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![[EN] Microbiota and Epigenetics: How Our Bacteria Influence Gene Expression.](https://methode-espinasse.com/wp-content/uploads/2026/02/cdc-Omo_LR_480x480.webp)
For a long time, the gut microbiota was approached almost exclusively through a digestive lens. It was primarily viewed as a collection of microorganisms involved in the breakdown of dietary fibres, the synthesis of certain vitamins, and protection against pathogenic organisms. While this perspective was not incorrect, it proved to be profoundly incomplete.
Over the past two decades, scientific advances have radically transformed our understanding of the microbiota. It is no longer seen as a peripheral actor in digestion, but rather as a metabolic, immune and informational organ, capable of continuous interaction with human cells.
This paradigm shift carries major implications. The microbiota does not act solely through what it produces, but through the biological signals it generates, modulates and disseminates. These signals directly influence inflammation, metabolism, mitochondrial function—and, more fundamentally, gene expression via epigenetic mechanisms [1–3].
In other words, part of our genetic activity depends not only on our diet and environment, but also on the way our microbiota interprets and transforms these inputs.
From this perspective, nutrition can no longer be considered independently of the microbiota. Likewise, epigenetics cannot be fully understood without integrating the central role of this microbial interface.
In other words
The microbiota is not merely a digestive intermediary: it actively participates in the dialogue between environment and genome.
The human gut microbiota is composed of tens of thousands of bacterial species, representing a genetic heritage—the microbiome—that vastly exceeds that of the human genome itself [1]. This genetic richness confers remarkable metabolic capacities that are absent from human cells.
These microorganisms are able to:
Experimental and clinical data converge on a central idea: the microbiota functions as a systemic regulatory organ, integrated into the major biological networks of the body [2,3].
This recognition has led to a profound shift in scientific status. The microbiota is no longer studied as a simple environmental factor, but as a physiological actor in its own right, whose imbalances are associated with metabolic, inflammatory, neurological and ageing-related disorders [4–6].
This systemic role is largely based on its ability to produce signalling metabolites—true biological messengers.
In other words
The microbiota does not merely accompany human physiology: it actively modulates how it functions.
One of the major contributions of contemporary research has been the identification of microbial metabolites as central mediators of host–microbiota communication.
Among the most extensively studied are:
These compounds are not simple fermentation by-products. They function as genuine biological signals, capable of binding to cellular receptors, modulating enzymatic activity, and influencing key regulatory pathways [3,7].
SCFAs, for example, play a critical role in:
Butyrate occupies a particularly important position. It serves as the primary energy source for colonocytes, but also acts as a histone deacetylase (HDAC) inhibitor—a major epigenetic mechanism [9].
Thus, a microbiota-derived metabolite is capable of directly modifying chromatin structure and, consequently, the expression of numerous genes involved in inflammation, metabolism and cellular differentiation.
In other words
The microbiota communicates with our cells through a molecular language—and that language is largely epigenetic.
Interactions between the microbiota and epigenetic regulation rely on several complementary mechanisms.
Certain microbial metabolites influence the availability of methyl donors required for DNA methylation. Folate, vitamin B12, choline and methionine status—partly dependent on the microbiota—directly conditions the activity of methylation enzymes [11,12].
Alterations in the microbiota can therefore modify methylation profiles associated with inflammatory or metabolic pathways.
As previously discussed, SCFAs—particularly butyrate—modulate histone acetylation by inhibiting HDACs. This mechanism promotes a more open, anti-inflammatory gene expression profile in specific contexts [9,10].
Emerging evidence shows that certain microbial metabolites influence the expression of microRNAs involved in immune and metabolic regulation [13].
These mechanisms do not operate in isolation. They form part of a dynamic network that depends on the overall nutritional, inflammatory and metabolic context.
In other words
The microbiota does not alter genes themselves, but it profoundly influences how they are used.
When microbial balance is disrupted—dysbiosis—the nature of the biological signals produced changes. Microbial diversity declines, pro-inflammatory species proliferate, and the production of protective metabolites collapses.
This situation promotes:
Chronic inflammation is one of the most powerful negative modulators of the epigenome. It alters methylation patterns, disrupts cellular repair pathways, and accelerates biological ageing [14–16].
Research on inflammaging shows that this persistent inflammatory state acts as biological background noise, durably shifting gene expression towards profiles of stress, insulin resistance and reduced resilience [15,16].
In this context, dysbiosis appears not as a secondary consequence, but as an active driver of epigenetic dysregulation.
In other words
A disrupted microbiota sends incoherent biological signals, which cells interpret as a state of chronic threat.
Nutrition is the primary lever through which the microbiota is shaped. Yet here again, the issue is not merely nutrient intake, but the functional coherence of biological signals.
A diet low in fermentable fibres, rich in ultra-processed foods and associated with repeated glycaemic spikes favours pro-inflammatory microbial profiles [17,18].
Conversely, regular intake of diverse fibres, polyphenols, high-quality fats and essential micronutrients supports favourable microbial metabolic activity [8,17].
Cellular Nutrition fits squarely within this framework. Its aim is not only to nourish human cells, but to optimise the entire biological ecosystem, with the microbiota as a central actor.
It acts simultaneously on:
Within this approach, the microbiota is not treated as an isolated variable, but as an integrated component of the cellular network.
In other words
Cellular Nutrition does not bypass the microbiota—it works with it.
With age, microbiota diversity tends to decline, while interindividual variability increases. Microbial profiles associated with healthy ageing are characterised by high richness, functional stability and sustained production of anti-inflammatory metabolites [19–21].
Studies conducted in centenarians reveal distinct microbial signatures associated with improved immune and metabolic regulation [20].
These observations align with epigenetic data: favourable biological environments—nutritional, microbial and inflammatory—are associated with slower, more resilient ageing trajectories [14–16].
The microbiota thus emerges as either an amplifier or a buffer of biological ageing, depending on the quality of the signals it produces over time.
In other words
Ageing does not depend solely on chronological age, but on the stability of biological signals sent to cells—of which the microbiota is a key contributor.
Current evidence allows for a clear distinction.
What can be influenced
What is partially modifiable
What cannot be changed
Within this framework, nutrition and Cellular Nutrition do not offer absolute control, but a powerful, continuous and well-documented biological steering mechanism.
In other words
The microbiota does not determine everything—but it influences far more than was once assumed.
Findings from cell biology, epigenetics and microbiota research converge on a single conclusion: the gut microbiota constitutes one of the major interfaces between environment and genome.
It transforms food into biological signals, modulates inflammation, influences mitochondrial function, and directly participates in epigenetic regulation.
In this context, thinking about nutrition without integrating the microbiota means overlooking a central actor of human physiology. Cellular Nutrition precisely allows this fragmentation to be overcome, by building a coherent, systemic approach aligned with the current state of scientific knowledge.
It does not promise magical reprogramming, but an intelligent optimisation of the biological environment—an essential condition for long-term health and functional ageing.
[1] The Human Microbiome Project Consortium (2012)
Structure, function and diversity of the healthy human microbiome. Nature, 486, 207–214.
https://www.nature.com/articles/nature11234
This landmark paper establishes the scale and functional diversity of the human microbiome (interindividual variation, metabolic functions by body site) and supports the concept of the microbiota as a genuine “microbial organ”. It provides the baseline for understanding why, even with comparable dietary intakes, biological responses can differ substantially: the microbial context changes how signals are interpreted.
[2] Qin, J. et al. (2010)
A human gut microbial gene catalogue established by metagenomic sequencing. Nature, 464, 59–65.
https://www.nature.com/articles/nature08821
This study quantifies the genetic dimension of the gut microbiome by establishing a gene catalogue, highlighting an extensive metabolic potential that can exceed the human genome in certain functional domains. It directly supports the logic “microbiota = transformation capacity”, i.e., the production of metabolites and biological signals that can act on the host.
[3] Zhang, Q. et al. (2025)
Implications of gut microbiota-mediated epigenetic modifications in human health and disease. (Review; PMC access)
https://pmc.ncbi.nlm.nih.gov/articles/PMC12143691/
A recent review focused on epigenetic pathways influenced by the microbiota (DNA methylation, histone modifications, non-coding RNAs, etc.). It provides a comprehensive framework—“microbiota → metabolites/inflammation → epigenome → gene expression”—which mirrors the conceptual backbone of this article.
[4] Rubas, N.C. et al. (2025)
The Gut Microbiome and Epigenomic Reprogramming. International Journal of Molecular Sciences.
https://www.mdpi.com/1422-0067/26/17/8658
A synthesis centred on operational mechanisms (fermentation products, one-carbon metabolism and methylation pathways, inflammation) through which the microbiota may influence epigenomic regulation. Useful to anchor the argument in actionable mechanisms rather than purely associative findings.
[5] Guo, S. et al. (2025)
Epigenetic modifications of gut microbiota and their… (Review; PDF) Frontiers in Pharmacology.
https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2025.1638240/pdf
A structured review covering DNA methylation, histone modifications and non-coding RNAs, framed as microbiota–epigenome “crosstalk”. It strengthens the academic robustness of the topic and supports the main conceptual blocks (SCFAs/HDAC, inflammation, nuclear signalling pathways, etc.).
[6] Waldecker, M. et al. (2008)
Inhibition of histone-deacetylase activity by short-chain fatty acids and some polyphenol metabolites formed in the colon. Journal of Nutritional Biochemistry.
https://www.sciencedirect.com/science/article/abs/pii/S095528630700188X
A key paper documenting SCFAs—particularly butyrate—as HDAC inhibitors in the colon. This is one of the central mechanistic pivots: a microbiota-derived metabolite can alter chromatin accessibility and therefore gene expression.
[7] Chen, J.S. et al. (2003)
Short-chain fatty acid inhibitors of histone deacetylases. (PubMed record)
https://pubmed.ncbi.nlm.nih.gov/12769690/
An older but foundational reference establishing the concept of SCFAs as HDAC inhibitors. It functions as an early anchor for the butyrate → epigenetics literature.
[8] Wu, W. et al. (2017)
Microbiota metabolite short-chain fatty acid acetate… (Review) Mucosal Immunology.
https://www.nature.com/articles/mi2016114
A clear review describing two major SCFA axes: (1) GPCR signalling (GPR41/43), and (2) HDAC inhibition, with downstream immune and inflammatory consequences. Particularly useful to show that SCFA actions are not “digestive” but signalling-driven and transcriptionally relevant.
[9] Stein, R.A. (2023)
Epigenetic effects of short-chain fatty acids from the large intestine. FEMS Microbes / MicroLife.
https://academic.oup.com/microlife/article/doi/10.1093/femsml/uqad032/7199775
A review focused specifically on SCFA epigenetic effects (gene expression, proliferation/differentiation, immunity). It helps connect “microbial metabolite” to concrete, measurable cellular consequences.
[10] Lee, D.H. et al. (2024)
GPR41 and GPR43: From development to metabolic… (Review)
https://www.sciencedirect.com/science/article/pii/S075333222400619X
A review on GPR41/GPR43 as key metabolic signalling nodes influenced by SCFAs. Useful to substantiate the “microbiota modulates metabolism” angle through membrane sensors, complementing HDAC/epigenetic mechanisms.
[11] Crider, K.S. et al. (2012)
Folate and DNA Methylation: A Review of Molecular Mechanisms and the Evidence for Folate’s Role. Nutrients (PMC access).
https://pmc.ncbi.nlm.nih.gov/articles/PMC3262611/
A reference review on DNA methylation and the role of folate in one-carbon metabolism. It supports a rigorous explanation of why methyl donor availability influences methylation patterns and therefore gene expression.
[12] Sfakianoudis, K. et al. (2024)
The Role of One-Carbon Metabolism and Methyl Donors… International Journal of Molecular Sciences.
https://www.mdpi.com/1422-0067/25/9/4977
A synthesis of folate/methionine/transsulfuration pathways and their dependence on key nutrients (B9, B12, choline, betaine, methionine). Useful to secure the “microbiota + nutrition → methylation substrates → epigenome” passage without oversimplification.
[13] Chamberlain, J.A. et al. (2018)
Dietary intake of one-carbon metabolism nutrients and DNA methylation…
https://www.sciencedirect.com/science/article/pii/S0002916522029513
A human study examining associations between one-carbon nutrient intake and DNA methylation patterns. It helps keep the narrative evidence-based: nutritional influences exist, but are tissue- and context-dependent rather than “magical”.
[14] Gutiérrez-Vázquez, C. & Quintana, F.J. (2018)
Regulation of the immune response by the aryl hydrocarbon receptor. (Review; PMC access)
https://pmc.ncbi.nlm.nih.gov/articles/PMC5777317/
A major review on AhR as an integrator of environment–metabolism–immunity, activated by ligands including indole derivatives linked to microbial tryptophan metabolism. It supports the role of tryptophan metabolites in immunity/inflammation with downstream gene-regulatory effects.
[15] Barroso, A. et al. (2021)
The aryl hydrocarbon receptor and the gut–brain axis. Cellular & Molecular Immunology.
https://www.nature.com/articles/s41423-020-00585-5
A review explaining how AhR may influence epigenetic states via microRNAs and histone modifications. Useful to link “microbial metabolites → receptors → epigenetic regulation” beyond butyrate alone.
[16] Konopelski, P. et al. (2022)
Biological Effects of Indole-3-Propionic Acid, a Gut Microbiota-Derived Metabolite… (Review; PubMed record)
https://pubmed.ncbi.nlm.nih.gov/35163143/
A review on indole-3-propionic acid (IPA), a tryptophan-derived metabolite produced by specific gut bacteria, associated with metabolic and anti-inflammatory effects depending on context. It supports the “indole derivatives = systemic signals” section without overclaiming, highlighting context-dependence.
[17] Cani, P.D. et al. (2007)
Metabolic Endotoxemia Initiates Obesity and Insulin Resistance. Diabetes.
https://diabetesjournals.org/diabetes/article/56/7/1761/12590/Metabolic-Endotoxemia-Initiates-Obesity-and
A foundational paper supporting the “metabolic endotoxaemia” hypothesis (LPS): gut-derived inflammatory signalling contributing to low-grade inflammation and metabolic consequences. It underpins the dysbiosis/permeability → chronic inflammation → network dysregulation logic, creating a context conducive to altered gene expression.
[18] Chen, B. et al. (2025)
Gut-derived lipopolysaccharides and metabolic endotoxemia. American Journal of Physiology – Endocrinology and Metabolism.
https://journals.physiology.org/doi/10.1152/ajpendo.00355.2025
A recent review revisiting and refining the LPS hypothesis (mechanisms, limits, nuance, context). Useful to strengthen the “LPS/inflammation” section while avoiding reliance on a single historical reference.
[19] Anhê, F.F. et al. (2021)
Metabolic endotoxemia is dictated by the type of lipopolysaccharide. Cell Reports.
https://www.sciencedirect.com/science/article/pii/S2211124721011384
An important study demonstrating that LPS structure varies and not all LPS species trigger the same metabolic/inflammatory outcomes. This prevents an overly simplistic “LPS = always toxic” narrative and adds mechanistic precision.
[20] Cai, J. et al. (2022)
Gut microbiota-derived bile acids in intestinal immunity, inflammation, and tumorigenesis. Cell Host & Microbe.
https://www.cell.com/cell-host-microbe/fulltext/S1931-3128%2822%2900090-7
A reference review on microbiota-derived bile acids: immune and inflammatory roles, nuclear signalling and distant-organ effects. It anchors the “bile acids as signals” section and complements the SCFA/indole axis with another major messenger system.
[21] Sato, Y. et al. (2021)
Novel bile acid biosynthetic pathways are enriched in the microbiome of centenarians. Nature.
https://www.nature.com/articles/s41586-021-03832-5
A major study in Japanese centenarians showing enrichment of specific secondary bile acid pathways with pathogen-resistance properties (including inhibition of C. difficile by certain derivatives). This is a strong piece for the “microbiota & ageing” section: longevity is associated with concrete microbial metabolic signatures, not merely a list of bacterial taxa.
[22] Kisthardt, S.C. et al. (2023)
The microbial derived bile acid lithocholate and its epimers… (PMC access)
https://pmc.ncbi.nlm.nih.gov/articles/PMC10274734/
Experimental work on LCA epimers (secondary bile acids) and anti-C. difficile activity, including effects on membranes/toxins. Useful for adding mechanistic depth to the centenarian/bile-acid section by moving from narrative association to plausible causal pathways via metabolites.
Short-chain fatty acids (SCFAs)
A family of metabolites produced mainly through microbial fermentation of dietary fibres in the colon. The principal SCFAs are acetate, propionate and butyrate. They play a central role in regulating inflammation, energy metabolism, intestinal barrier integrity and epigenetic signalling, notably through histone deacetylase inhibition.
Secondary bile acids
Molecules derived from primary bile acids produced by the liver, then transformed by the gut microbiota. Certain secondary bile acids act as potent biological signals via nuclear receptors (including FXR and TGR5), influencing immunity, metabolism and inflammation. Specific signatures have been associated with longevity.
AhR (Aryl hydrocarbon receptor)
A ligand-activated transcription factor sensitive to a wide range of environmental, dietary and microbial compounds, including indole derivatives produced by microbial tryptophan metabolism. It plays a key role in immune regulation, inflammation and several gene-regulatory pathways that intersect with epigenetic control.
Non-coding RNAs
RNAs that do not encode proteins but regulate gene expression. This category includes microRNAs (miRNAs) and long non-coding RNAs (lncRNAs). Their expression can be influenced by nutritional environment, inflammation and microbial metabolites.
Intestinal barrier
A set of structures (intestinal epithelium, tight junctions, mucus layer and local immune components) separating the gut lumen from the internal milieu. When compromised, permeability increases and pro-inflammatory signals more readily enter systemic circulation.
Butyrate
An SCFA produced by certain gut bacteria from fermentable fibres. It is the primary fuel for colonocytes and also acts as an HDAC inhibitor, directly influencing gene expression, inflammation and cellular differentiation.
Cellular Nutrition
A systemic nutritional approach designed to support the cell’s core biological mechanisms. It extends micronutrition by integrating systems biology, the microbiota, chronic low-grade inflammation, mitochondrial function and the concept of nutrition as a biological signal.
Chromatin
The structure formed by DNA and histone proteins. Its degree of compaction determines how accessible genes are to transcription machinery. Epigenetic modifications directly shape chromatin organisation.
Dysbiosis
A qualitative and/or quantitative disruption of the gut microbiota, typically characterised by reduced diversity, altered community structure and decreased protective metabolic functions. It is associated with chronic inflammation, metabolic dysregulation and accelerated ageing.
Epigenetics
The set of mechanisms that modulate gene expression without changing DNA sequence. The main mechanisms include DNA methylation, histone modifications and regulation by non-coding RNAs.
Gene expression
The process by which genetic information is transcribed and translated into RNA and/or proteins. Gene expression is dynamic and highly dependent on cellular and environmental context.
HDAC (Histone deacetylase)
Enzymes that remove acetyl groups from histones, generally leading to more compact chromatin and reduced gene expression. Certain molecules—most notably butyrate—can inhibit HDACs, promoting a more open transcriptional state.
Epigenetic clocks
Biological age estimators based on DNA methylation patterns. They are used to approximate ageing pace and potential divergence from chronological age.
Chronic low-grade inflammation
A persistent, low-intensity inflammatory state, often subclinical, implicated in many chronic disorders and in biological ageing. It durably alters cellular environment and gene-regulatory programmes.
Inflammaging
The concept describing chronic low-grade inflammation as a central driver of biological ageing and functional decline, arising from complex interactions between immunity, metabolism, the microbiota and environmental factors.
Microbial metabolites
Molecules produced by the microbiota from dietary substrates or endogenous compounds. They act as biological messengers that can influence local and systemic physiology, including epigenetic regulation.
DNA methylation
The addition of methyl groups to DNA, influencing transcriptional activity. This mechanism depends on methyl-donor availability (folate, vitamin B12, choline, methionine).
Microbiome
The collective genetic material of the microorganisms composing the microbiota. It underpins the microbiota’s broad metabolic and functional capabilities.
Gut microbiota
The community of microorganisms inhabiting the gastrointestinal tract. It plays a major role in digestion, immunity, metabolism, production of signalling metabolites and epigenetic regulation.
MicroRNA (miRNA)
Small non-coding RNAs that regulate multiple genes by influencing mRNA stability and translation. Their expression is sensitive to biological and nutritional environment.
Nutrient sensing
Cellular pathways that detect and interpret nutritional state (energy availability, nutrient supply, stress). Key pathways include mTOR, AMPK, sirtuins and insulin/IGF-1 signalling.
One-carbon metabolism
A network of biochemical pathways involved in methyl-group transfers, essential for DNA methylation and cellular synthesis processes. It depends on key micronutrients.
Intestinal permeability
An increased passage of molecules from the gut lumen into the bloodstream, often associated with dysbiosis and chronic inflammation.
Polyamines
Small molecules produced by both the host and the microbiota, involved in cell proliferation, differentiation and regulation of certain metabolic and gene-regulatory pathways.
Polyphenols
Plant-derived bioactive compounds that are partially metabolised by the microbiota. Their microbial metabolites can exert anti-inflammatory and gene-regulatory effects.
Biological signals
Molecular information perceived by cells (nutrients, hormones, metabolites, cytokines) and integrated to regulate function. Nutrition acts largely through the quality and coherence of these signals.
Biological ageing
A functional process characterised by progressive loss of coherence, resilience and adaptability of biological systems, distinct from chronological age.
Can the microbiota really influence gene expression?
Yes. The microbiota influences gene expression indirectly—but in a well-documented way—through the metabolites it produces (SCFAs, tryptophan-derived compounds, secondary bile acids). These molecules can modulate DNA methylation, histone modifications and non-coding RNA expression, which are three core mechanisms of epigenetic regulation. The microbiota therefore acts as an intermediary between diet, environment and genetic activity.
Can the microbiota change DNA itself?
No. The microbiota does not alter DNA sequence. What it can influence is how certain genes are expressed or silenced. This distinction is precisely what separates genetics from epigenetics: genetic information remains stable, while its use by the cell varies depending on biological context.
Which microbial metabolites matter most for epigenetics?
The most studied are SCFAs—especially butyrate, which functions as an HDAC inhibitor. Indole derivatives produced from tryptophan metabolism and certain secondary bile acids are also key, acting via nuclear or ligand-activated receptors involved in immune regulation, metabolism and gene expression.
Why are dietary fibres so important for the microbiota?
Fibres are the microbiota’s primary energy substrate. Without sufficient fermentable fibre intake, the production of protective metabolites—particularly SCFAs—declines. Low-fibre diets promote dysbiosis, low-grade inflammation and a deterioration of beneficial epigenetic signalling.
Can you “repair” your epigenetics through the microbiota?
“Repair” is an overstatement. However, it is possible to steer certain epigenetic mechanisms in a favourable direction by improving the biological environment—appropriate nutrition, a more functional microbiota and reduced chronic inflammation. Epigenetic regulation is gradual and context-dependent; it does not operate like an on/off switch.
Can dysbiosis accelerate biological ageing?
Yes. Chronic dysbiosis promotes low-grade inflammation, increased intestinal permeability and pro-inflammatory signalling. These states are associated with unfavourable epigenetic patterns and accelerated biological ageing—an effect often described within the inflammaging framework.
Does the microbiota change with age?
Yes. With age, microbiota diversity often declines and functional stability can deteriorate. However, studies in healthy older adults and centenarians show that certain microbial profiles are associated with better metabolic and immune resilience. The microbiota does not change only because of age; lifestyle and nutritional environment matter substantially.
Is there an “ideal” microbiota for longevity?
No. There is no single universally optimal microbiota. That said, several characteristics recur across longevity studies: higher diversity, sustained production of anti-inflammatory metabolites, and stability over time. Functionality matters more than the presence or absence of any single bacterial species.
Are probiotics enough to improve epigenetic regulation?
No. Probiotics can be helpful in specific contexts, but they do not replace an overall strategy. Without appropriate substrates (fibres, polyphenols), reduced inflammation and nutritional coherence, their effects tend to be limited and often transient. Epigenetic outcomes depend on the whole biological environment—not on an isolated product.
What is the link between microbiota, inflammation and epigenetics?
Chronic low-grade inflammation alters cellular environment and directly influences epigenetic mechanisms. The microbiota can either amplify inflammation (in dysbiosis) or help regulate it (via anti-inflammatory metabolites). It therefore acts as a central modulator of both inflammatory and epigenetic terrain.
Can nutrition compensate for an imbalanced microbiota?
Partially. Nutrition is the primary lever to reshape the microbiota, but effects are progressive. A coherent dietary pattern can improve diversity and microbial function over time, but long-standing or severe imbalances may require time and a structured approach. There is no instant correction.
What is the specific contribution of Cellular Nutrition in this context?
Cellular Nutrition is not limited to “feeding” human cells. It aims to optimise the coherence of biological signals at a systems level, integrating the microbiota as a central actor. It acts simultaneously on inflammation, metabolism, mitochondrial function and the quality of epigenetic signals perceived by the cell.
Can we measure the microbiota’s impact on epigenetics?
Indirectly, yes. Epigenetic clocks, inflammatory and metabolic markers, and microbiota analyses can help characterise biological trajectories. However, epigenetics remains complex, and no single test can summarise overall biological state on its own.
Microbiota and epigenetics: hype or scientific reality?
It is a robust research field supported by hundreds of experimental, clinical and population studies. Media narratives can overpromise, but the microbiota’s role as an interface between nutrition, environment and gene expression is now widely established in the scientific literature.