• Wendy Finkelstein

What is Post Prandial Endotoxemia? Why is it becoming a leading cause of sudden death?

By Wendy Finkelstein PA-C, owner of Nephesh Enlightened Health and Functional Medicine

Post prandial endotoxemia AKA “Metabolic Endotoxemia” (ME) is an becoming increasingly more common. ME essentially is an exacerbation of a leaky gut process which activates the immune system and inflammatory cascades in the body. In severe cases ME can cause death due to an acute cardiovascular event such as MI or stroke.

What is Metabolic Endotoxemia?

Metabolic endotoxemia like leaky gut can start as an acute low grade persistent, inflammatory driver of many underlying diseases. When the mucosal barrier of the gut lining is permeable, increased toxins from food enter the bloodstream. This as a result, can exacerbate food allergies and sensitivities, cause bloating gas, diarrhea and general malaise.

Our microbiome is colonized with millions of diverse bacteria. When our diets lack diversity and are high in processed food and saturated fat, overgrowth of unwanted strains of bacteria thrive. These bacteria increase an inflammatory mediator known as Lipopolysaccharide (LPS) LPS can increase to dangerous levels up to five hours after eating a meal. LPS symptoms, although many not recognized affect approximately 50% of the western population and it is caused by eating high fat and calorie-dense processed foods.

LPS-induced Endotoxemia is linked to

· Leptin resistance and weight gain

· Chronic Constipation

· Mood disorders such as depression and anxiety

· Cognitive decline and memory issues

· Anorexia and other eating disorders

· Chronic pain

· Parkinson’s disease and Alzheimer’s disease

· Low testosterone

· Autoimmune disease

Symptoms of Metabolic endotoxemia include:

· Food sensitivities

· Histamine intolerance

· Nutrient deficiencies (B12, ferritin/iron, minerals and fat soluble vitamins)

· Autoimmune disease

· Fatigue

· Anxiety and depression

· Weight gain

· Hyperlipidemia and high triglycerides

· Insulin resistance and diabetes

· Inflammation and pain

The presence of LPS in the body causes the same signaling factors as minor inflammation which overtime increase your risk of chronic inflammatory conditions such as:

  • Cardiovascular disease

  • Diabetes

  • Obesity

  • Auto-immunity

  • Anxiety

  • Depression

How can you Prevent Metabolic Endotoxemia?

1. Plant Based Whole Food Diet

As simple as it sounds, eating a plant based whole food diet with diversity can be a challenge in today’s fast paced society. Polyphenol-rich plants, including fruits, vegetables, and nuts, are an important component of a health promoting diet, and such foods and their component phytochemicals are known to have significant prebiotic effects in humans. Polyphenols are poorly absorbed in the upper gastrointestinal tract but do reach the colon to be fermented by bacteria, where they can enhance the growth of beneficial microorganisms and influence the physiological sequel associated with metabolic endotoxemia. (3)

2. Decrease Stress

Unfortunately, our bodies have become adapted to such high levels of stress and cortisol. This not only drives our cravings for sugar and saturated fat, but we barely even slow down enough to chew our food. Cortisol not only increases the tendency towards inflammation, but it lowers our immune response and causes leaky gut. In order to stop this epidemic, we must slow down and be more mindful around food. We must chew and activate our own digestive enzymes. As mentioned earlier, a poor diet will naturally release more LPS (Lipopolysaccharides) into your digestive system. The now leaky barrier loses its immune surveillance allowing foreign food additives, preservatives, undigested food to be absorbed.

3. Probiotics

Studies have shown that in just 30 days of probiotic supplementation without any other lifestyle changes such as exercise or dietary changes, can reduce LPS induced ME by up to 45%.. Aside from the benefits of reducing ME symptoms, probiotics are helpful to the gut in many other ways. The most important function of a true probiotic is to:

  • Reduce the amount of gas and bloating.

  • Improve your bowel movements.

  • Reduce the inflammatory effects of processed and fatty foods

  • Improve gut health associated with an unhealthy diet.

4. Lactoferrin

Lactoferrin is a protein found in colostrum. It can inhibit the pathogen from binding to the host by binding to the lipopolysaccharide of the bacterial wall, ultimately resulting in bacterial cell lysis. Lactoferrin promotes the growth of beneficial bacteria, such as Lactobacillus and Bifidobacterium. Lactoferrin can both upregulate and downregulate the inflammatory response. It can bind to lipopolysaccharides, and microbial signals present in the intestine and can block their attachment to Toll-like receptors.(1)

5. Glutamine

The amino acid glutamine is considered an important nutritional intervention for leaky gut because it plays a principal role in gastrointestinal function, in particular in the maintenance of the integrity of the intestinal epithelium, and nutritional depletion has been shown to result in increased intestinal permeability and translocation of endotoxins.111 Supplementation with glutamine has also been shown to reduce endotoxemia-induced inflammation. (2)

6. Berberine

Berberine has many known cardiovascular and gut implications. It mitigates overgrowth of bacteria and high cholesterol through its inhibition of endotoxin-induced inflammation

7. Evidence Based Interventions to Reduce LPS-induced endotoxemia

Physical Exercise





EPA DHA omega fatty acids

Bifidobacteria sp.

Megaspore probiotic

8. Zinc, Magnesium, Vitamin A, and C

These nutrients all play a role in the microbiome and its role in inflammation caused by endotoxins. A deficiency in zinc has been shown to reduce the integrity of the intestinal epithelium and alter the immune responses. Zinc helps with villous atrophy, which associated with leaky gut. Some evidence from human studies has suggested that zinc supplementation alone, or as part of an integrated treatment, can reduce intestinal permeability and circulating endotoxins. Vitamin A helps to heal the tight junctions and improve the barrier function which decreases permeability.

ME is at it’s root cause a condition of a poor microbiome. It causes a leaky permeable instestinal lining which actives the immune system. In some medical circles, It is considered to be the number one cause of morbidity and mortality worldwide. It has been linked to the underlying cause of obesity, heart disease, autoimmunity, diabetes, Alzheimer’s, and many other serious health conditions. Plant based nutrition, specific micronutrient supplementation along with a lifestyle that rewards self-care, mindfulness and meditation are the best predictors of longevity free of disease.


  1. https://www.sciencedirect.com/topics/neuroscience/lactoferrin

  2. 2.https://www.researchgate.net/publication/319749744_Nutritional_Management_of_Metabolic_Endotoxemia_A_Clinical_Review

  3. 3. Cani PD, Bibiloni R, Knauf C, et al. Changes in gut microbiota control metabolicendotoxemia-induced inflammation in high-fat diet-induced obesity anddiabetes in mice. Diabetes. 2008;57(6):1470–148

4. Erridge C, Attina T, Spickett CM, et al. A high-fat meal induces low-grade endotoxemia: Evidence of a novel mechanism of postprandial infammation. Am J Clin Nutr. 2007;86(5):1286–1292

5. Ghanim H, Abuaysheh S, Sia CL, et al. Increase in plasma endotoxinconcentrations and the expression of Toll-like receptors and suppressor ofcytokine signaling-3 in mononuclear cells aer a high-fat, high-carbohydratemeal: Implications for insulin resistance. Diabetes Care. 2009;32(12):2281–228

6. Maes M, Kubera M, Leunis JC. The gut-brain barrier in major depression:Intestinal mucosal dysfunction with an increased translocation of LPS from gramnegative enterobacteria (leaky gut) plays a role in the inflammatory pathophysiology of depression. Neuro Endocrinol Lett. 2008;29(1):117–124

7. Pastor Rojo O, López San Román A, et al. Serum lipopolysaccharide-bindingprotein in endotoxemic patients with inflammatory bowel disease. Inflamm Bowel Dis. 2007;13(3):269–277


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