Cooked meat bacteria endotoxemia- Inflammation and diet

The emerging role of chronic inflammation in modern society’s major chronic diseases has sparked research into the impact of nutrition and dietary patterns on inflammatory status. The majority of human studies have linked dietary intake to systemic inflammation markers such as high-sensitivity C-reactive protein (HS-CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-).

Significant dietary influences have been established for glycemic index (GI) and load (GL), fiber, fatty acid composition, magnesium, carotenoids, and flavonoids. Whole food plant-based diet or even a traditional Mediterranean dietary pattern, which typically has a high ratio of monounsaturated (MUFA) to saturated (SFA) fats and ω-3 to ω-6 polyunsaturated fatty acid (PUFAs) and supplies an abundance of fruits, vegetables, legumes, and grains, has shown anti-inflammatory effects when compared with typical North American and Northern European dietary patterns in most observational and interventional studies. There is a wide range of factors that influence inflammation caused by diet but a whole food antioxidant-rich, nutrient-rich diet may become the diet of choice for diminishing chronic inflammation in clinical practice.

Prolonged low-grade inflammation is linked to increased oxidative stress and altered glucose and lipid metabolism in fat (adipose) cells, muscle, and the liver. As a result, research indicates that certain dietary components can influence these key inflammatory pathways.

One of the factors that creates inflammation spikes after animal product consumption is a process known as endotoxemia. `Diet-induced metabolic endotoxemia has been proposed as a major root cause of inflammation, and these pathways appear to be detrimental to healthy aging.

We as humans, unlike carnivores species, have very low resistance filters meaning any live bacteria we eat will be creating inflammation, and diet can kill us if bacteria is dangerous. We cannot eat uncooked meat. Carnivorous animals have extremely corrosive bile acids that are able to kill any living microorganism and their digestive system is practically sterile. We as any other plant eater have mild bile acid and low resistance filters and have to cook meat and any other food item that has the potential to spread an infectious disease. For example, pasteurization is mandatory.

What people don’t understand is that even if we do cook meat we do not magically dematerialize all of the bacteria that were present in there. We only kill them by heat but they are still in there. Microorganisms are still in the meat just dead. They will not pose any risk of infection anymore.

But that does not mean that they don’t pose a risk anymore.

Even dead non-probiotic bacteria do count as toxins.

Some of the world’s most toxic substances are these dead meat bacteria endotoxins.

These substances known as endotoxins (Greek éndon within; cognate with Old Irish ind-) are thermally (250C) and chemically stable and extremely toxic. Endotoxin is a complex lipopolysaccharide (LPS) found in the outer cell membrane of gram-negative bacteria (E.coli, Salmonella typhi, Shigella).

Bacteria shed endotoxins in large amounts upon cell death creating an endotoxemia state in the body. Meaning, the bacteria can be dead or cooked for a long time, but their endotoxins are still there. Endotoxins are chemically very stable and can withstand our body’s best attempts at acid and enzyme degradation. One of the leading causes of hundreds of studies that display enlarged inflammation from animal foods, but not from most plant foods, maybe is a consequence of a toxic load of dead bacteria endotoxins in animal products. These bacteria shed endotoxins after death and then when we eat them they are absorbed into our system, leading to the endotoxemia inflammation we see after egg, meat, and dairy consumption, as well.

This would cause damage to our internal organs and the entire body and will increase the chances of chronic diseases (Ghosh et al., 1993).

If we already have an autoimmune disease such as atherosclerosis, for example, this will just agitate our immune system even worse and would create even more of an immune response (Stoll et al., 2004).

Here is one study that discovered a link between endotoxin exposure and diabetes type 2 (Harte et al., 2012).

What a low level of chronic endotoxemia inflammation does is that it causes damage like any other inflammation just in a prolonged period. What that translates to is faster and more noticeable DNA damage, a higher mortality rate from chronic diseases, and decreased longevity.

In contrast, plant foods do not show this trait, and actual consumption is correlated with the anti-inflammatory reaction after a meal because of the antioxidants and other anti-inflammatory phytochemicals. It would be interesting to see how much inflammation meat consumption causes in carnivorous species. So far I was unable to find research that looks into dead meat bacteria endotoxemia exposure in carnivorous species. This could be potentially interesting because if meat causes no inflammation in carnivorous animals, we might look at a way how to lower the same inflammation in our own bodies. 

Consumption of meat, therefore, is associated with an increase in inflammation even if we disregard the risk of live infectious bacteria. This mechanism is natural and normal, and all of the carnivorous species had it to some extent but are more adept at coping with it.

A fresh hamburger contains approximately a hundred million bacteria per quarter pounder. Eating meals high in bacterial endotoxins could develop mild but systemic inflammatory episodes that predispose subjects to the development of chronic diseases.

The animal fat that comes in the same package may play a role in the pathogenesis of this after-meal inflammation. Endotoxins hold a powerful attraction for saturated fat, so they stick to it and then get absorbed through the gut wall and into the bloodstream (Erridge, 2011).

Would this happen if we eat food that is high in saturated fat from plant origin? It would, but the difference is that there are no high levels of these toxins in plant-based foods. For example, cocoa has a high fat content. It is one of the plants that has energy stored in a form of saturated fat, the same fat that is found in the animal kingdom. But cocoa also has a large number of antioxidants and in studies always decreases the level of C-reactive protein in subjects (a marker for inflammation) (Erridge et al., 2007), (Herieka et al., 2014).

The high antioxidant content of cocoa prevails and is able to neutralize the pro-inflammatory effects of endotoxins that are not present in the plants in high numbers, to begin with (Gu et al., 2014).

The problem with meat is a high concentration of bacteria. This means that eating a standard Western diet rich in animal protein and refined sugar and fat will require a much higher level of antioxidants to negate the bad pro-inflammatory effects.

The question will be where can we use these findings and can we diminish the bed proinflammatory effects of high animal protein meals with antioxidant-rich food. In other words, can we still eat meat but also add some high-antioxidant vegetables or fruits to the same meal to avoid the risk (Burton-Freeman, 2010).

There was a large number of studies done on a topic and the conclusion is yes, we can, but only to some extent. Avoidance of toxin exposure is our primary goal. If you really have to eat animal products then at least incorporate an adequate amount of anti-inflammatory food sources and calculate your optimal ORAC (Oxygen radical absorbance capacity) intake. You can find ORAC values here (ORAC Values). This would not completely negate the toxicity of dead meat bacteria endotoxemia exposure. These toxins are very potent and hard to detoxify. There are genetically susceptible individuals that have a harder time detoxifying these compounds. Antioxidant-rich food will lower the risk to a relevant degree and my advice is to optimize the antioxidant intake.

The best course of action would be to have a whole food plant-based diet that has an optimal level of ORAC units and a wide range of proinflammatory food sources with an adequate level of all essential micronutrients.

This is what the British Journal of Nutrition has to say about it.

“Postprandial (fed) state is a pro-oxidant state. The postprandial period is a time of active oxidative metabolism and formation of ROS (free radicals). There is increasing evidence that the postprandial state is an important contributing factor to chronic disease. Two main questions are posed: first, what is the role of plant foods, specifically fruits rich in complex and simple phenolic compounds in postprandial metabolic management; and second, does the evidence support consuming these fruits with meals as a practical strategy to preserve health and lower risk for disease? The collected data suggest that consuming phenolic-rich fruits increases the antioxidant capacity of the blood, and when they are consumed with high fat and carbohydrate ‘pro-oxidant and pro-inflammatory’ meals, they may counterbalance their negative effects. Given the content and availability of fat and carbohydrate in the Western diet, regular consumption of phenolic-rich foods, particularly in conjunction with meals, appears to be a prudent strategy to maintain oxidative balance and health.“

References:

1. Ghosh, S., Latimer, R. D., Gray, B. M., Harwood, R. J., & Oduro, A. (1993). Endotoxin-induced organ injury. Critical care medicine, 21(2 Suppl), S19–S24. https://doi.org/10.1097/00003246-199302001-00005
2. Stoll, L. L., Denning, G. M., & Weintraub, N. L. (2004). Potential role of endotoxin as a proinflammatory mediator of atherosclerosis. Arteriosclerosis, thrombosis, and vascular biology, 24(12), 2227–2236. https://doi.org/10.1161/01.ATV.0000147534.69062.dc
3. Harte, A. L., Varma, M. C., Tripathi, G., McGee, K. C., Al-Daghri, N. M., Al-Attas, O. S., Sabico, S., O’Hare, J. P., Ceriello, A., Saravanan, P., Kumar, S., & McTernan, P. G. (2012). High fat intake leads to acute postprandial exposure to circulating endotoxin in type 2 diabetic subjects. Diabetes care, 35(2), 375–382. https://doi.org/10.2337/dc11-1593
4. Erridge C. (2011). The capacity of foodstuffs to induce innate immune activation of human monocytes in vitro is dependent on food content of stimulants of Toll-like receptors 2 and 4. The British journal of nutrition, 105(1), 15–23. https://doi.org/10.1017/S0007114510003004
5. Erridge, C., Attina, T., Spickett, C. M., & Webb, D. J. (2007). A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation. The American journal of clinical nutrition, 86(5), 1286–1292. https://doi.org/10.1093/ajcn/86.5.1286
6. Herieka, M., & Erridge, C. (2014). High-fat meal induced postprandial inflammation. Molecular nutrition & food research, 58(1), 136–146. https://doi.org/10.1002/mnfr.201300104
7. Gu, Y., Yu, S., Park, J. Y., Harvatine, K., & Lambert, J. D. (2014). Dietary cocoa reduces metabolic endotoxemia and adipose tissue inflammation in high-fat fed mice. The Journal of nutritional biochemistry, 25(4), 439–445. https://doi.org/10.1016/j.jnutbio.2013.12.004
8. Burton-Freeman B. (2010). Postprandial metabolic events and fruit-derived phenolics: a review of the science. The British journal of nutrition, 104 Suppl 3, S1–S14. https://doi.org/10.1017/S0007114510003909

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