparation, recipe modification, meal planning, food-label interpretation, grocery shopping strategies, portion management, and the selection of cooking methods. Some programs also incorporate goal setting, self-monitoring, problem-solving, and discussion of clinical cases. Crucially, the authors note that a defining characteristic of a genuine culinary medicine intervention is that it is delivered by healthcare professionals—physicians, nurses, or registered dietitians—rather than by chefs alone. The field emerged partly in response to the long-recognized inadequacy of nutrition education in medical training, and its scope has since expanded from health-professional education into patient care and community health promotion.

The review situates culinary medicine within a wider ecosystem of food-focused approaches. Medical nutrition therapy, the individualized disease-specific nutrition care provided by qualified nutrition professionals, establishes what a patient must achieve through assessment, diagnosis, intervention, and monitoring. Food-is-Medicine interventions, including medically tailored meals, medically tailored groceries, and produce prescriptions, primarily improve access to health-promoting foods. Precision nutrition identifies individualized dietary strategies based on metabolic and other personal characteristics. Yet, as the authors argue, each of these approaches stops short of the practical competencies required to select, plan, prepare, and consume meals consistent with individualized recommendations. Culinary medicine is proposed as the practical interface that completes the chain: general culinary education provides foundational skills, medical nutrition therapy defines therapeutic targets, Food-is-Medicine programs supply access, precision nutrition individualizes the strategy, and culinary medicine translates all of it into feasible meal-level behavior.

The potential health effects of this approach operate through interrelated behavioral and physiological pathways. On the behavioral side, the review frames culinary education within social cognitive theory, in which self-efficacy—the confidence to perform a behavior—is a principal determinant of change, acquired chiefly through mastery experience. Hands-on cooking classes are structured to generate exactly such experiences: participants observe a technique, perform it under guidance, receive immediate feedback, and then eat the result. Repeated successful preparation of simple meals reduces perceived difficulty and builds confidence in handling unfamiliar foods and modifying recipes. The authors emphasize that teaching a flexible framework—such as combining a whole grain, a protein source, vegetables, and a minimally processed sauce—transfers better to real life than a single fixed recipe, and can be adapted to available foods, cultural preferences, and dietary restrictions.

Perhaps the most technically intriguing section of the review concerns how cooking methods themselves alter the biochemical properties of food. Moderate heating can unfold protein structures and expose peptide bonds to digestive enzymes, improving protein digestibility in some foods. In contrast, high-temperature dry-heat techniques such as prolonged grilling, roasting, baking, and frying promote Maillard reactions, lipid oxidation, and the formation of advanced glycation end products, compounds linked to metabolic and inflammatory processes. Moist-heat methods like boiling, steaming, stewing, and poaching generally generate fewer of these compounds under comparable conditions. The review highlights a recent randomized crossover study in which lower-advanced-glycation-end-product cooking methods reduced circulating measures of these compounds and improved lipid profiles compared with higher-exposure methods. Intense dry-heat cooking of animal protein can also produce heterocyclic aromatic amines, and large prospective U.S. cohorts have associated frequent high-temperature meat cooking with higher risk of type 2 diabetes, independent of total meat intake—although the authors caution that residual confounding means causality remains unestablished.

Starch digestibility offers another mechanistic pathway. Cooking disrupts starch granules and promotes gelatinization, which generally increases enzymatic accessibility and postprandial glucose availability. However, when cooked starch cools, its chains reassociate through retrogradation, generating resistant starch that resists small-intestinal digestion. This resistant starch reaches the colon, where the gut microbiota ferment it into short-chain fatty acids—acetate, propionate, and butyrate—that support colonocyte energy metabolism, intestinal barrier integrity, immune regulation, and host metabolic signaling. Consistent with this chemistry, one clinical study found that white rice cooked, refrigerated, and then reheated produced a lower glycemic response than freshly cooked rice. Such findings give culinary technique a plausible role in glycemic management that goes far beyond simply choosing which foods to eat.

Food combinations matter as well. The review cites human intervention research showing that tomatoes cooked with olive oil significantly increased plasma lycopene concentrations compared with tomatoes cooked without oil, and that adding avocado or avocado oil to vegetable-based meals increased absorption of carotenoids including lycopene, beta-carotene, and lutein. Mineral absorption is similarly context-dependent: ascorbic acid enhances non-heme iron absorption by reducing ferric to ferrous iron and forming soluble complexes in the intestinal lumen, supporting practical pairings such as legumes with tomatoes or leafy greens with citrus juice. Vinegar or acetic acid consumed with carbohydrate-rich meals has been shown in clinical trials and meta-analyses to attenuate postprandial glucose and insulin responses. Within the precision nutrition framework the authors propose, precision nutrition determines what should be modified, while culinary medicine provides strategies for how those modifications are enacted at the level of the meal.

The clinical evidence, however, comes with important caveats. The review summarizes numerous intervention studies, including a Canadian phase 2 trial of meal-preparation training in type 2 diabetes that reported modest reductions in weight and HbA1c, a Mediterranean-diet-based teaching kitchen trial showing improvements in diastolic blood pressure and total cholesterol, a twelve-month remote culinary medicine trial demonstrating net weight loss of over four percent, and virtual programs improving cooking self-efficacy and diabetes self-management in low-income populations. Yet across studies, improvements in cooking confidence, self-efficacy, dietary behavior, and self-management are reported far more consistently than sustained changes in body weight, glycemic control, blood pressure, lipid profiles, or disease incidence. The literature is constrained by small samples, short follow-up periods, heterogeneous intervention components, non-randomized designs, reliance on self-reported outcomes, and self-selection bias among motivated participants. The authors are careful to state that cooking competence should be regarded as a behavioral mediator of potential benefit rather than a surrogate for clinical benefit.

Implementation faces further structural obstacles. The review notes conceptual imprecision in commonly invoked terms such as real food and home cooking, pointing out that home-prepared meals can be high in sodium, added sugars, saturated fat, or energy density—it is cooking method and ingredient selection, not home preparation per se, that determines biochemical exposure. Physical teaching kitchens entail significant costs in facilities, equipment, food procurement, trained personnel, and protected time, none of which are routinely reimbursed. Equity concerns loom large: culinary medicine presupposes time, cooking skill, kitchen access, food literacy, and financial resources that are least reliably available to the populations bearing the greatest burden of diet-related disease, who may simultaneously face food insecurity, unstable work schedules, and inadequate cooking facilities. Recommending daily fresh-ingredient cooking to such populations risks increasing burden rather than improving health.

Looking forward, the authors argue that culinary medicine should be evaluated as an implementation strategy embedded within nutrition care rather than a stand-alone cooking program. They call for programs that define core components and professional roles—physicians identifying clinical priorities, dietitians setting individualized goals, culinary professionals translating those goals into feasible meals, and community workers supporting access and retention—while adapting delivery to cultural, economic, functional, and food-access contexts through community co-design. Future trials, they contend, should measure the full causal pathway from culinary competencies to sustained dietary behavior to clinically meaningful outcomes such as glycemic control, blood pressure, and lipids, with extended follow-up to confirm durability. If the field can meet these standards, culinary medicine may fulfill its promise as a rigorous bridge between nutritional science and the everyday act of putting a meal on the table—turning dietary prescriptions from abstract targets into dinners people can actually cook, eat, and sustain.

Subject of Research: Culinary medicine as an interdisciplinary field integrating clinical nutrition, precision nutrition, and food preparation skills into medical practice

Article Title: Culinary medicine as a new paradigm integrating clinical nutrition and medical practice: a narrative review

Article References: Park, H. G., & Lim, H. (2026). Culinary medicine as a new paradigm integrating clinical nutrition and medical practice: a narrative review. Frontiers in Nutrition, 13, Article 1963264. https://doi.org/10.3389/fnut.2026.1963264

Image Credits: AI Generated

DOI: 10.3389/fnut.2026.1963264

Keywords: culinary medicine, clinical nutrition, precision nutrition, medical nutrition therapy, Food-is-Medicine, cooking self-efficacy, advanced glycation end products, resistant starch, teaching kitchens, dietary behavior, type 2 diabetes, narrative review

The scale of the problem is growing. Pediatric-onset inflammatory bowel disease is rising in incidence worldwide, and children tend to carry a more aggressive disease phenotype than adults, facing decades of potential inflammation, hospitalization and surgery. Biologic agents such as infliximab and adalimumab have transformed outcomes, but long-term cohort data show that a substantial fraction of children lose response over time, and drug approval pathways for young patients remain constrained. Against this backdrop, nutritional therapy occupies a unique position: it is the only induction strategy recommended by European guidelines as first-line for pediatric Crohn’s disease that simultaneously improves inflammation, supports growth and avoids pharmacological side effects. The catch, as the review emphasizes, is that remission rates vary considerably across studies depending on research design, treatment population and how remission is defined in the first place.

The authors frame the field’s central challenge as a transition away from a one-treatment-suits-all strategy toward a tailor-made, precision-based approach. In principle, a clinician armed with a reliable treatment-responsiveness phenotype could match each child to the therapy most likely to work before the first formula feed or the first injection. The benefits would cascade through the healthcare system: fewer months spent on ineffective regimens, less exposure to unnecessary immunosuppression, earlier escalation for the children who need it, and reduced lifetime costs of a disease whose economic burden is among the highest of any chronic inflammatory condition. The obstacle is that, despite decades of research, the evidence base for definitive predictors of response to nutritional therapy remains insufficient, a conclusion the review states plainly rather than glossing over.

What does the existing evidence actually suggest? Among the most consistently reported signals are early clinical improvement and a reduction in faecal calprotectin, the stool-based marker of intestinal inflammation that has become a workhorse of pediatric IBD monitoring. Serial measurements during exclusive enteral nutrition have been shown to track with disease activity and treatment response, and falling calprotectin concentrations during therapy have been linked to better outcomes and to the prediction of clinical relapse after treatment ends. Early mucosal healing, visible at endoscopy in newly diagnosed children, is also associated with improved long-term outcomes. But the picture is not clean: at least one prospective pediatric study concluded that faecal calprotectin is not a clinically useful marker for predicting early non-response to exclusive enteral nutrition, and the review notes that the rapid fall in calprotectin seen during treatment is lost quickly once food is reintroduced. Timing, it seems, matters as much as the marker itself.

Disease location offers another thread of evidence, though a tangled one. Classic work from the early 2000s suggested that colonic Crohn’s disease without ileal involvement responds less well to enteral nutrition, hinting that the intestinal segment where inflammation resides shapes the therapy’s effectiveness. Later studies complicated this view, with some reporting that disease phenotype does not influence clinical remission at all, and others examining whether specific scoring systems can predict short- and long-term mucosal healing across different gastrointestinal segments. The review also highlights practical determinants that have nothing to do with biology: adherence. Real-world studies of children starting exclusive enteral nutrition have identified factors associated with higher adherence and better response, and parent-perspective research underscores how difficult the diet’s social and psychological demands can be for families. Whether the formula is polymeric or elemental, and whether it is delivered orally or by tube, appears to have little effect on outcomes, which at least simplifies one clinical decision.

The most scientifically vibrant frontier, and the one the review treats as the field’s future horizon, lies in the gut microbiome. Nutritional therapy works, at least in part, by reshaping the microbial communities that drive intestinal inflammation, and several prospective studies have now reported microbial signatures that predict response. Children whose baseline gut communities contain particular bacterial taxa and functional profiles have been shown more likely to achieve sustained remission after exclusive enteral nutrition, and early shifts in microbial community structure during treatment have been associated with durable remission. Metabolomic analyses add another layer, with gut metabolome signatures alongside microbiota profiles predicting response in prospective pediatric cohorts. Even a child’s pre-diagnosis diet has been found to correlate with the microbiome and to predict response to enteral nutrition, suggesting that long-term dietary habits may prime the gut environment for success or failure before therapy even begins.

These findings align with a broader conceptual shift captured in a 2024 position paper from the European Society for Paediatric Gastroenterology, Hepatology and Nutrition, which called for precision nutrition in pediatric IBD. The logic is compelling: if exclusive enteral nutrition remodels the microbiome and its metabolic output, then the composition of a child’s starting microbial community should, in theory, determine how far that remodeling can go. Multidisciplinary consensus work on microbiome-based biomarkers published in The Lancet Microbe has begun to define the standards such biomarkers would need to meet before clinical deployment, and the review argues that integrating clinical data with multiomic information, spanning genomics, microbiomics and metabolomics, into a unified decision-making framework could eventually enable genuinely personalized treatment selection. Machine learning approaches developed for targeted therapies elsewhere in medicine offer a template for how such heterogeneous data streams might be combined.

The authors are careful, however, to temper enthusiasm with rigor. Anticipating treatment response, they write, transcends simple stratification based on clinical characteristics, meaning that no checklist of age, disease location, severity or laboratory values currently suffices to forecast outcome. The literature they surveyed provides insufficient evidence for definitive predictors, and many of the most promising microbiome and metabolome studies are small, single-center and retrospective, vulnerable to the confounding and overfitting that plague biomarker research. The path forward, they suggest, involves prospective validation of candidate predictors in large, well-phenotyped cohorts, harmonized definitions of remission and response, and ultimately the kind of integration of clinical and multiomic data that precision medicine initiatives in other fields have begun to demonstrate at scale.

For families facing a new diagnosis, the practical message of the review is one of cautious optimism. Nutritional therapy remains a first-line, evidence-based option, whether as exclusive enteral nutrition or as partial enteral nutrition combined with the Crohn’s disease exclusion diet, and randomized trial evidence shows the dietary approach can induce rapid, sustained remission in children. Early clinical improvement and falling faecal calprotectin during the first weeks of treatment are reasonable indicators that the therapy is working, and clinicians can use them to guide decisions about continuing or switching. What the field cannot yet do is predict, before the first sip of formula, which child will respond. Closing that gap, the review concludes, may be a small but crucial step toward individualized therapy for every child with Crohn’s disease, transforming a treatment that sometimes works brilliantly into one that works brilliantly for the right patients, chosen in advance.

Subject of Research: Predictors of response to nutritional therapy in pediatric Crohn's disease

Article Title: Current perspectives and future horizons in predicting response to nutrition therapy in children with Crohn’s disease – a narrative review

Article References: Krawiec, P., & de Ridder, L. (2026). Current perspectives and future horizons in predicting response to nutrition therapy in children with Crohn’s disease – a narrative review. Pediatric Research. https://doi.org/10.1038/s41390-026-05559-3

Image Credits: AI Generated

DOI: 10.1038/s41390-026-05559-3

Keywords: Crohn's disease, exclusive enteral nutrition, pediatric IBD, precision nutrition, faecal calprotectin, gut microbiome, Crohn's disease exclusion diet, personalized medicine, multiomics, biomarkers, mucosal healing, narrative review

The biological rationale rests on a century-old observation. Otto Warburg first showed that cancer cells preferentially burn glucose through aerobic glycolysis, converting it to lactate even when oxygen is plentiful—a metabolic reprogramming now recognized as a hallmark of cancer. This dependence on external nutrients makes tumors vulnerable to changes in nutrient supply, and the review catalogs a striking list of examples. Many cancer cells cannot synthesize methionine and must obtain it from the diet, a dependency known as the Hoffman effect. Arginine is essential for tumor growth in high-grade neuroendocrine carcinoma of the bladder, serine and glycine fuel intestinal tumors, and the glutamate transporter ASCT2 supports growth in gastric, triple-negative breast, and prostate cancers. Lipids matter too: the fatty acid receptor CD36 marks aggressive metastasis-initiating cells in breast, ovarian, and oral cancers, and dietary palmitic acid can enhance their metastatic potential.

Diet also shapes the hormonal and immune environment in which tumors grow. Elevated blood glucose and amino acids activate growth factor signaling through insulin, insulin-like growth factor 1, and downstream pathways such as PI3K/AKT/mTOR and Ras/MAPK, promoting cell survival and proliferation. Adipose tissue converts androgens to estrogen, linking obesity to tumor growth and angiogenesis. Meanwhile, the gut microbiome—directly sculpted by diet—maintains energy homeostasis, mucosal barriers, and immunity, and emerging evidence suggests it modulates responses to immunotherapy. In one prospective study of 128 melanoma patients treated with anti-PD-1 antibodies, higher dietary fiber intake was associated with better immunotherapy response and longer progression-free survival, while probiotic supplements were linked to reduced microbiome diversity and poorer outcomes. Even more striking, a phase II pilot trial of fecal microbiota transplantation in 15 patients with metastatic melanoma refractory to anti-PD-1 therapy saw six patients achieve renewed partial or complete responses after rechallenge.

What does the clinical evidence actually show about diet and prognosis? The picture is nuanced. In a study of 1,011 patients with stage III colon cancer, red and processed meat intake did not significantly reduce or increase recurrence or death risk in multivariable analysis, with hazard ratios of 0.84 for unprocessed red meat and 1.05 for processed meat. But other dietary signals are stronger. Among 1,149 patients with metastatic colorectal cancer, higher intake of specific fatty acids was associated with lower all-cause mortality, and patients in the highest quartile had a lower risk of cancer progression or death than those in the lowest. A validated model incorporating diet and lifestyle variables alongside clinicopathologic factors improved prognostic accuracy for stage III colon cancer, particularly for patients at higher baseline risk. Most dramatically, a longitudinal cohort of 1,340 patients with high-risk breast cancer found that those who adhered to lifestyle-related cancer prevention guidelines had a 37 percent lower risk of recurrence and a 58 percent lower risk of mortality—though only about 15 percent of patients fully adhered to all recommendations.

Diet may also blunt the toxicities of chemotherapy itself. The long-standing practice of prescribing neutropenic or low-bacterial diets to prevent infections during chemotherapy-induced immune suppression has now been largely debunked. A Cochrane systematic review of five randomized trials involving 350 patients found no clear benefit in infection prevention, and individual trials in hematologic malignancies, pediatric oncology, and acute myeloid leukemia all showed similar infection rates between restrictive and standard diets. Accordingly, the American Society of Clinical Oncology explicitly does not recommend neutropenic diets for infection prevention, citing insufficient scientific evidence. For other side effects, gentler food-based strategies show promise: a systematic review of 17 trials found that dietary counseling, peppermint drinks, chamomile, ginger with protein, and bland colorless diets significantly reduced chemotherapy-induced nausea and vomiting, though evidence quality was generally low. Cognitive health may benefit as well—one prospective study of 80 patients found that higher diet quality, particularly greater monounsaturated and lower saturated fat intake, was associated with smaller declines in cognitive performance during chemotherapy.

The most buzzed-about intervention is the fasting-mimicking diet, a plant-based, low-amino-acid regimen designed to mimic the metabolic effects of fasting without full deprivation. In mouse xenograft models of breast cancer and melanoma, the diet suppressed HO-1 expression, increased tumor-infiltrating lymphocytes, and slowed tumor growth. The phase II DIRECT trial tested it in 131 patients with early HER2-negative breast cancer undergoing neoadjuvant chemotherapy: patients followed a protocol limiting energy to 1,200 kilocalories on day one with a 3.5:1:2 carbohydrate-to-protein-to-fat ratio, then 200 kilocalories of carbohydrates on days two through four, followed by a recovery diet. The intervention proved feasible and safe, reducing grade III vomiting and neutropenia, lowering IGF-1 and high-sensitivity C-reactive protein, and producing biological signals consistent with improved chemosensitivity. A subanalysis of a related phase Ib trial even reported exceptional tumor responses in a subset of patients with hard-to-treat cancers, including KRAS-mutant colorectal cancer and metastatic triple-negative breast cancer, when the diet was combined with standard therapies.

Importantly, the review does not oversell these results. Quality-of-life scores measured with EORTC questionnaires declined in both fasting-mimicking diet and control groups during treatment, returning to baseline six months after surgery, and a systematic review found no difference in severe neutropenia or adverse events. With few studies conducted, the authors caution that firm conclusions remain out of reach. They also emphasize that dietary interventions cannot be offered universally given limited medical resources, so identifying who needs them most is critical. A Chinese study of ovarian cancer patients found malnutrition rates of roughly 12 to 19 percent across chemotherapy cycles, with C-reactive protein levels significantly affecting quality of life—suggesting that serum biomarkers should complement body mass index in screening. Another study of 293 breast cancer patients showed that nutrition literacy, self-efficacy, and social support strongly influenced dietary practice, pointing to specific patient profiles—obesity, rural residence, low education, multiple chemotherapy cycles—that should be prioritized for intervention.

Looking forward, the review maps out a pipeline of clinical trials pairing diets with drugs, most commonly combining fasting-mimicking diets, calorie restriction, ketogenic diets, or amino acid restriction with conventional chemotherapy, particularly in breast cancer. But the more provocative frontier is combining diet with molecular-targeted agents. Because PI3K inhibitors trigger feedback loops that raise insulin and glucose, pairing them with very low-carbohydrate or fasting-mimicking diets could enhance efficacy in PIK3CA-mutated breast and endometrial cancers. Preclinical work suggests serine- and glycine-depleted diets might synergize with PHGDH inhibitors in tumors with elevated serine synthesis, while low-fat diets could complement de novo lipogenesis inhibitors in prostate and liver cancers, and low-sugar diets might pair with ketohexokinase inhibitors in gastrointestinal malignancies. Each pairing is grounded in the specific metabolic substrate a tumor depends on, turning the diet into a pharmacologic partner rather than a general wellness measure.

The authors also see digital health tools as the missing infrastructure for making precision nutrition practical. Mobile applications, wearable devices, and digital coaching platforms could enable real-time collection of metabolic and dietary data, allowing clinicians to dynamically adjust personalized nutrition plans as a patient’s physiology shifts through treatment. Such platforms could also improve adherence to demanding protocols like fasting-mimicking diets or amino acid restrictions by providing immediate feedback and support. As healthcare costs rise and patients increasingly seek agency in their own care, the review’s central proposal—that integrating precision nutrition with molecular precision medicine constitutes the true future of personalized oncology—offers a compelling, testable vision. Whether the clinic can deliver on it will depend on the next generation of rigorously designed trials now underway.

Subject of Research: Precision nutrition and dietary interventions as adjuncts to cancer therapy

Article Title: Precision Nutrition as the Concept of Dietary and Nutritional Interventions for Patients With Malignancies: A Narrative Literature Review and Perspectives

Article References: Yamaguchi, K., Yamanoi, K., Ogura, J., Koike, A., Umemiya, M., Higashiyama, N., Kou, K., Inayama, Y., Mizuno, R., Miyamoto, T., Taki, M., Murakami, R., Hamanishi, J., & Masaki, M. (2026). Precision Nutrition as the Concept of Dietary and Nutritional Interventions for Patients With Malignancies: A Narrative Literature Review and Perspectives. Cancer Reports, 9(10), Article e70702. https://doi.org/10.1002/cnr2.70702

Image Credits: AI Generated

DOI: 10.1002/cnr2.70702

Keywords: precision nutrition, cancer, chemotherapy, fasting-mimicking diet, gut microbiome, cancer metabolism, immunotherapy, nutritional guidelines, PI3K inhibitors, colorectal cancer, breast cancer, digital health

The review, led by researchers at Inner Mongolia Agricultural University, organizes decades of evidence into a Mechanism-Technology-Application framework designed to separate what has actually been demonstrated from what has merely been inferred. The authors are blunt about the distinction. Cross-feeding, as they define it, is any interaction in which a resource produced, released, or made accessible by one microorganism is acquired or further transformed by another. It is not inherently cooperative, not always beneficial to the host, and not a universal organizing principle of the gut ecosystem. The same resource transfer that sustains a health-associated butyrate producer can, in a different context, feed a dangerous pathogen.

The clearest examples come from sequential degradation, sometimes called a trophic relay. Complex dietary polysaccharides and host-derived mucus glycans are too large for most gut bacteria to touch. Specialist degraders such as Bacteroides species, Akkermansia muciniphila, and Bifidobacterium bifidum cleave these polymers into sugars and oligosaccharides that downstream consumers can use. In one well-characterized relay, Bacteroides ovatus releases breakdown products during inulin degradation that support B. vulgatus, B. thetaiotaomicron, and Parabacteroides goldsteinii. In another, Akkermansia muciniphila liberates mucin-derived sugars and acetate that fuel the butyrate producer Anaerostipes caccae, linking mucus turnover to the production of a short-chain fatty acid that nourishes the colonic lining and modulates immune signaling through receptors such as GPR43.

But relays have a dark side. In antibiotic-treated mice, the same liberation of host sugars becomes a lifeline for pathogens: sialic acid and fucose released from mucus by the depleted community boost the competitive fitness of Salmonella enterica serovar Typhimurium, while sialic acid catabolism supports the post-antibiotic expansion of Clostridioides difficile. Amino acid exchange tells a similar story. In antibiotic-perturbed mice, enterococci supply leucine and ornithine that enhance C. difficile fitness, and their arginine catabolism simultaneously generates metabolic signals associated with increased virulence. Metagenomic surveys suggest that more than 40 percent of gut microbes lack complete pathways for making branched-chain amino acids, implying that such dependencies are widespread, though predicted auxotrophy alone does not prove that transfer actually occurs.

Diffusible metabolites add another layer of coupling. Hydrogen produced by fermentative bacteria such as Roseburia intestinalis can be consumed by acetogens like Ruminococcus hydrogenotrophicus or by the methanogen Methanobrevibacter smithii, keeping fermentation thermodynamically favorable while shifting the end products toward acetate or methane. Elevated methane has been associated with delayed transit and constipation-predominant irritable bowel syndrome, although the review stresses that these associations do not establish hydrogen cross-feeding as a direct cause of disease. Perhaps the most elegant demonstrated exchange is bidirectional: Bacteroides xylanisolvens supplies folate to Clostridium butyricum, which in turn provides p-aminobenzoic acid that B. xylanisolvens needs to synthesize folate, a reciprocal loop shown under controlled culture conditions but not yet traced in a living gut.

Micronutrients reveal an even more competitive dimension. Bacteroides thetaiotaomicron makes no siderophores of its own yet steals iron from enterobactin and salmochelin secreted by Enterobacteriaceae using its XusABC system, a capacity that improves its colonization fitness during inflammation. Remarkably, the XusB protein captures enterobactin and shields it from the host’s iron-sequestering lipocalin-2, but Salmonella can then reacquire the protected complex. A single iron-trafficking route can therefore bolster a commensal, blunt host nutritional immunity, and still hand iron to a pathogen. Vitamin provisioning shows similar ambiguity: auxotrophic strains in humanized germ-free mice maintain stable abundances despite dietary swings, consistent with community-level sharing, yet the actual donors and transfer routes remain unidentified.

Given this complexity, the review proposes a tiered evidence framework that mirrors a Design-Build-Test-Learn engineering cycle. Multi-omics and computational platforms such as COMETS, MICOM, and the Gut Cross-feeding Predictor generate candidate donor-resource-recipient hypotheses, but correlation networks cannot establish causality. Causal attribution demands co-culture experiments, targeted metabolite perturbation, and genetic disruption of production or uptake pathways, exemplified by a study in which paired mutants of Bifidobacterium breve and Limosilactobacillus reuteri confirmed that a nutritional interaction depended on the intermediate 1,2-propanediol. Stable-isotope tracing then resolves metabolite fate directly: labeled acetate has been shown to be incorporated into butyrate by Faecalibacterium prausnitzii and Roseburia strains, and labeled lactate and acetate traced the carbon route from Bifidobacterium adolescentis into butyrate synthesis by Eubacterium hallii via acetyl-CoA.

Even validated pairwise exchanges, however, may not survive contact with a real community. In a twelve-member synthetic gut community, pairwise interactions explained only part of the observed dynamics, and initial abundances and negative interactions imposed strong historical contingency. Functional redundancy complicates matters further: depleting specific Bacteroides members triggers compensatory expansion of relatives that partially restores glycan degradation. Host-associated models add spatial architecture, dietary fluctuation, and colonization history, all of which can attenuate or redirect interactions that looked stable in a flask. The authors argue that no single method suffices; only convergent evidence across candidate identification, causal validation, and ecological robustness testing can support claims of functional cross-feeding.

The translational implications are sobering but instructive. Cross-feeding-informed synbiotics would require a primary responder to release a defined intermediate that a secondary consumer then transforms, with a combination-specific benefit demonstrated against substrate-only and microbe-only controls, a standard that current human evidence does not meet. Among live biotherapeutic products, the dual-strain pairing of B. xylanisolvens and C. butyricum improved metabolic and barrier parameters in high-fat-diet mice, but the folate exchange was never traced in vivo. The seventeen-strain consortium GUT-103 attenuated colitis in gnotobiotic mice without resolving any donor-metabolite-recipient chain, and a thirty-seven-strain synthetic microbiota suppressed C. difficile through competitive proline depletion rather than resource transfer at all. Engineered examples cut both ways: redirecting polysaccharide-utilization loci in Bacteroides uniformis altered glycan flow to downstream consumers, a relatively direct case of engineered cross-feeding, while the clinical candidate NOV-001 achieved porphyran-dependent, largely reversible engraftment in a Phase 1/2a trial yet showed variable colonization, genetic instability, and no significant benefit over placebo for urinary oxalate. The Phase 2b ECO-RESET trial of SER-287 similarly failed its primary endpoint despite confirmed engraftment, demonstrating that colonization is not efficacy.

The review’s conclusion is neither dismissive nor utopian. Cross-feeding offers a rigorous, mechanistically grounded framework for prioritizing dietary substrates, strain combinations, and engineered resource-allocation strategies, and emerging tools, from spatially resolved transcriptomics to gut-on-chip platforms and digital-twin modeling, should progressively narrow the gap between inference and demonstration. But a reproducible, closed engineering cycle for gut microbial communities has not been achieved across heterogeneous human hosts, and the immediate priority is prospective validation of the full causal chain linking substrate availability, microbial activity, metabolite transfer, ecological persistence, safety, and clinically meaningful benefit. Cross-feeding, the authors emphasize, must be evaluated within the competitive, host-regulated ecology of the gut rather than as an isolated, programmable switch. The microbial economy of the intestine is real, increasingly legible, and, in carefully defined cases, already manipulable. Turning that legibility into reliable medicine is the task the field now faces.

Subject of Research: Metabolic cross-feeding interactions in the gut microbiome and their application to live biotherapeutic development

Article Title: Programming Gut Microbiome Function Through Cross‐Feeding: From Ecological Mechanisms to Live Biotherapeutics

Article References: Sun, C., Ma, T., Jin, H., Li, Z., Cheng, Y., Li, J., Kwok, L.-Y., & Sun, Z. (2026). Programming Gut Microbiome Function Through Cross‐Feeding: From Ecological Mechanisms to Live Biotherapeutics. Advanced Science, 13(55), Article e77267. https://doi.org/10.1002/advs.77267

Image Credits: AI Generated

DOI: 10.1002/advs.77267

Keywords: gut microbiome, cross-feeding, microbial metabolism, live biotherapeutics, synbiotics, butyrate, short-chain fatty acids, synthetic communities, stable-isotope tracing, microbiome therapeutics, colonization resistance, precision nutrition

The review is careful about what it can and cannot claim. Because the evidence base for this breed is limited and heterogeneous, the authors screened 42 records published between January 2000 and January 2026 and retained 18 empirical studies as their core evidence, synthesizing the findings as a structured narrative rather than a meta-analysis. They explicitly frame their age-stratified suggestions as hypothesis-generating compositional alignments, not clinical dietary guidance. That caution matters, because most of the data come from laboratory profiling of meat composition rather than from controlled human trials, and the authors repeatedly warn that compositional plausibility is not the same as proven health benefit.

The physiological story begins with how these goats live. Korean native black goats are raised primarily as a meat breed, often under grazing-based systems in mountainous terrain. Their small body size and active foraging behavior are associated with limited fat deposition and a higher proportion of lean tissue. That leanness has a biochemical consequence: with less storage fat in the muscle, the overall lipid pool shifts toward membrane-associated polar lipids, which are typically richer in unsaturated fatty acids than the triacylglycerols that dominate fat depots. The result, according to the synthesis, is meat whose saturated fatty acid proportion hovers around 35 to 38 percent across major cuts, compared with figures approaching 45 percent in selected Hanwoo beef loin samples and exceeding 50 percent in a crossbred goat comparator.

Those numbers come with caveats. Fatty-acid composition is shaped by intramuscular fat levels, lipid-class distribution, breed, age, feeding system, muscle function, and postmortem handling, so cross-study comparisons are vulnerable to confounding. The review notes, for instance, that some pork cuts show saturated fat proportions as low as or lower than those of the goat leg cuts, and that marbling grade in beef reflects fatness and grain finishing as much as species identity. The consistent signal, the authors argue, is directional rather than quantitative: across shoulder, loin, foreleg, hind leg, and rib, Korean native black goat meat tends toward lower saturated and higher unsaturated fat than cattle, pigs, and crossbred goats, and even outperforms other goat crossbreeds. In the rib cut, the native goats measured 41.95 percent saturated fatty acids against 51.44 percent in the crossbred comparator.

Beyond the lipid profile, the meat is protein-dense in ways that matter for human nutrition. Its crude protein content is comparable to beef while its crude fat is exceptionally low, and its cholesterol level, roughly 35.73 to 37.48 milligrams per 100 grams, sits below typical beef or pork values. The meat is particularly rich in histidine, important for growth and tissue development, and arginine, which participates in ammonia detoxification and blood-flow regulation. It also carries high concentrations of L-carnitine, 20.8 to 26.0 milligrams per 100 grams, a compound that shuttles fatty acids into mitochondria for oxidation. Linoleic acid and oleic acid are the dominant unsaturated fatty acids, and linoleic acid serves as a precursor for eicosanoids that modulate inflammatory responses.

The most intriguing components may be the bioactive dipeptides and related metabolites. Creatine, carnosine, and anserine appear at notable levels, and each has a defined biochemical role: creatine supports rapid energy regeneration in muscle, carnosine buffers intracellular pH and mitigates oxidative stress, and anserine facilitates the removal of reactive oxygen species and recovery from muscle fatigue. These findings rest mainly on biochemical and experimental evidence, but they give the meat a functional profile that few mainstream livestock products can match. Rib cuts showed the highest antioxidant capacity among the major cuts in one analysis, while another study found the chuck, with its distinctive magnesium and phosphorus content, displayed the greatest antioxidative potential, suggesting that mineral composition may modulate antioxidant enzyme activity.

Cut-specific differences are where the review becomes genuinely practical. The hind leg is a branched-chain amino acid powerhouse, containing 2,672 milligrams of valine, 2,487 milligrams of leucine, and 1,565 milligrams of isoleucine per 100 grams, for a total of 6.72 grams, a substantial contribution toward World Health Organization reference intakes. It is also rich in the antioxidant amino acids histidine and methionine. The back loin, by contrast, has low collagen content and a favorable protein-to-unsaturated-fat ratio, making it tender and highly digestible, and it carries meaningful amounts of creatine, carnosine, and anserine. Rib meat is fattier but shows the strongest antioxidant activity in the assays used, while shoulder meat contains about 2.8 percent crude fat and notably high magnesium and phosphorus.

From these profiles the authors build their life-stage framework. For children and adolescents, whose rapid growth elevates protein and branched-chain amino acid requirements, the hind leg emerges as a plausible protein source supporting muscle accretion. For adults focused on cardiovascular and metabolic health, the loin or sirloin, with its lower saturated fat proportion and its creatine, carnosine, and anserine content, fits dietary patterns emphasizing a favorable fatty-acid balance; physically active adults might combine loin and hind leg cuts to support both protein synthesis and muscle energetics. For older adults, who face reduced protein digestibility and progressive muscle loss, the tender, easily chewed sirloin with its leucine-rich essential amino acid profile is the recommended starting point, while the dense hind leg may demand too much chewing and the fattier rib cuts warrant moderation.

The review situates these suggestions within established geriatric nutrition guidance, including the PROT-AGE position paper and ESPEN recommendations, stressing that protein needs in older people should be individualized according to health status, appetite, and comorbidities, with goat meat as one food-based option among many. It also confronts the sensory hurdle that has limited the breed’s market reach: the characteristic goaty odor, driven by volatile branched-chain fatty acids whose concentrations vary with genetics, age, feeding, and postmortem handling. Some consumers read that odor as traditional restorative value; others find it off-putting. Because the odor is a modifiable attribute rather than an immutable breed trait, the authors point to integrated control points spanning feeding, management, and processing, noting that high-pressure treatment has been reported to attenuate off-odor intensity, though commercial feasibility remains unproven.

The path forward, the authors conclude, requires coordinated work on several fronts: metabolic and genetic studies to explain how the goats’ physiology produces their nutritional advantages; standardized cross-species comparisons normalized for intramuscular fat; controlled human trials measuring bioavailability and dose-response relationships for the bioactive compounds; pilot studies of protein digestibility and amino acid kinetics; and consumer research on acceptability and flavor reduction. Breeding programs are already underway, crossing three indigenous Korean lines with the New Zealand Boer breed to develop improved commercial strains. Until human intervention data arrive, the review’s message is measured but striking: a traditional medicinal meat may be one of the most nutritionally interesting protein sources in the modern livestock portfolio, provided consumers and scientists alike resist the temptation to treat compositional promise as clinical proof.

Subject of Research: Nutritional composition of Korean native black goat meat and age-specific consumption strategies

Article Title: Physiological and nutritional characteristics of Korean native black goats and their implications for age-specific consumption strategie

Article References: Lee, H. W., Kim, W. J., Jang, H. G., Kim, D. B., Lee, H. J., Kim, J. H., & Lee, S. Y. (2026). Physiological and nutritional characteristics of Korean native black goats and their implications for age-specific consumption strategie. Food Science of Animal Resources, 46(1), Article 51. https://doi.org/10.1007/s44463-026-00065-w

Image Credits: AI Generated

DOI: 10.1007/s44463-026-00065-w

Keywords: Korean native black goat, meat quality, fatty acids, essential amino acids, bioactive compounds, carnosine, anserine, creatine, nutrition, functional food, precision nutrition, aging