April 16, 2025
The Microbiome: You’re More Bacteria Than Human

How many dumb doctors do you know?
In medical school, I learned that, up until about 100 years ago, doctors prescribed cigarettes as a treatment for asthma¹. Equally perplexing is the lobotomy (a procedure in which the corpus callosum, a structure which joins the two hemispheres of the brain), is severed. Not only was this common practice, but it won a Nobel Prize². Consistent with this madness, heroin was once used to treat morphine addiction³.
It’s natural to think these doctors were really dumb, though, of course, they weren’t. They simply knew less. That’s why I often wonder about what I’m doing (or not doing) now, that will make me look dumb to people in the future. Science and medicine continue to achieve extraordinary things. For instance, there is the ROSA ONE Brain System⁴ for performing neurosurgery, CRISPR for editing genes⁵, and Google Deep Mind’s AI making rapid progress⁶ in both disease diagnosis and drug development.
We’re good, but we’re not that good. I say that because medicine as a profession overwhelmingly ignores the human microbiome, which happens to contain 3.3 million genes⁷, as compared with our own 20,000 genes. Ignoring its impact on physical and mental health, quality of life or susceptibility to disease, won’t age well. It’s a modern day ‘cigarette for asthma’.
From Microscope to Footpath
In the 1600s, Antonie van Leeuwenhoek⁸ peered into a handmade microscope and saw bacteria for the first time.
The best part of 400 years later, Australian scientists Barry Marshall and Robin Warren, demonstrated it was a bacterium, H. pylori, and not stress, that caused stomach ulcers⁹. Data 1, Dogma 0.
Thousands of years before the discovery of microbes including H. Pylori, however, Chinese Medicine was using faecal preparations¹⁰ to treat gut infections—what we now call FMT (faecal microbiota transplant). Sounds revolting but works brilliantly!
Dogs will never need FMT. Their sniffing, licking, and generally disgusting behaviour is innate behaviour that reinforces microbial diversity¹¹—for them (and us). Our ancestors, not so distant, used to gain diversity from dirt, shared meals, and unfiltered environments, whereas now, many seem more interested in antibacterial sprays and sterile packaging.

As our tools have improved, so too has our language¹². We now separate microbiota (the bugs) from the microbiome (their genes and the environment they contribute to). This has allowed us to evolve from carpet-bombing interventions to those more sniper-rifle—like, such as narrow spectrum antibiotics, prebiotics, probiotics, postbiotics, and curated exposures.
What a Healthy Microbiome Looks Like
In the last 100 years, we’ve lost 30% of microbial diversity¹³, representing erosion as opposed to evolution. Indeed, the best way to think of your gut microbiome is as a garden-like ecosystem. When it’s healthy, it’s:
- Diverse and Stable – Different species doing different jobs. Diversity means resilience.¹⁴
- Functionally Rich and Productive – Producing short-chain fatty acids (SCFAs), breaking down fibre, making vitamins, metabolising bile acids.¹⁵
- Conditions are Optimised – The gut thrives at a pH between 5.5–7.0, with oxygen gradients and a strong mucosal barrier.¹⁶
- Key Players are Playing – Akkermansia muciniphila, Fecalibacterium prausnitzii, and phyla like Bacteroidota, Bacillota, and Actinobacteriota are the backbone of a robust microbiome.¹⁷
We’re Cyborgs! (trust me, it’s a good thing)
Most of the genetic material in your body isn’t yours. The vast majority belongs to trillions of bacteria, viruses, and fungi that call your body home. Despite what you may think, a bit like the 10-year-old at my house, they actually run the joint!
Top 10 Functions of the Microbiome
- Digestion
Microbes break down complex carbohydrates and plant fibres that human enzymes can’t touch¹⁸. In doing so, they produce SCFAs — particularly butyrate, acetate and propionate — which fuel colon cells, modulate appetite and suppress inflammation. Butyrate¹⁹, in particular, helps keep inflammation in check by blocking pro-inflammatory pathways and supporting regulatory T-cells — the immune cells that tell your body when to calm down.
2. Immune Calibration
Nearly 70% of your immune cells reside in the gut²⁰. Microbes help train it — teaching the body to tolerate the self and harmless antigens, while still mounting proportionate responses to pathogens. This is how we build immune tolerance and avoid chronic inflammation or autoimmunity.
- Pathogen Defence
Through a process called competitive exclusion, beneficial microbes outcompete pathogens for food and space²¹. Many also produce acids and antimicrobial peptides that directly inhibit pathogens. This microbial barrier is your immune system’s first line of defence.
- Metabolic Regulation
Your microbiome influences how you process food, store fat and regulate blood sugar²². Some species enhance insulin sensitivity and mitochondrial function. Others promote inflammation and metabolic dysfunction. This is why gut health is foundational to preventing metabolic disease.
- Nutrient Synthesis
Certain microbes synthesise essential vitamins including K2, folate, and several B vitamins.²³ They also help with mineral absorption by creating the right pH conditions in the gut. Without these bugs, dietary nutrients don’t get converted into usable fuel.
- Homeostasis and Hormonal Signalling
Microbes produce molecules that influence appetite, energy balance and even temperature regulation.²⁴ They interact with hormones like GLP-1 (the class of peptide found in Ozempic), and modulate the hypothalamic-pituitary-adrenal axis — the command centre for your stress response and circadian rhythm.
- Neurotransmission
The gut and brain talk constantly. Microbes produce neurotransmitter precursors, including serotonin and dopamine.²⁵ This communication loop — the gut-brain axis — affects mood, cognition and resilience. When the balance is off, so are you.
- Inflammatory Control
Some bacteria dial down inflammation by producing SCFAs and stimulating T cells.²⁶ Others provoke inflammation by activating (the master transcription factor) NF-κB and releasing endotoxins. Your long-term inflammatory state often reflects who’s winning that tug of war.
- Developmental Programming
The early microbiome plays a critical role in immune and brain development.²⁷ A baby’s delivery, feeding and environmental exposures all influence this programming window. A disrupted early microbiome increases risk for allergy, obesity and chronic disease later on.
- Detoxification and Waste Management
Microbes help metabolise bile acids, degrade hormones like oestrogen, and break down environmental toxins.²⁸ They even influence how your liver handles pharmaceuticals. When this system stalls, toxins linger and inflammation rises.
There Are Many Ways To Ruin A Perfectly Good Microbiome.
These are varied and complex²⁹, but at the top of the list come antibiotics, highly processed and sugary foods and foods stripped of nutrients, excessive alcohol, chronic stress, environmental toxins and living “too cleanly” for our own good.
When the ecosystem breaks down, it’s called dysbiosis³⁰—too many bad bugs, not enough good ones. The effects can be quantified using comprehensive microbiome and stool testing (including sequencing, metabolomics, or functional panels) which often reveal certain patterns:
- Reduced microbial diversity – Healthy guts demonstrate 20–30% more species richness than those with chronic digestive or inflammatory conditions.³¹
- Low SCFA production – Butyrate, acetate, and propionate are critical for colonocyte health, immune regulation, and inflammation control.³² These are consistently depleted in IBS and IBD patients.
- Digestive dysfunction markers – Undigested fat (steatorrhoea), occult blood, high calprotectin, or low pancreatic elastase usually point to deeper issues—enzyme insufficiency, inflammation, or mucosal breakdown.³³ These can explain fatigue, bloating, or nutrient loss.
- Leaky gut indicators – Elevated zonulin and the translocation of lipopolysaccharides (LPS) into circulation correlate with increased intestinal permeability (“leaky gut”) and are strongly associated with autoimmune activation and systemic inflammation.³⁴
- Dysbiosis and toxic overgrowth – Excess Proteobacteria, low Firmicutes to Bacteroidetes ratios, or blooms of species like Klebsiella or Clostridium difficile are red flags.³⁵ These bugs pump out LPS and other metabolic byproducts that keep the gut wall inflamed and the immune system reactive.
- Low secretory IgA – This is your mucosal immune forcefield. We often see it tanked in people with chronic stress, repeat infections, or immune suppression.³⁶ Low sIgA creates vulnerability to things ranging from pathogens to food antigens.
Microbiome results can explain a person’s symptoms or can be harbingers of impending illness. They can explain why someone’s gut is dysfunctional, even when their blood tests are normal. More importantly, they guide more precise, targeted interventions.
If You’re Feeling Like Crap, Your Microbiome Could Hold Some Answers
I’ve had inflammatory bowel disease since I was 17 — and until fairly recently, not one gastroenterologist mentioned the microbiome. That tells you something about where mainstream medicine still stands. But now, having seen firsthand the impact of restoring microbial balance in my patients, it’s the first place I look when the clinical picture doesn’t add up.
When the gut ecosystem loses diversity³⁷, resilience³⁸, or microbial signalling³⁹, symptoms follow. That can happen gradually, or suddenly — after a course of antibiotics⁴⁰, a bout of food poisoning⁴¹, or travel-related exposure⁴² to unfamiliar microbes. Evidence⁴³ shows that microbial disruption from travel can occur within 24 hours, and while the microbiome may begin reverting⁴⁴ to baseline within a week, full recovery often takes weeks to months — and sometimes doesn’t happen without support.
Restoring microbial balance is more than theory. With the right inputs, it can build back. I’ve seen it — repeatedly in clinical practice, and personally. Some of the maladies that may be driven, or exacerbated by dysbiosis include:
- IBS, Crohn’s, and Ulcerative Colitis – Loss of SCFA-producing species increases inflammation, impairs healing, and worsens symptom severity.⁴⁵
- Atherosclerosis and Cardiovascular Disease – Gut-derived metabolites like trimethylamine-N-oxide (TMAO)—produced by dysbiotic microbes metabolising choline and carnitine—have been associated with increased plaque formation and cardiovascular risk. Low SCFA levels may also impair lipid metabolism and endothelial function.⁴⁶
- Metabolic Conditions – Obesity and Type 2 diabetes are linked to microbial imbalance, insulin resistance, and chronic low-grade inflammation.⁴⁷
- Autoimmunity – Bacteria like Prevotella copri are disproportionately present in rheumatoid arthritis, MS, and Hashimoto’s thyroiditis—possibly driving immune misfiring.⁴⁸
- Mental Health & Neurological Disorders – Dysbiosis alters stress hormone output, disrupts neurotransmitters, and may accelerate neurodegeneration in conditions like Parkinson’s.⁴⁹
- Skin Conditions – Eczema, acne, and psoriasis often reflect gut inflammation and loss of microbial balance.⁵⁰
- Immune Dysfunction – The immune system either overreacts (autoimmunity) or underperforms (recurrent infections)—both patterns linked to a compromised gut.⁵¹
A healthier gut means better digestion, as well as feeling stronger, thinking clearer, and living better, longer.
A Framework for Repairing the Microbiome
The 4 R’s – A Smarter Way to Support the Gut
Understanding what’s happening in the gut allows for a more structured, targeted approach to treatment. One such framework is the 4 R’s — a method that can be used and adapted to a patient’s unique findings.
The 4Rs serve as a flexible, data-driven approach that may involve general practitioners, allied health, and when needed, specialist input.

1. Remove
The first step is to eliminate what does not belong. This may include using targeted antimicrobials to reduce bacterial overgrowth or parasites, removing aggravating foods, and addressing inflammatory drivers⁵² such as alcohol, chronic stress, or environmental toxins. This is a deliberate and test-informed intervention to disrupt the patterns sustaining dysfunction as opposed to a detox.
2. Replace
When digestion is impaired due to factors like low pancreatic enzyme output, bile insufficiency, or prolonged inflammation, nutrient absorption is compromised. Digestive processes may be supported with pancreatic enzymes⁵³ or bile acid replacement where clinically indicated. Micronutrient deficiencies⁵⁴ identified through testing are typically addressed at this stage. The focus is on restoring physiological function.
3. Reinoculate
With dysbiosis and digestion attended to, the third R aims to improve microbial diversity. This involves reintroduction of depleted species with specific probiotics, informed by stool testing. Interventions usually include specific probiotic strains, prebiotic fibres, and fermented foods⁵⁵. The aim is to restore ecological balance, since microbial resilience⁵⁶ depends on both diversity and function.
4. Repair & Rebalance
The gut lining is metabolically active and immune-responsive. When compromised, it permits translocation of antigens, pathogens, and toxins. Nutritional support may include glutamine, zinc carnosine, polyphenols, omega-3 fatty acids, or immunoglobulin supplementation⁵⁷. Additional strategies to restore circadian rhythm⁵⁸, autonomic tone, and inflammatory balance⁵⁹ are also considered, depending on clinical context. In complex cases, this phase often deploys experts within a multidisciplinary collaboration.
Further Reading
This article began by questioning what aspects of current medical thinking might seem misguided in hindsight. One strong candidate is the widespread neglect of the human microbiome. Having explored its importance, how it becomes disrupted, and how it can be repaired, readers who want to go further will find Your Best Gut: The 28 Day Guide to Transform Your Life by Dr. Paul Froomes an extremely helpful next step.
References
¹ Valenstein, Elliot S. 2010. “The Discovery of the Leukotomy.” Dialogues in Clinical Neuroscience 12 (1): 79–92. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2844275/.
² NobelPrize.org. 1949. “The Nobel Prize in Physiology or Medicine 1949 – António Egas Moniz.” NobelPrize.org. Nobel Prize Outreach AB. https://www.nobelprize.org/prizes/medicine/1949/moniz/facts/.
³ United Nations Office on Drugs and Crime (UNODC). 1953. “The Hallucinogens.” Bulletin on Narcotics 2 (January 1): 4–21. https://www.unodc.org/unodc/en/data-and-analysis/bulletin/bulletin_1953-01-01_2_page004.html.
⁴ Zimmer Biomet. ROSA ONE Brain Robotic Platform. Last modified 2023. https://www.zimmerbiomet.com/en/products-and-solutions/zb-edge/robotics/rosa-brain.html.
⁵ Doudna, Jennifer A., and Emmanuelle Charpentier. “The New Frontier of Genome Engineering with CRISPR-Cas9.” Science 346, no. 6213 (2014): 1258096. https://doi.org/10.1126/science.1258096.
⁶ Jumper, John, Richard Evans, Alexander Pritzel, et al. “Highly Accurate Protein Structure Prediction with AlphaFold.” Nature 596, no. 7873 (2021): 583–589. https://doi.org/10.1038/s41586-021-03819-2.
⁷ Song, Hong, and Guangmei Yang. 2010. “Neuroinflammation and Microglia: The Potential Targets of Disease-Modifying Treatment for Alzheimer’s Disease.” Protein & Cell 1 (8): 718–21. https://academic.oup.com/proteincell/article/1/8/718/6874114.
⁸ Lederberg, Joshua, and Alexa T. McCray. “‘Ome Sweet ‘Omics: A Genealogical Treasury of Words.” The Scientist, July 2001. U.S. National Library of Medicine. https://lhncbc.nlm.nih.gov/LHC-publications/PDF/pub2001047.pdf.
⁹ Marshall, Barry, and Robin Warren. “The Nobel Prize in Physiology or Medicine 2005.” Nobel Lecture, December 2005. https://www.nobelprize.org/uploads/2018/06/marshall-lecture.pdf.
¹⁰ Pollak, Thomas A., B. Neil R. Lennox, Sina Müller, Michael E. Benros, Harald Prüss, Ludger T. van Elst, et al. 2020. “Autoimmune Psychosis: An International Consensus on an Approach to the Diagnosis and Management of Psychosis of Suspected Autoimmune Origin.” The Lancet Psychiatry 7 (1): 93–108. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8155486/.
¹¹ Valles-Colomer, Mireia, Gwen Falony, Youssef Darzi, Eran F. Tigchelaar, Jingyuan Wang, Raul Y. Tito, et al. 2019. “The Neuroactive Potential of the Human Gut Microbiota in Quality of Life and Depression.” Microbiome 7 (1): 15. https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-018-0450-3.
¹² Lederberg, Joshua, and Alexa T. McCray. “‘Ome Sweet ‘Omics: A Genealogical Treasury of Words.” The Scientist, July 2001. U.S. National Library of Medicine. https://lhncbc.nlm.nih.gov/LHC-publications/PDF/pub2001047.pdf.
¹³ Blaser, Martin J. “Disappearance of the Gut Microbiota: How We May Be Losing Our Most Important Allies.” American Society for Microbiology, November 2019. https://asm.org/Articles/2019/November/Disappearance-of-the-Gut-Microbiota-How-We-May-Be.
¹⁴ Lloyd-Price, Jason, Galeb Abu-Ali, and Curtis Huttenhower. “The Healthy Human Microbiome.” Genome Medicine 8, no. 1 (2016): 51. https://doi.org/10.1186/s13073-016-0307-y.
¹⁵ Koh, Andrea, et al. “From Dietary Fiber to Host Physiology: Short-Chain Fatty Acids as Key Bacterial Metabolites.” Cell 165, no. 6 (2016): 1332–1345. https://doi.org/10.1016/j.cell.2016.05.041.
¹⁶ Fallingborg, Jan. “Intraluminal pH of the Human Gastrointestinal Tract.” Danish Medical Bulletin 46, no. 3 (1999): 183–196. https://pubmed.ncbi.nlm.nih.gov/10421978/.
¹⁷ Qin, Jun, et al. “A Human Gut Microbial Gene Catalogue Established by Metagenomic Sequencing.” Nature 464, no. 7285 (2010): 59–65. https://doi.org/10.1038/nature08821.
¹⁸ Flint, H. J., Scott, K. P., Louis, P., & Duncan, S. H. (2012). The role of the gut microbiota in nutrition and health. Nature Reviews Gastroenterology & Hepatology, 9(10), 577–589. https://doi.org/10.1038/nrgastro.2012.156.
¹⁹ Parada Venegas, Daniela, et al. “Short Chain Fatty Acids (SCFAs)–Mediated Gut Epithelial and Immune Regulation and Its Relevance for Inflammatory Bowel Diseases.” Frontiers in Immunology 10 (2019): 277. https://doi.org/10.3389/fimmu.2019.00277.
²⁰ Belkaid, Y., & Hand, T. W. (2014). Role of the microbiota in immunity and inflammation. Cell, 157(1), 121–141. https://doi.org/10.1016/j.cell.2014.03.011.
²¹ Kamada, N., Chen, G. Y., Inohara, N., & Núñez, G. (2013). Control of pathogens and pathobionts by the gut microbiota. Nature Immunology, 14(7), 685–690. https://doi.org/10.1038/ni.2608.
²² Bäckhed, F., Ding, H., Wang, T., Hooper, L. V., Koh, G. Y., Nagy, A., … & Gordon, J. I. (2004). The gut microbiota as an environmental factor that regulates fat storage. Proceedings of the National Academy of Sciences, 101(44), 15718–15723. https://doi.org/10.1073/pnas.0407076101.
²³ LeBlanc, J. G., Milani, C., de Giori, G. S., Sesma, F., van Sinderen, D., & Ventura, M. (2013). Bacteria as vitamin suppliers to their host: a gut microbiota perspective. Current Opinion in Biotechnology, 24(2), 160–168. https://doi.org/10.1016/j.copbio.2012.08.005.
²⁴ Neufer, P. D., Bamman, M. M., Muoio, D. M., Bouchard, C., Cooper, D. M., Goodpaster, B. H., … & Booth, F. W. (2015). Understanding the cellular and molecular mechanisms of physical activity-induced health benefits. Cell Metabolism, 22(1), 4–11. https://doi.org/10.1016/j.cmet.2015.05.011.
²⁵ O’Mahony, S. M., Clarke, G., Borre, Y. E., Dinan, T. G., & Cryan, J. F. (2015). Serotonin, tryptophan metabolism and the brain-gut-microbiome axis. Behavioural Brain Research, 277, 32–48. https://doi.org/10.1016/j.bbr.2014.07.027.
²⁶ Cani, P. D., & Delzenne, N. M. (2009). The role of the gut microbiota in energy metabolism and metabolic disease. Current Pharmaceutical Design, 15(13), 1546–1558. https://doi.org/10.2174/138161209788168164.
²⁷ Rook, G. A. W., & Lowry, C. A. (2008). The hygiene hypothesis and psychiatric disorders. Trends in Immunology, 29(4), 150–158. https://doi.org/10.1016/j.it.2008.01.002.
²⁸ Ridlon, J. M., Kang, D. J., & Hylemon, P. B. (2006). Bile salt biotransformations by human intestinal bacteria. Journal of Lipid Research, 47(2), 241–259. https://doi.org/10.1194/jlr.R500013-JLR200.
²⁹ Zmora, Niv, Jotham Suez, and Eran Elinav. “You Are What You Eat: Diet, Health and the Gut Microbiota.” Nature Reviews Gastroenterology & Hepatology 16, no. 1 (2019): 35–56. https://doi.org/10.1038/s41575-018-0061-2.
³⁰ Petersen, Charisse, and June L. Round. “Defining Dysbiosis and Its Influence on Host Immunity and Disease.” Cell Microbiology 16, no. 7 (2014): 1024–1033. https://doi.org/10.1111/cmi.12308.
³¹ Sonnenburg, Erica D., and Justin L. Sonnenburg. “Starving Our Microbial Self: The Deleterious Consequences of a Diet Deficient in Microbiota-Accessible Carbohydrates.” Cell Metabolism 20, no. 5 (2014): 779–786. https://doi.org/10.1016/j.cmet.2014.07.003.
³² Parada Venegas, Daniela, et al. “Short Chain Fatty Acids (SCFAs)–Mediated Gut Epithelial and Immune Regulation and Its Relevance for Inflammatory Bowel Diseases.” Frontiers in Immunology 10 (2019): 277. https://doi.org/10.3389/fimmu.2019.00277.
³³ Manz, Michael, et al. “Small bowel endoscopy, capsule and device-assisted enteroscopy: the present and future.” Gut 67, no. 1 (2018): 1–13. https://doi.org/10.1136/gutjnl-2017-314711.
³⁴ Fasano, Alessio. “Zonulin and Its Regulation of Intestinal Barrier Function: The Biological Door to Inflammation, Autoimmunity, and Cancer.” Physiological Reviews 91, no. 1 (2011): 151–175. https://doi.org/10.1152/physrev.00003.2008.
³⁵ Rinninella, Emanuele, et al. “What Is the Healthy Gut Microbiota Composition? A Changing Ecosystem across Age, Environment, Diet, and Diseases.” Microorganisms 7, no. 1 (2019): 14. https://doi.org/10.3390/microorganisms7010014.
³⁶ Brandtzaeg, Per. “Secretory IgA: Designed for Anti-Microbial Defense.” Frontiers in Immunology 4 (2013): 222. https://doi.org/10.3389/fimmu.2013.00222.
³⁷ Lozupone, Catherine A., et al. “Diversity, Stability and Resilience of the Human Gut Microbiota.” Nature 489, no. 7415 (2012): 220–30. https://doi.org/10.1038/nature11550.
³⁸ Gagliardi, Alessandra, et al. “Rebuilding the Gut Microbiota Ecosystem.” International Journal of Environmental Research and Public Health 15, no. 8 (2018): 1679. https://doi.org/10.3390/ijerph15081679.
³⁹ Belkaid, Yasmine, and Timothy W. Hand. “Role of the Microbiota in Immunity and Inflammation.” Cell 157, no. 1 (2014): 121–41. https://doi.org/10.1016/j.cell.2014.03.011.
⁴⁰ Dethlefsen, Les, and David A. Relman. “Incomplete Recovery and Individualized Responses of the Human Distal Gut Microbiota to Repeated Antibiotic Perturbation.” Proceedings of the National Academy of Sciences 108, Suppl 1 (2011): 4554–61. https://doi.org/10.1073/pnas.1000087107.
⁴¹ Ferreira, Ricardo B.R., et al. “Pathogen-Induced Changes in the Intestinal Microbiota Contribute to Inflammatory Bowel Disease.” Inflammatory Bowel Diseases 27, no. 4 (2021): 515–27. https://doi.org/10.1093/ibd/izaa332.
⁴² David, Lawrence A., et al. “Host Lifestyle Affects Human Microbiota on Daily Timescales.” Genome Biology 15, no. 7 (2014): R89. https://doi.org/10.1186/gb-2014-15-7-r89.
⁴³ David, Lawrence A., et al. “Host Lifestyle Affects Human Microbiota on Daily Timescales.” Genome Biology 15, no. 7 (2014): R89. https://doi.org/10.1186/gb-2014-15-7-r89.
⁴⁴ Lozupone, Catherine A., et al. “Diversity, Stability and Resilience of the Human Gut Microbiota.” Nature 489, no. 7415 (2012): 220–30. https://doi.org/10.1038/nature11550.
⁴⁵ Parada Venegas, Daniela, et al. “Short Chain Fatty Acids (SCFAs)–Mediated Gut Epithelial and Immune Regulation and Its Relevance for Inflammatory Bowel Diseases.” Frontiers in Immunology 10 (2019): 277. https://doi.org/10.3389/fimmu.2019.00277.
⁴⁶ Ahmadmehrabi, S., and W. H. W. Tang. “Gut Microbiome and Its Role in Cardiovascular Diseases.” Current Opinion in Cardiology 32, no. 6 (November 2017): 761–66. https://doi.org/10.1097/HCO.0000000000000445.
⁴⁷ Qin, Jun, et al. “A metagenome-wide association study of gut microbiota in type 2 diabetes.” Nature 490, no. 7418 (2012): 55–60. https://doi.org/10.1038/nature11450.
⁴⁸ Scher, Jose C., et al. “Expansion of intestinal Prevotella copri correlates with enhanced susceptibility to arthritis.” eLife 2 (2013): e01202. https://doi.org/10.7554/eLife.01202.
⁴⁹ Sampson, Timothy R., et al. “Gut microbiota regulate motor deficits and neuroinflammation in a model of Parkinson’s disease.” Cell 167, no. 6 (2016): 1469–1480.e12. https://doi.org/10.1016/j.cell.2016.11.018.
⁵⁰ De Pessemier, B., et al. “The Microbiome and Psoriasis: A Comprehensive Review.” Journal of Dermatological Science 104, no. 1 (2021): 42–49. https://doi.org/10.1016/j.jdermsci.2021.07.005.
⁵¹ Belkaid, Yasmine, and Timothy W. Hand. “Role of the Microbiota in Immunity and Inflammation.” Cell 157, no. 1 (2014): 121–141. https://doi.org/10.1016/j.cell.2014.03.011.
⁵² Link, Springer. “Inflammatory Drivers.” In Neuroinflammation and Neurodegeneration, edited by Phillip K. Peterson and Michal Toborek, 2014. https://link.springer.com/chapter/10.1007/978-3-319-09614-8_6.
⁵³ Domínguez-Muñoz, J. E., et al. “Optimization of Nutrition and Pancreatic Enzyme Replacement Therapy in Chronic Pancreatitis.” Current Opinion in Clinical Nutrition and Metabolic Care 14, no. 5 (2011): 570–576. https://doi.org/10.1097/MCO.0b013e328349b812.
⁵⁴ Di Sabatino, Antonio, and Gino R. Corazza. “Micronutrient Deficiencies in Celiac Patients.” Clinical Reviews in Allergy & Immunology 42, no. 3 (2014): 298–310. https://www.researchgate.net/publication/389057929_Micronutrient_deficiencies_in_patients_with_celiac_disease_A_systematic_review_and_meta-analysis.
⁵⁵ Rastall, Robert A., and Glenn R. Gibson. “Recent developments in prebiotics to selectively impact beneficial microbes and promote intestinal health.” Current Opinion in Biotechnology 16, no. 2 (2005): 186-192. https://doi.org/10.1016/j.copbio.2005.02.005.
⁵⁶ Lozupone, Catherine A., et al. “Diversity, Stability and Resilience of the Human Gut Microbiota.” Nature 489, no. 7415 (2012): 220–30. https://doi.org/10.1038/nature11550.
⁵⁷ Soler, Dulcineia, et al. “Modulation of intestinal epithelial barrier function by immunoglobulin-derived proteins.” Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease 1802, no. 5 (2010): 451-457. https://doi.org/10.1016/j.bbadis.2010.01.006.
⁵⁸ Voigt, Robin M., et al. “Circadian Disruption: Potential Implications in Inflammatory and Metabolic Diseases Associated with Gut Barrier Dysfunction.” Journal of Leukocyte Biology 100, no. 5 (2016): 987–996. https://pubmed.ncbi.nlm.nih.gov/24313168/.
⁵⁹ Kiecolt-Glaser, Janice K., et al. “Chronic Stress and Age-Related Increases in the Proinflammatory Cytokine IL-6.” Proceedings of the National Academy of Sciences 100, no. 15 (2003): 9090–9095. https://doi.org/10.1073/pnas.1531903100.

ABOUT THE AUTHOR
For over 30 years, Dr. Weisinger has been dedicated to improving health, performance, and well-being. His expertise spans clinical care, research, and academic instruction. Discover why so many trust Dr. Weisinger for personalised, proactive healthcare—because true health is about thriving, not just surviving.