Diet Soda and Microbiome Epigenetics: What We Inherit Through the Gut

April 17, 2026 ·

Thaena Inc.

New research shows that what your grandparents drank may still be editing the DNA in your liver today. The microbiome, not genes alone, is how biological inheritance bends within a single lifetime, and the papers mapping that bridge are rewriting what we thought actually gets passed down.

Lit Review Friday · Learn Something with Thaena · Published 2026 · Reading time: ~18 minutes

Lamarck Was Right (He Just Didn't Know the Mechanism)

Darwin had a competitor. A French naturalist named Jean-Baptiste Lamarck, who argued that organisms could adapt within a single lifetime, and that those adaptations could be passed to their offspring. Lamarck's version of inheritance was disdained. His name became shorthand for bad science. He was essentially driven out, and Darwinian evolution, with its slow, multi-generational pace and random mutation engine, became the textbook view.

It turns out Lamarck was right about the pattern. He just could not have known the mechanism. The mechanism is the microbiome. Bacteria sitting in the human colon, responding to what we eat and drink and breathe, produce chemical signals that reach the nucleus of our cells and decide which of our genes are accessible and which are silenced. When those signals change, so does the expression of our DNA. And critically, the altered expression pattern gets copied into the cells that become sperm and egg. Whatever the microbiome has been hearing gets passed forward to children and grandchildren who never encountered the signal themselves.

A 2026 paper by Concha Celume and colleagues in Frontiers in Nutrition documents this exact handoff with unusual precision. The input was a common dietary additive. The output was a metabolic and inflammatory phenotype measurably altered across three generations of mice, where only the first generation was ever exposed. Pair that paper with a foundational 2014 study by Yotam Suez in Nature, a 2022 follow-up in Cell, a 2016 multigenerational experiment by Justin Sonnenburg in Nature, and review papers by Zhang in 2025 and Shock in 2021 that map the molecular bridge between the gut microbiome and host epigenetics, and you have a research arc that fundamentally changes how we should think about diet, inheritance, and therapeutic intervention.

This blog walks through those papers in sequence, lands on the molecular mechanism, and closes with what it all means for the emerging class of therapeutics built on microbial metabolites rather than live bacteria. Specifically, postbiotics.

The Zero-Calorie Paradox: Suez 2014

For half a century, the food industry has sold consumers a biological loophole: artificial sweeteners. The premise was straightforward. Saccharin, sucralose, and aspartame bind to the sweet taste receptors on the tongue but are not metabolized by human cells. No calories absorbed. No metabolic consequence. This was the scientific consensus, and it drove the substitution of non-nutritive sweeteners into diet sodas, yogurts, coffee additives, and the broader architecture of weight-loss eating.

Population-level data quietly argued with that premise. Extensive epidemiological studies showed that regular non-nutritive sweetener consumption correlated with weight gain and increased risk of type 2 diabetes. The very chemicals used to prevent metabolic disease were appearing disproportionately in populations suffering from it.

Yotam Suez and colleagues at the Weizmann Institute ran the controlled trial that resolved the paradox. They took lean mice and supplemented their drinking water with either caloric sugars (glucose, sucrose) or commercial non-nutritive sweeteners (saccharin, sucralose, aspartame) at doses matched to human equivalents. Not chemical vats. The equivalent of a daily diet soda habit at FDA acceptable intake levels.

The Finding That Disrupted the Consensus

Within eleven weeks, the mice drinking the artificial sweeteners developed marked glucose intolerance. The control mice drinking actual sugar water did not. The chemical marketed to prevent metabolic dysfunction was producing it.

This alone would have been a significant finding. What made the Suez paper a landmark was the causal machinery they then demonstrated. They treated the sweetener-consuming glucose-intolerant mice with a broad-spectrum antibiotic regimen of ciprofloxacin and metronidazole. Following the antibiotic wipeout, the sweetener-induced glucose intolerance completely vanished. The metabolic disruption required the presence of gut bacteria to exist.

To firmly establish causation, they performed fecal microbiota transplantation. They extracted stool from the sweetener-consuming mice and transferred that microbial community into germ-free mice raised in sterile isolators with no prior exposure to any microorganisms. Six days after transplant, those sterile recipient mice developed impaired glucose tolerance. They had never consumed a drop of artificial sweetener in their lives. The disease phenotype was entirely decoupled from the host's direct ingestion of the chemical. The metabolic derangement was encoded within and transmitted by the altered configuration of the microbiome.

The shotgun metagenomics added mechanistic detail. The researchers didn't just count which bacteria were present, they looked at what functional capabilities the altered community was exercising. They found a dramatic over-representation of Bacteroidales species and an upregulation of glycan degradation pathways. The microbial community had shifted into a metabolic configuration that was aggressively harvesting energy from complex carbohydrates and sending elevated levels of short-chain fatty acid signals to the host. Too much of a good thing, in a signaling environment the host was not calibrated for.

Humans Aren't Exempt: Suez 2022

Animal models are a starting point, not an ending point. The obvious question: does this happen in humans? Suez and his team answered it in a 2022 paper in Cell.

They recruited 120 healthy adults who strictly abstained from non-nutritive sweeteners. Finding participants who genuinely did not consume diet products proved harder than expected, a telling detail in its own right. The participants were randomized to receive daily sachets of saccharin, sucralose, aspartame, or stevia for two weeks, at doses well below the FDA's acceptable daily intake.

Two weeks. In that short window, saccharin and sucralose significantly impaired human glycemic responses. The impairment was personalized, not universal: the magnitude depended on the individual's pre-existing microbiome configuration. Some participants responded dramatically. Others showed only mild shifts. The microbiome, not the chemical dose, was the primary mediator.

To confirm the causal chain in humans as cleanly as in mice, the researchers took stool from the top human responders (those whose glucose control deteriorated the most) and transferred it into germ-free mice. The recipient mice developed the same glycemic impairment. The causal chain held: sweetener exposure, altered microbiome, metabolic disruption transmissible via the bacteria themselves.

This was the state of the literature by early 2025. Sweeteners disrupted the microbiome. The altered microbiome produced metabolic consequences. The consequences were transmissible by the bacteria alone. What the field had not yet asked, at least not rigorously, was whether those consequences could travel beyond the exposed individual into the next generation.

The Generational Leap: Celume 2026

Concha Celume and colleagues, publishing in Frontiers in Nutrition in 2026, set up the experiment to answer that question. The design was elegant and the findings, if they held up, would be genuinely paradigm-shifting.

The Experimental Design

The researchers took male and female mice, designated them the F0 generation (the parents), and supplemented their drinking water with either sucralose, stevia, or plain water as control. The exposure lasted 16 weeks, roughly a fifth of the mouse's total lifespan. This modeled a human consuming diet beverages for years before having children.

The F0 generation was then bred. Their offspring, the F1 generation, received only plain drinking water their entire lives. The F1 mice were bred to produce an F2 generation, the grandchildren of the originally exposed animals. The F2 generation also received only plain drinking water. The grandchildren and great-grandchildren had never encountered sucralose or stevia in any form.

By classical genetic logic, those F1 and F2 generations should have been metabolically unremarkable. Their DNA sequence was not mutated by the parental exposure. Sucralose is not a mutagen. Radiation was not involved. The genetic code itself was intact.

The Finding

The F1 and F2 male mice whose grandparents had consumed sucralose showed altered glycemic responses. Their blood sugar control was measurably impaired. They also displayed persistent compositional changes in their fecal microbiota relative to control lineages, along with persistently lower overall concentrations of short-chain fatty acids. The fermentative capacity of their gut ecosystems had been recalibrated downward across three generations.

The gene expression data was sharper still. In the F0 sucralose-consuming parents, a gene called SREBP1, a master metabolic regulator responsible for lipid and cholesterol homeostasis in the liver, was significantly downregulated. At the same time, two inflammatory genes in the intestinal tissue, TLR4 (toll-like receptor 4) and TNF (tumor necrosis factor), were intensely upregulated. These are canonical inflammatory alarm bells, and they were ringing in F0 animals exposed to a supposedly inert dietary additive.

The same gene expression pattern appeared in the F1 and F2 offspring. The dialed-down metabolic regulator and the dialed-up inflammatory genes traveled through generations that had never been exposed to the initial trigger.

The stevia arm of the experiment deserves its own note. Stevia did not alter glycemic response in the F0 parents, which initially seemed like good news for the natural plant extract. However, it did cause inflammatory marker spikes (TLR4 and TNF) in the F1 generation. Those spikes normalized by the F2 generation. The natural plant extract left a transient inflammatory echo that the biology was able to resolve within two generations. Sucralose left a structural alteration that persisted.

Different chemicals, different inheritance profiles. The microbiome and the epigenome are not uniformly sensitive to all inputs; they respond in species-specific, molecule-specific ways. But the basic principle held: what the grandparent consumed shaped the gene expression of the grandchild.

Mapping the Bridge: The Microbiome-Epigenome Axis

The Celume finding raises a mechanistic question that cannot be deferred. Bacteria in the colon do not have hands. How does a microbial community in the lower intestine physically reach the nucleus of a liver cell, let alone the nucleus of a germ cell destined to become the next generation, and flip a regulatory switch on specific genes?

Two review papers map the bridge with unusual clarity: Zhang et al. 2025 in Gut Microbes, which focuses on the intestinal disease side of the axis, and Shock et al. 2021, which walks through the broader landscape of diet, gut microbes, and host epigenetics across multiple tissues and disease states.

The picture they collectively paint is that the gut microbiome is not merely a digestion machine. It is a distributed chemical factory, constantly producing signaling molecules that cross the gut wall, enter systemic circulation, reach every tissue in the body, and in many cases pass through the nuclear membrane to interact directly with the machinery that reads DNA.

The Signaling Molecule Inventory

The molecular categories produced by gut bacteria and documented to influence host epigenetic state include:

Short-chain fatty acids (acetate, propionate, butyrate) produced by bacterial fermentation of dietary fiber. Butyrate in particular is a well-characterized histone deacetylase inhibitor, as detailed below.

Bile acid derivatives produced by microbial modification of host-derived primary bile acids. Secondary and tertiary bile acids act as ligands for host nuclear receptors including FXR and TGR5, regulating lipid metabolism, glucose homeostasis, and inflammatory gene expression.

Tryptophan metabolites, particularly indoles and indole-derivatives, produced by bacterial tryptophan catabolism. These are ligands for the aryl hydrocarbon receptor (AhR), which regulates intestinal barrier integrity, immune tolerance, and antimicrobial peptide expression.

Polyamines such as putrescine, spermidine, and agmatine. These molecules influence chromatin organization and can cross the nuclear envelope to modulate gene expression.

Methyl donors including folate derivatives and vitamin B12, which provide the methyl groups used in DNA methylation. Microbial synthesis of these cofactors directly influences the availability of methylation substrate in host cells.

Small peptides and bacterial wall fragments, which act as pattern recognition receptor ligands and drive inflammatory transcriptional programs.

The Epigenetic Mechanisms These Molecules Engage

The Zhang and Shock reviews catalogue three principal ways that these microbial signals modify the host epigenome:

Histone modification. Your DNA is wound around structural proteins called histones. Chemical tags added to or removed from those histones physically change how tightly the DNA is packaged. Tightly packaged DNA is silent. Loosely packaged DNA is accessible for transcription. Butyrate and related metabolites modify the enzymes that regulate this packaging.

DNA methylation. Methyl groups attached directly to cytosine bases in the DNA sequence can silence gene expression over long timescales. Microbial metabolites influence methylation by providing methyl donors and by altering the activity of the enzymes (DNMTs) that write methylation marks.

Non-coding RNA regulation. Microbial signals influence the expression of microRNAs and other regulatory RNAs that fine-tune which host genes are transcribed and translated.

Critically, all three mechanisms are heritable. When a cell divides, the histone modification patterns and the DNA methylation patterns are largely copied to the daughter cells. When a cell divides to produce sperm or egg, a portion of those patterns travels forward to the next generation. This is the physical substrate of epigenetic inheritance.

Butyrate as the Clearest Worked Example

Among the microbial signals that reach the epigenome, butyrate is the best-characterized and the most directly relevant to the Celume findings. A 2014 paper by Bultman in Clinical Cancer Research established the foundational mechanism linking dietary fiber, microbial butyrate production, and host epigenetic regulation. The mechanism works like this.

Certain gut bacteria, particularly species in the Bacteroidales and Firmicutes phyla, ferment dietary fiber (specifically the microbiota-accessible carbohydrates, or MACs, that escape digestion in the small intestine) into short-chain fatty acids. Butyrate is the most abundant of these in the colon. It serves two simultaneous functions: it is the primary energy source for colonocytes, and it acts as a histone deacetylase inhibitor (HDAC inhibitor) throughout the host body.

Histone deacetylases (HDACs) are enzymes that remove acetyl groups from histone proteins. When acetyl groups are on a histone, the associated DNA is loosened and transcriptionally accessible. When HDACs remove those acetyl groups, the DNA wraps tighter and becomes silenced. Butyrate binds to HDAC3 and related enzymes and prevents them from functioning. In the presence of adequate butyrate, specific metabolic and anti-inflammatory genes stay relaxed and readable. In its absence, HDAC activity runs unopposed, metabolic genes wind tight, and the inflammatory program rises in compensation.

This is the molecular handoff that links the Celume finding to the Zhang and Shock frameworks. When parental mice consumed sucralose, the sweetener disrupted their microbial community. The fermentative bacteria that produced butyrate declined. Butyrate production fell. HDAC activity was no longer held in check. SREBP1 in the liver was wound tight and silenced. TLR4 and TNF in the intestinal tissue were left in an accessible, transcriptionally active state. The epigenetic profile of those F0 animals was altered not by direct chemical mutagenesis, but by the withdrawal of a single microbial metabolite.

And because histone modification and DNA methylation patterns copy forward during cell division, including during the formation of germ cells, the altered state was inherited. The F1 and F2 generations were born with a recalibrated epigenetic baseline even though their own microbiomes had never been challenged by sucralose.

The Older, Slower Version: Sonnenburg 2016 and Microbial Extinction

Artificial sweeteners are one way to starve the microbiome of butyrate. They are also a recent one, tied to the post-1960s explosion of industrial food science. A much older, slower, and more widespread version of the same basic insult has been running quietly in the background of every Western life for several generations: fiber depletion.

Justin Sonnenburg and colleagues at Stanford, publishing in Nature in 2016, set up one of the most carefully designed multigenerational microbiome experiments in the literature. They took germ-free mice, colonized them with a human fecal microbiome, and fed them a diet severely deficient in microbiota-accessible carbohydrates (a low-MAC, low-fiber Western-style diet).

In the first generation, microbial diversity crashed. Specific taxa, especially the Bacteroidales responsible for complex polysaccharide fermentation, were driven to low abundance. Importantly, when these first-generation mice were switched back to a high-fiber diet, the microbial diversity largely recovered. The depleted bacteria were still present, hiding at low numbers in the crypts and interstitial spaces of the gut, waiting for their substrate to return.

The researchers then did something most studies do not do. They bred the mice, kept the F1 generation on the low-MAC diet, and then bred again. Then again. Four generations in, on a continuous low-fiber diet, the specific fiber-degrading Bacteroidales were no longer present at low abundance. They were gone. Undetectable in the gut microbiome. And when the fourth-generation mice were returned to a high-fiber diet, the previously hidden microbes did not come back. The taxa were extinct within the host lineage.

Think about the farm again. Depleted soil can be restored if the microbial ecology is still present, hiding at low levels in the crypts between the rows. Depleted soil in which the entire decomposer community has been driven to extinction is something different. You can pour on all the compost and plant all the cover crops you want, but if the organisms that process them into usable nutrients are no longer there, the ecological function does not return. You cannot feed a microbe that does not exist.

Pair Sonnenburg with the Celume/Zhang framework and the through-line sharpens. Whatever shapes your microbiome becomes signal into the next generation's epigenome. The input can be a chemical insult (sucralose). It can be fiber starvation over generations. It can, presumably, be antibiotic courses, chronic stress, environmental exposures like PFAS, or any of the myriad inputs that reshape which microbes thrive and which do not. The specific input matters for the specific downstream consequence. But the channel is the same: gut bacteria, then metabolite output, then host epigenetic modification, then inheritance.

When the Microbes Are Depleted: FMT as Epigenetic Reprogramming

Standard clinical advice for a patient with metabolic dysfunction has historically been some combination of dietary change, exercise, and, in many cases, the substitution of artificial sweeteners for sugar to reduce caloric intake. The Suez work shows that the sweetener substitution is likely counterproductive. The Sonnenburg work shows that dietary fiber recommendations, however correct in principle, may not produce the expected response if the specific fiber-degrading microbes have been depleted in the patient's lineage. Fiber flowing through a depleted community is fiber that does not get converted into butyrate.

This is where fecal microbiota transplantation (FMT) earns its clinical attention. Most people encounter FMT as a last-line treatment for severe recurrent Clostridioides difficile infection, where it works with striking efficacy. But van der Vossen and colleagues, publishing in Gut Microbes in 2021, ran a different kind of FMT trial that speaks directly to the epigenetic questions raised by Celume and Sonnenburg.

The van der Vossen Trial

The team recruited patients with metabolic syndrome and performed allogenic fecal microbiota transplants from healthy, lean donors. The donor pool was rigorously screened for diverse, intact microbial ecosystems of the kind that have become scarce in the general population.

The outcomes they measured went beyond the usual FMT endpoints. They looked at the recipient patients' plasma metabolome, their peripheral blood mononuclear cells, and critically, the DNA methylation patterns on those immune cells.

The FMT altered the recipient patients' metabolome, as expected. It also produced significant changes in DNA methylation patterns on the recipients' own immune cells. The epigenetic marks on the host's own DNA were measurably rewritten after the transplanted microbial community had established itself.

This is a genuinely important finding. It means that epigenetic inheritance is not a sentence. The altered marks copied forward from a grandparent's diet do not have to remain in place. If the missing microbes can be reintroduced, and if those microbes begin producing the metabolites that regulate the epigenome, the transcriptional state of the host can shift. Silenced metabolic genes can become accessible again. Elevated inflammatory genes can return to baseline.

FMT works. But FMT is invasive, logistically demanding, dependent on rigorous donor screening, and limited in its accessibility. It is not a pill you pick up at a pharmacy. And for patients whose microbial ecosystems have been depleted in the Sonnenburg sense (specific taxa extinct across generations of industrialized diet), FMT may not even be a durable solution. The transplanted microbes can be re-extinguished if the hostile dietary environment that drove the original extinction is still present.

The Postbiotic Argument: Signals Without the Source

If the therapeutic target of FMT is not the live bacteria but the chemical output those bacteria produce, then a more direct intervention becomes available: deliver the chemical output itself.

This is the logic behind postbiotics. A postbiotic is not a fiber to feed the bugs (prebiotic) and not a live organism (probiotic). A postbiotic is the finished metabolic product of a healthy microbial community: short-chain fatty acids, secondary bile acids, indoles, polyamines, antimicrobial peptides, cell wall fragments, and the other non-living products that collectively represent the signaling output of a functional ecosystem.

Zhang 2025 explicitly points to postbiotics as a therapeutic frontier for exactly the reason this research arc makes clear: if the critical signal is the metabolite, and if the patient's native microbiome is incapable of producing adequate levels of that metabolite because the producing species are depleted or extinct, then delivering the metabolite directly is a logical intervention. You bypass the need to reconstitute a complex ecosystem. You deliver the epigenetic regulators that the missing microbes would have made.

Where Thaena Sits in This Frame

This is the scientific premise behind Thaena's work on postbiotics. Thaena is building a full-spectrum postbiotic derived from the microbiomes of rigorously screened, exceptionally healthy human donors. The goal is not to seed new bacteria into a patient's gut. The goal is to restore the signaling environment that a healthy microbiome would have generated, in a form that can be delivered orally, shelf-stable, and without the logistical demands of FMT.

In the framework of this blog, a full-spectrum postbiotic is positioned as a way to restore epigenetic signaling lost intergenerationally. The next best thing after FMT when FMT is not accessible, or when the producing microbes in the recipient are so depleted that FMT-reintroduced populations cannot establish durable colonization. Postbiotics deliver the downstream output directly. They do not depend on the recipient's microbiome being in any particular state to produce their signaling effect.

The postbiotic argument is not that live bacteria are unimportant, that dietary fiber does not matter, or that probiotics have no role. All three remain part of a well-functioning gut ecosystem. The argument is narrower and more specific. For individuals whose microbiomes have been depleted enough that they can no longer produce adequate levels of the metabolites the body depends on, and who cannot easily access or maintain the results of FMT, delivering the metabolites themselves is a logical and direct therapeutic strategy. Especially when the downstream consequences of that metabolite loss include inherited epigenetic dysregulation affecting the next generation.

The Honest Limitations

Every paper in this arc has important limitations that the field will need to resolve before the clinical picture is complete.

Scientific integrity requires acknowledging these gaps. The framework is coherent and the supporting data is substantial, but the clinical picture is still in active construction. Useful intervention can happen in parallel with the science; it does not have to wait for perfect data.

The Bottom Line

The core claim of this research arc is that biological inheritance is not a locked vault. The DNA sequence is stable. But the annotations on that sequence, the chemical tags that determine which genes are accessible and which are silenced, are dynamic. They are written in large part by the signaling molecules produced by the gut microbiome. And they are heritable. What shapes your microbiome today may still be reading genes in your grandchildren tomorrow.

Modern life places sustained pressure on this system from multiple directions simultaneously. Artificial sweeteners alter microbial communities and drive measurable glucose intolerance that has now been shown to propagate across three generations. Low-fiber diets drive specific microbial taxa to local extinction within a human lineage, such that simply reintroducing fiber in the present generation cannot restore the lost ecological function. Antibiotics, PFAS exposure, chronic physiological stress, and other modern inputs all press on the same axis.

The therapeutic options include restoring the missing microbes (FMT), feeding the surviving microbes (fiber), seeding new microbes (probiotics), and delivering the microbial output directly (postbiotics). Each has its place in the emerging toolkit. Postbiotics are particularly suited to the scenario in which the specific microbial producers have been depleted or lost across generations, and in which rebuilding the full ecosystem is either not feasible or not durable. In that scenario, delivering the chemical signals themselves becomes a direct route to restoring the epigenetic regulation those signals support.

Lamarck was right about inheritance bending within a single lifetime. He was wrong about the mechanism, because the mechanism was invisible to nineteenth-century biology. The microbiome fills in the missing piece. And the interventions that support a healthy microbiome-epigenome axis, including the direct delivery of its chemical output through full-spectrum postbiotics, are a logical next step in translating this understanding into clinical benefit.

The vault of genetic inheritance is not locked. The ink on the blueprints is still wet. What we eat, drink, and expose ourselves to is writing instructions that may still be read by descendants we will never meet. That is a sobering realization. It is also, in the clinical frame this research opens, a hopeful one. If the epigenetic marks are writable, they are also rewritable.

Stay curious. Take care of your ecosystem.

References

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This post accompanies the Lit Review Friday episode of Learn Something with Thaena.