Gastrointestinal Health: Dysbiosis and Metabolic Endotoxaemia Flashcards
Q: What is dysbiosis?
A: Dysbiosis is an imbalance in the colonies of bowel flora, potentially disrupting both local and systemic health.
Q: What are common causes of dysbiosis (Aetiology)?
A: Causes of dysbiosis include poor diet (highly processed, low fiber, low polyphenols), infections, medications (antibiotics, antacids, OCP), chronic stress, low digestive secretions (HCl, bile), C-section birth, non-breastfeeding, GI surgery, and abdominal scar tissue.
Q: How is dysbiosis linked to atopic diseases?
A: C-section infants fed formula milk instead of breastmilk have a lower abundance of Bifidobacteria and Lactobacilli, which has been associated with increased risk of atopic diseases later in life. Probiotics can reduce incidence and symptoms.
Q: How does dysbiosis contribute to metabolic syndrome?
A: Dysbiosis in metabolic syndrome is associated with lower levels of Bifidobacteria and Akkermansia spp., increased E. coli, and a high Firmicutes to Bacteroidetes ratio. A fiber-rich diet with SCFA-producing bacteria (probiotics) can improve the condition.
Q: What role does dysbiosis play in colorectal cancer (CRC)?
A: Fiber-rich diets increase beneficial SCFA-producing bacteria (e.g., Roseburia, Eubacterium, Bifidobacterium), while pathogens like B. fragilis, E. coli, Fusobacterium spp., and Campylobacter spp. are linked to promoting CRC.
Q: How is dysbiosis connected to neurodegenerative diseases?
A: Alzheimer’s, Parkinson’s, and motor neuron disease (MND) are associated with increased pro-inflammatory bacterial species. Periodontal pathogens like P. gingivalis and T. denticola have also been linked to Alzheimer’s disease, with LPS from P. gingivalis detected in the brain tissue of AD patients.
Q: What is metabolic endotoxaemia?
A: Metabolic endotoxaemia is a subclinical rise in bacterial LPS in the blood, leading to chronic low-grade inflammation. It is associated with chronic diseases like cardiovascular disease, diabetes, autoimmunity, and degenerative disorders.
Q: How does metabolic endotoxaemia contribute to inflammation?
A: LPS from gram-negative bacteria interacts with toll-like receptors (especially TLR4), triggering pro-inflammatory cytokines like TNF-α and IL-β. Dysbiosis, mucosal degradation, and increased gut permeability further raise LPS levels in the blood.
Q: What dietary factors can worsen metabolic endotoxaemia?
A: High-fat diets (including ketogenic diets) can increase LPS transport across the intestinal membrane, exacerbating metabolic endotoxaemia.
Q: What is a natural approach to managing metabolic endotoxaemia?
A: Avoid alcohol, dietary irritants, and NSAIDs. Increase dietary fiber to bind and clear LPS, and feed butyrate-producing bacteria (e.g., Roseburia, Akkermansia spp.). Avoid Western or ketogenic diets, and focus on polyphenol-rich foods to reduce inflammation.
Q: What lifestyle interventions can help reduce metabolic endotoxaemia?
A: Breathing techniques and cold exposure (e.g., cold showers) can help reduce systemic LPS load.
Q: How can the GI barrier and liver function be supported in metabolic endotoxaemia?
A: Reinoculate the gut and support the GI barrier. For liver support, use herbs like milk thistle (hepatoprotective), burdock root, artichoke, and chlorella. Increase dietary antioxidants (vitamins C, E, carotenoids), and support glutathione production with selenium, NAC, cruciferous vegetables, and resveratrol.
Q: What are some Nrf2 inducers that help scavenge reactive oxygen species (ROS)?
A: Nrf2 inducers include broccoli sprouts, green tea, lycopene (tomatoes), rosemary, and curcumin.
