Cibus Medicina Est – 'Let Food Be Thy Medicine'

What is endotoxin?

It is probably quite likely that the reader has never heard of endotoxin before. Endotoxin, specifically lipopolysaccharide (LPS), the most potent form, is a toxic component found in the outer membrane of Gram-negative bacteria. When these “bad” bacteria die, or are destroyed in our guts by white blood cells, these endotoxins break off and can enter the circulating bloodstream (a process known as endotoxemia). LPS has a very high binding affinity for the TLR4 receptor, which in turn creates inflammation, and has been implicated in many chronic diseases.

The harmful effects of endotoxin on energy and structure

Endotoxin is, unfortunately, somewhat uniquely evil in how many biological systems it can impair. The main toxic mechanism of LPS involves inappropriate excitation of cells, followed by inflammation and mitochondrial dysfunction. This inflammation causes cells to swell, taking up water and losing their structure. When a cell lacks structure, it also lacks energy, and vice versa. Think of a tidy home; that order (structure) took energy. When cells lack order, they lack the means and infrastructure to generate energy, gradually resulting in less and less structure and energy. High-energy cells are highly specialised and differentiated, and it’s that abundance of cellular energy which allowed them to develop and carry out their specialised roles in the first place. Therefore, when mitochondrial function is impaired by LPS (whether through cytokine release, accumulation of excess oestrogen, or the swelling-induced mechanical distortion of mitochondria) and cellular energy is decreased, cells can no longer carry out their individual roles and the whole organism suffers, leading to disease. These faulty, impaired mitochondria produce more reactive oxygen species (ROS), which in turn creates more DNA damage, eventually leading to cancer.

Endotoxin and Cancer: Why we shouldn’t overlook it

“I’m inclined to think that even cancer is largely an endotoxin problem. Chronic, year after year, bad food, irritating the intestine, causing increased histamine and serotonin and oestrogen. A constant stream of endotoxin flowing through the system, shaking up chromosomes, creating inflammation, fatiguing the repair systems. Finally, when the repair systems are down, to a certain extent, the cancers that are constantly popping up stop being removed. And so if you don’t die of acute sepsis, then heart disease and cancer are the result of chronic exposure to the endotoxin.” – Dr Raymond Peat

Until only fairly recently, endotoxin was not suspected to be involved in cancer. Fortunately, now we know that not only can it provide a favourable environment for cancers to thrive in, but it can even directly cause tumours to form. 

One of the ways in which chronic endotoxin exposure can lead to cancer formation is through its ability to allow oestrogen to accumulate in excess, and thus skew its relationship with the opposing factors like thyroid hormone and progesterone. Endotoxin’s inhibition of the glucuronidation system (the system which helps export substances from the body through urine or faeces via bile) leads to oestrogen accumulation in our cells, as well as prolonging circulation of endotoxin in the body (Bánhegyi, et al., 1995). The liver is constantly inactivating hormones, like oestrogen, and when this ability is shut down, it can no longer stabilise hormone balances as normal. Excess oestrogen (also known as ‘oestrogen dominance’) has been shown to play roles in breast, ovarian, prostate, uterine, pituitary, lung, and skin cancers (Steinberg et al., 1994; Langdon et al., 2020; Lafront et al., 2024; Grady et al., 1995; Heaney, Fernando and Melmed, 2002; Li, Pei and Feng, 2023; Smida et al., 2020). 

Excess oestrogen can be metabolised into catechol oestrogens which mimic compounds such as adrenaline, and it’s in these forms when they can be oxidised into quinones which produce toxic free radicals, leading to tumour formation (Cavalieri and Rogan, 2021).

Furthermore, LPS forces macrophages and the Kupffer cells in the liver to synthesise more tumour necrosis factor (TNF). Good, right? Unfortunately not. Despite its name, in reality TNF significantly enhances tumour growth and metastasis of numerous cancers (Wang and Lin, 2008). I think a more appropriate name is needed.

It’s important and helpful to look at endotoxin as this chronic, baseline stressor on the body. Like the quote above suggests, when your gut lining is damaged, you have a constant flow of endotoxin being absorbed and creating inflammation. At these sites of inflammation, immune cells become activated, and their evolutionary advantage is that they produce free radicals and inflammatory enzymes to kill pathogens. However, these compounds also break DNA strands. And so when you have chronic inflammation over the long term, although we have DNA repair systems to fix these damages, these systems become overloaded, and mutations accumulate. Have enough of the correct mutations in the right places, and cancers start forming.

Why endotoxin is becoming such a large problem today

Endotoxin and its mechanisms of damage have never been more of a serious issue than they are right now. We consume too much ultra-processed ‘food’ and lace it with biological toxins. Our fields, waters, and skies are riddled with environmental poisons which leach into the animals and crops we eat. And as it turns out, consumption of these ultra-processed foods, emulsifiers, pesticides, and pollutants wages war on our biology. Overconsumption of, and overexposure to these things, unhealthy farming practices, and more generally “stressful modern conditions”, tear apart our epithelial gut lining, increasing permeability and leading to endotoxemia, systemic inflammation, and metabolic disorders (Camilleri et al., 2019; Poto et al., 2023; Do, 2024; Mallardi et al., 2025). 

Consequently, young people – who have notoriously bad diets – are becoming ill at higher rates than ever before. And if you have a population wherein both the old and the young are sick, it creates an unsustainable dual strain on the healthcare services and medical resources. In combination, a healthcare system which doesn’t effectively heal the patient but instead suppresses the symptoms of a complicated underlying problem which is never fixed, only ever prolongs the patients’ poor health and thus the financial burden on the state.

One particularly striking study was carried out last year and it explored endotoxin’s impact on human emotions. In the study, the researchers discovered that in the test subjects that were exposed to LPS, there was a significant reduction in people’s empathy for others’ psychological pain (Flasbeck et al., 2024). It was the “endotoxin-induced acute inflammation” which led to the volunteers becoming more callous and less empathetic towards others. Evolutionarily, this makes sense; it likely reflects an adaptive strategy to conserve one’s energy through not responding empathetically when sick oneself. However, it begs an interesting question, that perhaps those who seem to be ‘more apathetic by nature’ are actually just chronically inflamed on the inside? 

Endotoxin has also been shown to:

• Drive obesity, diabetes, and cardiovascular disease (Perng et al., 2022; Lin et al., 2022)
• Accelerate the cognitive decline of ageing (Fei et al., 2022)
• Cause chronic inflammation (Shan et al., 2020)
• Cause infertility and lower testosterone levels in men (Tremellen, 2016)
• Cause infertility and lower progesterone levels in women (Tremellen et al., 2014)
• Cause depression and anxiety (Radjabzadeh et al., 2022)
• Trigger social withdrawal and isolation (Stockmaier et al., 2020)
• Potentially cause cancerisation of normal cells (Tang et al., 2021)
• Increase serum oestrogen and cortisol levels (Christeff et al., 2002; Grigoleit et al., 2011)
• Accelerate atherosclerosis (Reifenberg et al., 2009; Mastrangelo et al., 2025)
• Cause metastasis of some cancers (Cao et al., 2023)
• Increase serotonin release from platelets, suppressing mitochondria, and impairing circulation (J. Hawiger et al., 1977)
• Attenuate empathy for others (Flasbeck et al., 2024)
• Cause muscle weakness/damage (myopathy) (Hashida, Steelman and Erdman, 2024)
• Drive Alzheimer’s disease (Pogue et al., 2022; Brown and Heneka, 2024)

… to name but a few. So, it’s hopefully pretty clear that endotoxin is really rather awful for us. But, if it’s so bad, why haven’t I ever heard about it before? Well, I believe it’s largely because our culture and education systems haven’t assimilated many of the scientific discoveries of the past 100 years or so. Endotoxin has been known to be toxic for decades now, but money drives research, and sometimes, if research isn’t deemed to be profitable for investors, said investors are less likely to cough up funding. 

It’s not all doom and gloom though, because in light of the heightened interest in microbiome research over the last few decades, researchers are now becoming increasingly curious about endotoxin. Partly as a result, it is now known that there are many simple and effective ways to protect oneself against endotoxin.

Carrots? 

Yes, really. Allow me to explain. While the discovery of gut-derived endotoxin as a driver of chronic inflammation has led to the development of pharmaceutical strategies, some have long suggested simple dietary interventions to mitigate their damage. Decades before mainstream science linked endotoxin to chronic disease, biologist and author Dr Raymond Peat suggested that raw carrot fibre could prevent this toxicity through binding and removing endotoxin from the intestine. 

“Endotoxin formed in the bowel can block respiration and cause hormone imbalances contributing to instability of the nerves, so it is helpful to optimize bowel flora, for example with a carrot salad; a dressing of vinegar, coconut oil and olive oil, carried into the intestine by the carrot fiber, suppresses bacterial growth while stimulating healing of the wall of the intestine [thus preventing endotoxemia].” – Dr Raymond Peat, PhD

How does it work?

Carrot fibre, specifically raw carrot fibre, acts like a non-digestible, hydrophobic sponge that collects endotoxin through various mechanisms, and escorts it out of the gut before it can be absorbed into the bloodstream. In other words, it acts as a vessel for all sorts of toxins to be cleared from the digestive system.

The insoluble nature of raw carrot possesses hydrophobic regions, which are excellent at interacting with the lipid-rich region of endotoxin, as well as a rigid and porous matrix which is effective at physically trapping LPS. It’s also poorly fermented by gram negative gut bacteria, which means that it doesn’t feed excess bacterial growth, and thus create more endotoxin. Raw fibre is also more resistant to being broken down, therefore it maintains its structural integrity throughout the whole digestive tract, continuing to successfully adsorb endotoxin.

Coconut oil reduces the source of endotoxin by inhibiting gut bacterial overgrowth, and apple cider vinegar also discourages bacterial proliferation and supports digestive efficiency, through lowering the pH of the salad and improving upper GI digestion.

Recipe: The Ray Peat Carrot Salad (Serves one)

• 1 large raw carrot, peeled lengthwise (or grated)
• 1 tablespoon apple cider vinegar
• 1 teaspoon coconut oil
• 1 teaspoon olive oil
• Pinch of salt

What else can be utilised to prevent absorption of endotoxin?

White button mushrooms

Well-cooked, white button mushrooms help to clear endotoxin from the gut because they contain indigestible polysaccharides and beta-glucans that bind LPS in the gut and modulate immune cell activity to reduce inflammation. 

It is paramount, though, that the mushrooms are boiled for 1-3 hours (or microwaved for 4-6 minutes). This is because raw or lightly cooked mushrooms contain fungal toxins (e.g. hydrazine) and irritants (e.g. chitin) that can irritate the gut lining and trigger the immune system’s inflammatory cascade. Extended cooking denatures or evaporates away these toxins and that the chitin matrix is softened, reducing the potential for irritation. White button mushrooms are chosen for their very low polyunsaturated fatty acid (PUFA) content, lowering the potential for mitochondrial oxidative stress. You can follow this link for a recipe of mushroom soup, which adheres to the above information. 

Coffee

Coffee has numerous protective effects on the gut barrier and can reduce circulating endotoxin levels, regardless of the caffeine concentration. Coffee’s polyphenols and diterpenes strengthen gut lining integrity and, by increasing peristalsis, coffee can reduce constipation-related endotoxemia.

If you want to get really particular about your coffee and extract as much of the ‘good stuff’ as possible, such as the terpenoids, trigonelline, melanoidins, chlorogenic acid, and tocopherols etc., you could brew your coffee with ascending heat. This is because these unique beneficial compounds are most soluble at lower temperatures. So, if you dump boiling hot water over the grounds, you’re going to denature a lot of them. Therefore, you could moisten the grounds slightly with warm water first, then slowly add water of increasing temperature, allowing things with different solubilities to periodically release into the water. This process often gives the coffee this deep orange colour and introduces pleasant new aromas.

Orange juice

Fresh, unpasteurised orange juice has been shown to be extremely protective against endotoxin. The vitamin C, flavonoids, and sugars in orange juice all enhance tight junction stability and reduce oxidative stress in the gut. The sugar protects against stress-induced intestinal permeability through preventing cortisol-driven breakdown of tight junctions and supporting liver detoxification of LPS through glycogen replenishment. Naringenin, found in other citrus fruits as well as oranges, is a TLR4 antagonist, meaning it binds to the receptor in a way which prevents the correct substrate from binding, inhibiting the inflammatory process.

A classic study in 2010 discovered that drinking a glass of fresh orange juice alongside a high-fat, high-carbohydrate breakfast meal (“similar to a McDonald’s-style fast food breakfast sandwich”) neutralised the typical proinflammatory response. The control group showed significant postprandial increases in plasma endotoxin and TLR4 expression, but the orange juice group did not (Ghanim et al., 2010).

Glycine

Glycine, an anti-inflammatory amino acid deficient in both modern diets and endogenous production in adults today (Meléndez-Hevia et al., 2009), decreases mortality in animals dosed with endotoxin. Glycine is abundant in gelatinous cuts of meat (think “eating nose to tail”) and plays key roles in maintaining integrity of the gut barrier. Unfortunately, glycine is often replaced by glyphosate (a toxic herbicide) in the epidermis, by mimicking glycine’s structure. It’s this replacement which leads to endotoxemia for many people.

To combine the positive effects of both orange juice and glycine, you could make orange juice gummies with gelatine (being 33% glycine). 600ml orange juice and 5 tablespoons of gelatine is a good place to start. Bloom your gelatine (add slowly) into your orange juice and heat very gently in a saucepan. Transfer to a container once the gelatine is dissolved and cool in the fridge for a couple of hours to set. Add more gelatine for a firmer texture.

Avoid polyunsaturated fatty acids

Polyunsaturated fatty acids (PUFAs; the reason why seed oils are bad for us) are highly prone to lipid peroxidation, and it’s this peroxidation in our gut which damages junctions and creates a ‘leaky gut’, allowing endotoxin to pass into our bloodstream. PUFAs are also precursors to pro-inflammatory mediators like prostaglandins, which intensify the inflammatory cytokine response when endotoxin activates TLR4. It’s likely because of this that septic shock (when the body releases too many cytokines into the bloodstream), caused by the injection of endotoxin, is 100% lethal to animals fed diets high in PUFA, whereas it’s only 24% lethal to PUFA-deficient animals (Cook et al., 1981).

The problem with reductionism in science

Problems like endotoxemia are complicated, and it’s arguably largely for this complexity as well as reductionist thinking in our scientific culture, that it’s taken so long for us to figure it out. 

Reductionism, which reduces the explanation for something to a description of its parts, the ways the parts interact, and a small number of physical laws, avoids bothering with physiological complexity in understanding something biological. It’s a way of drawing hypotheses based on a small set of binary principles and therefore ‘proving it scientifically’. With this reductionist mystique of imposing conclusions about things, of claiming that because we already have the knowledge of the parts we can sufficiently explain the problem as a whole, we miss out on the ‘unexpected’ links in disease. We would likely never have connected endotoxin to Alzheimer’s, or atherosclerosis, or cancer with this philosophy. Therefore, as Dr Raymond Peat wrote, “satisfactory solutions to complex problems will be possible only if we directly confront the complexity” (Peat, 2001). 

In order to progress scientifically in a qualitative manner, we have to unsubscribe from the reductionist notion of ‘logical deduction’ assigning general theory to solve specific problems, because in reality, biology doesn’t often work like that. We must try to avoid the mindset that nothing else is to be found within problems that have already been ‘solved’ so as to not thwart the development of new branches and ideas in science. This mirrors one of the current problems with academia, particularly in biosciences – that the emphasis is on imprinting information onto the students’ minds to be regurgitated when recalled upon, rather than on applying their own judgement upon the world to cause a material change. Niels Bohr was given the Nobel Prize for his incorrect electron shell model. The important takeaway is not that the model was quickly found to be incorrect, but that the development of our understanding of atomic structure was not obstructed, which allowed new ideas to build from it. Knowledge is somewhat fickle. If we can accept this and that we will develop our knowledge in the future, we would be less likely to automatically reject new information that conflicts with our current understanding.

Conclusion; What the future of food security could hold for us

“The current agricultural landscape prioritizes quantity rather than quality and chemistry rather than biology… but ending this isn’t impossible” – Peter Behrens

In order to tackle the increasingly large opponent that is endotoxemia and diet-induced chronic disease, the quality of our food, and therefore the food system in its entirety, needs to be confronted directly at the source. It’s not an easy job, but we need to address the complexity head-on. 

I believe that regenerative agriculture, primarily through its respect of the reality that healthy soil begets healthy plants and healthy plants beget healthy soil, offers the best foot forward in solving many of our systemic health problems. Regenerative agriculture protects and harnesses soil biota-plant symbiotic relationships (which usually take decades to develop), revoking the need for chemical pesticides and fertilisers, and halting the silent mass-poisoning of people (and plants).

Regenerative farming leverages data to gather insights relating plant diseases to nutrient deficiencies, understanding that pests and pathogens feed only on weak, unhealthy plants. Therefore, plants that are healthy, because their soil contains all the correct components in sufficient quantities, will either require fewer, or completely lack the need for harsh chemical pesticides and synthetic fertilisers.

Many assume regenerative agriculture is not sustainable in the long term because it is not profitable. While easier said than done, this is still far from the truth. A great restaurant and its tasty, high-quality food, attentive service, reasonable prices, and pleasant atmosphere creates happy customers that want to keep coming back for more. Prices don’t need to be insultingly high because the restaurant’s footfall is much higher – and will be for much longer – with this approach. Regenerative farming is much the same. John Kempf articulated this well: “When farmers make wise management decisions based on data, plant health improves, the need for inputs is reduced, and increased yields and profitability necessarily follow”.

In addition to regenerative farming, the importance of small farms and growing your own food cannot be emphasised enough right now. Small family farms are one of our last connections to real food. They’re not inefficient, nor are they outdated. They’re just ‘in the way’. In the way of a food system which is driven by profitable ultra-processed food products that can be mass produced cheaply and stacked high up on a shelf in a warehouse somewhere in Chongqing. If small, local farms disappear, the gap between us the consumer and where food really comes from widens enormously, and the more we depend on the harmful ‘food’ that isn’t really food anymore.

If we could finally taste the fruits of the cutting-edge modern research in ecology, agronomy, physiology, medicine, and nutrition, and offer farmers cost-effective, actionable solutions, we might just be able to set off a global cascade of positive change in food security and public health. By lobbying against ultra-processed foods and other toxins, being open minded to novel ideas about physiology, detaching ourselves from our profit-oriented medical culture, and investing in the provision of healthful environments, the pendulum will swing back in favour of the health of the people, rather than the profit of multinational corporations.

References (alphabetical order):

1. Bánhegyi, G., Mucha, I., Garzó, T., Antoni, F. and Mandl, J. (2000). Endotoxin inhibits glucuronidation in the liver: An effect mediated by intercellular communication. Biochemical Pharmacology, [online] 49(1), pp.65–68. doi:https://doi.org/10.1016/0006-2952(94)00389-4
2. Bitto, A., Galeano, M., Squadrito, F., Minutoli, L., Polito, F., Dye, J.F., Clayton, E.A., Calò, M., Venuti, F.S., Vaccaro, M. and Altavilla, D. (2008). Polydeoxyribonucleotide improves angiogenesis and wound healing in experimental thermal injury. Critical Care Medicine, 36(5), pp.1594–1602. doi:https://doi.org/10.1097/ccm.0b013e318170ab5c
3. Camilleri, M. (2019). Leaky gut: mechanisms, measurement and clinical implications in humans. Gut, [online] 68(8), pp.1516–1526. doi:https://doi.org/10.1136/gutjnl-2019-318427
4. Cao, H. (2023). Bacterial endotoxin lipopolysaccharides regulate gene expression in human colon cancer cells. BMC Research Notes, 16(1). doi:https://doi.org/10.1186/s13104-023-06506-9
5. Cavalieri, E. and Rogan, E. (2021). The 3,4-Quinones of Estrone and Estradiol Are the Initiators of Cancer whereas Resveratrol and N-acetylcysteine Are the Preventers. International Journal of Molecular Sciences, [online] 22(15), pp.8238–8238. doi:https://doi.org/10.3390/ijms22158238
6. Christeff, N., Auclair, M.-C., Thobie, N., Benassayag, C. and Nunez, E.A. (2002). Endotoxin induced changes in serum estrogen in male rats: Influence of testicular maturation. Life Sciences, [online] 48(24), pp.2341–2348. doi:https://doi.org/10.1016/0024-3205(91)90271-C
7. Chou, C.-H., Chen, S.-U., Chen, C.-D., Shun, C.-T., Wen, W.-F., Tu, Y.-A. and Yang, J.-H. (2019). Mitochondrial Dysfunction Induced by High Estradiol Concentrations in Endometrial Epithelial Cells. The Journal of Clinical Endocrinology & Metabolism, [online] 105(1), pp.126–135. doi:https://doi.org/10.1210/clinem/dgz015
8. Cook, J.A., Wise, W.C., Knapp, D.R. and Halushka, P.V. (1981). Essential fatty acid deficient rats: a new model for evaluating arachidonate metabolism in shock. Advances in Shock Research, [online] 6, pp.93–105. Available at: https://pubmed.ncbi.nlm.nih.gov/6818852/
9. Do, N.M. (2024). From Leaky Gut to Leaky Skin: A Clinical Review of Lifestyle Influences on the Microbiome. American Journal of Lifestyle Medicine. doi:https://doi.org/10.1177/15598276241292605
10. Fei, X., Dou, Y., Lv, W., Ding, B., Wei, J., Wu, X., He, X., Fei, Z. and Fei, F. (2022). TLR4 Deletion Improves Cognitive Brain Function and Structure in Aged Mice. Neuroscience, 492, pp.1–17. doi:https://doi.org/10.1016/j.neuroscience.2022.04.007
11. Flasbeck, V., Dersch, N., Engler, H., Manfred Schedlowski and Brüne, M. (2024). Acute experimental inflammation in healthy women attenuates empathy for psychological pain. Brain, Behavior, and Immunity, 119, pp.1–5. doi:https://doi.org/10.1016/j.bbi.2024.03.032
12. Ghanim, H., Sia, C.L., Upadhyay, M., Korzeniewski, K., Viswanathan, P., Abuaysheh, S., Mohanty, P. and Dandona, P. (2010). Orange juice neutralizes the proinflammatory effect of a high-fat, high-carbohydrate meal and prevents endotoxin increase and Toll-like receptor expression. The American Journal of Clinical Nutrition, [online] 91(4), pp.940–949. doi:https://doi.org/10.3945/ajcn.2009.28584
13. Grady, D., Gebretsadik, T., Kerlikowske, K., Ernster, V. and Petitti, D. (1995). Hormone replacement therapy and endometrial cancer risk: a meta-analysis. Obstetrics and Gynecology, [online] 85(2), pp.304–313. doi:https://doi.org/10.1016/0029-7844(94)00383-O
14. Grigoleit, J.-S., Kullmann, J.S., Wolf, O.T., Hammes, F., Wegner, A., Jablonowski, S., Engler, H., Gizewski, E., Oberbeck, R. and Schedlowski, M. (2011). Dose-Dependent Effects of Endotoxin on Neurobehavioral Functions in Humans. PLoS ONE, [online] 6(12), p.e28330. doi:https://doi.org/10.1371/journal.pone.0028330
15. Hashida, M., Steelman, A.J. and Erdman, J.W. (2024). α-Tocopherol Depletion Exacerbates Lipopolysaccharide-Induced Reduction of Grip Strength. The Journal of Nutrition, [online] 154(2), pp.498–504. doi:https://doi.org/10.1016/j.tjnut.2023.12.031
16. Hawiger, J., Hawiger, A., Steckley, S., Timmons, S. and Cheng, C. (1977). Membrane Changes in Human Platelets Induced by Lipopolysaccharide Endotoxin. British Journal of Haematology, 35(2), pp.285–299. doi:https://doi.org/10.1111/j.1365-2141.1977.tb00585.x
17. Heaney, A.P., Fernando, M. and Melmed, S. (2002). Functional role of estrogen in pituitary tumor pathogenesis. Journal of Clinical Investigation, 109(2), pp.277–283. doi:https://doi.org/10.1172/jci14264
18. Lafront, C., Germain, L., Campolina-Silva, G.H., Weidmann, C., Berthiaume, L., Hovington, H., Brisson, H., Jobin, C., Frégeau-Proulx, L., Cotau, R., Gonthier, K., Lacouture, A., Caron, P., Ménard, C., Atallah, C., Riopel, J., Latulippe, É., Bergeron, A., Toren, P. and Guillemette, C. (2024). The estrogen signaling pathway reprograms prostate cancer cell metabolism and supports proliferation and disease progression. Journal of Clinical Investigation, 134(11). doi:https://doi.org/10.1172/jci170809
19. Langdon, S.P., Herrington, C.S., Hollis, R.L. and Gourley, C. (2020). Estrogen Signaling and Its Potential as a Target for Therapy in Ovarian Cancer. Cancers, 12(6), p.1647. doi:https://doi.org/10.3390/cancers12061647
20. Lin, T., Chang, Y., Wu, M., Wu, T., Chen, C. and Lim, P. (2022). Serum lipopolysaccharide‐binding protein levels and cardiovascular events in hemodialysis patients: A prospective cohort study. Nephrology, 27(11), pp.877–885. doi:https://doi.org/10.1111/nep.14107
21. Mallardi, D., Maqoud, F., Guido, D., Aloisio, M., Linsalata, M. and Russo, F. (2025). Mapping Research Trends on Intestinal Permeability in Irritable Bowel Syndrome with a Focus on Nutrition: A Bibliometric Analysis. Nutrients, [online] 17(6), pp.1064–1064. doi:https://doi.org/10.3390/nu17061064
22. Mastrangelo, A., Robles-Vera, I., Mañanes, D., Galán, M., Femenía-Muiña, M., Redondo-Urzainqui, A., Barrero-Rodríguez, R., Papaioannou, E., Amores-Iniesta, J., Devesa, A., Lobo-González, M., Carreras, A., Beck, K.R., Ivarsson, S., Gummesson, A., Georgiopoulos, G., Rodrigo-Tapias, M., Martínez-Cano, S., Fernández-López, I. and Nuñez, V. (2025). Imidazole propionate is a driver and therapeutic target in atherosclerosis. Nature, [online] doi:https://doi.org/10.1038/s41586-025-09263-w
23. Meléndez-Hevia, E., de Paz-Lugo, P., Cornish-Bowden, A. and Cárdenas, M.L. (2009). A weak link in metabolism: the metabolic capacity for glycine biosynthesis does not satisfy the need for collagen synthesis. Journal of Biosciences, 34(6), pp.853–872. doi:https://doi.org/10.1007/s12038-009-0100-9
24. Peat, R. (2001). Generative Energy
25. Perng, W., Friedman, J.E., Janssen, R.C., Glueck, D.H. and Dabelea, D. (2022). Endotoxin Biomarkers Are Associated With Adiposity and Cardiometabolic Risk Across 6 Years of Follow-up in Youth. The Journal of Clinical Endocrinology & Metabolism, [online] 107(7), pp.e3018–e3028. doi:https://doi.org/10.1210/clinem/dgac149
26. Pogue, A.I., Jaber, V.R., Sharfman, N.M., Zhao, Y. and Lukiw, W.J. (2022). Downregulation of Neurofilament Light Chain Expression in Human Neuronal-Glial Cell Co-Cultures by a Microbiome-Derived Lipopolysaccharide-Induced miRNA-30b-5p. Frontiers in Neurology, [online] 13. doi:https://doi.org/10.3389/fneur.2022.900048
27. Poto, R., Fusco, W., Rinninella, E., Cintoni, M., Kaitsas, F., Raoul, P., Caruso, C., Mele, M.C., Varricchi, G., Gasbarrini, A., Cammarota, G. and Ianiro, G. (2024). The Role of Gut Microbiota and Leaky Gut in the Pathogenesis of Food Allergy. Nutrients, [online] 16(1), p.92. doi:https://doi.org/10.3390/nu16010092
28. Radjabzadeh, D., Bosch, J.A., Uitterlinden, A.G., Zwinderman, A.H., Ikram, M.A., van Meurs, J.B.J., Luik, A.I., Nieuwdorp, M., Lok, A., van Duijn, C.M., Kraaij, R. and Amin, N. (2022). Gut microbiome-wide association study of depressive symptoms. Nature Communications, 13(1), p.7128. doi:https://doi.org/10.1038/s41467-022-34502-3
29. Reifenberg, K., Lehr, H.-A., Fan, J., Koike, T., Wiese, E., Küpper, I., Tolga Atilla Sagban, Schaefer, S.C., Ulrich Zähringer, Torzewski, M., Lackner, K.J. and Sucharit Bhakdi (2009). Endotoxin accelerates atherosclerosis independent of complement activation. Thrombosis Research, 123(4), pp.653–658. doi:https://doi.org/10.1016/j.thromres.2008.06.017
30. Shan, B., Shao, M., Zhang, Q., Hepler, C., Paschoal, V.A., Barnes, S.D., Lavanya Vishvanath, An, Y.A., Jia, L., Malladi, V.S., Strand, D.W., Gupta, O.T., Elmquist, J.K., Oh, D. and Gupta, R.K. (2020). Perivascular mesenchymal cells control adipose-tissue macrophage accrual in obesity. Nature Metabolism, [online] 2(11), pp.1332–1349. doi:https://doi.org/10.1038/s42255-020-00301-7
31. Smida, T., Bruno, T.C. and Stabile, L.P. (2020). Influence of Estrogen on the NSCLC Microenvironment: A Comprehensive Picture and Clinical Implications. Frontiers in Oncology, 10. doi:https://doi.org/10.3389/fonc.2020.00137
32. Steinberg, K.K., Smith, S.J., Thacker, S.B. and Stroup, D.F. (1994). Breast Cancer Risk and Duration of Estrogen Use. Epidemiology, 5(4), pp.415–421. doi:https://doi.org/10.1097/00001648-199407000-00007
33. Stockmaier, S., Bolnick, D.I., Page, R.A., Josic, D. and Carter, G.G. (2020). Immune-challenged vampire bats produce fewer contact calls. Biology Letters, 16(7), p.20200272. doi:https://doi.org/10.1098/rsbl.2020.0272
34. Tang, S., Lian, X., Cheng, H., Guo, J., Ni, D., Huang, C., Gu, X., Meng, H., Jiang, J. and Li, X. (2021). Bacterial Lipopolysaccharide Augmented Malignant Transformation and Promoted the Stemness in Prostate Cancer Epithelial Cells. Journal of Inflammation Research, [online] 14, pp.5849–5862. doi:https://doi.org/10.2147/JIR.S332943
35. Tremellen, K., Syedi, N., Tan, S. and Pearce, K. (2014). Metabolic endotoxaemia – a potential novel link between ovarian inflammation and impaired progesterone production. Gynecological Endocrinology, 31(4), pp.309–312. doi:https://doi.org/10.3109/09513590.2014.994602
36. Tremellen, K. (2016). Gut Endotoxin Leading to a Decline IN Gonadal function (GELDING) – a novel theory for the development of late onset hypogonadism in obese men. Basic and Clinical Andrology, 26(1). doi:https://doi.org/10.1186/s12610-016-0034-7
37. Wang, X. and Lin, Y. (2008). Tumor necrosis factor and cancer, buddies or foes? Acta Pharmacologica Sinica, [online] 29(11), pp.1275–1288. doi:https://doi.org/10.1111/j.1745-7254.2008.00889.x
38. Wang, Y.S. and White, T.D. (1999). The Bacterial Endotoxin Lipopolysaccharide Causes Rapid Inappropriate Excitation in Rat Cortex. Journal of Neurochemistry, 72(2), pp.652–660. doi:https://doi.org/10.1046/j.1471-4159.1999.0720652.x