Bacteria (and their metabolites) and depression

Diethanolamine (DEA), consumer products & safety

• Commenters note DEA is an industrial surfactant in detergents, shampoos, cosmetics, CO₂ capture, etc., not a natural metabolite, yet can be incorporated into lipids via cardiolipin synthase.
• Concerns raised: mitochondrial membrane disruption, oxidative stress, possible links to cancer and depression; safe dose considered “unclear” and the focus here is chronic suffering, not acute toxicity.
• Some propose practical avoidance: DEA‑free products, reverse‑osmosis water, minimally processed foods, thorough rinsing of dishes, switching to natural fibers and “simple” soaps.
• Others correct chemistry (DEA is an amine that yields abnormal lipids) and stress “dose makes the poison,” warning against overgeneralizing from absorption anecdotes.

Skin, plastics, and exposure pathways

• Debate over how meaningful skin absorption is: examples of extreme toxins (hydrofluoric acid, dimethylmercury) versus the likely much lower permeability for DEA.
• Discussion about micro/nanoplastics from clothing: some fear dermal absorption and endocrine disruption, others argue skin uptake is an “extraordinary claim” with little evidence and that inhalation/ingestion via lint and dust are more plausible routes.

Statistics, GWAS, and causality

• The reported association between M. morganii and depression (very low p‑value ~1e‑37) prompts both excitement and skepticism.
• GWAS specialists explain that such tiny p‑values are common with large samples and many tests; they reflect strong statistical evidence but potentially small effects and heavy dependence on model assumptions.
• “Crud factor” is invoked: in rich datasets, almost everything weakly correlates with everything (diet, obesity, depression, microbiome), making causal inference hard. Mendelian randomization and biological follow‑up are viewed as essential.

Individual genetics and gut–brain tailoring

• Personal genomics anecdotes: FUT2 non‑secretor, NOD2 variants, partial PNP deficiency guiding diets high in seaweed, mushrooms, omega‑3 fish, low sugar, careful infection control.
• A shared NotebookLLM summary of the paper emphasizes gene–microbiome–diet interactions (LCT/lactose, ABO/secretor status, fiber) and suggests cautious, personalized dietary adjustments plus professional guidance.

Fasting, keto, microbiome & mood

• Multiple users report dramatic mood improvements from long fasts, repeated shorter fasts, or ketogenic diets; others describe depression triggered by low‑calorie/low‑carb regimens.
• Proposed mechanisms include microbiome reset (reducing overgrowth like M. morganii), lowered inflammation/oxidative stress, dopamine “reset,” behavioral activation, and “starvation euphoria”; all remain speculative.
• Some suggest structured low‑FODMAP protocols, specific probiotics (e.g., certain Bacillus strains), oregano oil/garlic extracts, or butyrate as more sustainable microbiome interventions.
• Skeptics caution against seeing diet as a universal cure‑all for depression and highlight bipolar spectrum, behavioral therapy effects, and placebo/psychosomatic possibilities.

Possible interventions on the microbiome

• Beyond general lifestyle changes (diet, fasting, stress reduction, probiotics), fecal microbiota transplant is mentioned as a more direct way to reshape gut flora.
• Idea floated of species‑specific antimicrobials against M. morganii; bacteriophages are cited as an existing, highly specific antibacterial approach.

Regulation, precaution, and “via negativa”

• Several commenters criticize regulatory regimes that treat chemicals as “safe until proven harmful,” citing historical drug and industrial scandals.
• Taleb’s “via negativa” is referenced: favor only long‑historical foods and exposures (water, wine, coffee) and avoid novel additives where long‑term effects are unknown.
• Others counter that while caution is warranted, depression and similar conditions are serious enough that experimental self‑interventions may still be justified.

Other biological links (Long Covid, serotonin)

• One thread connects Long Covid to reduced gut tryptophan uptake and low serotonin; a commenter reports benefit from hydrolyzed protein supplementation but another notes the underlying study has methodological issues and lacks replication.
• Overall, participants converge on the view that the gut–brain–immune axis is important but poorly understood, and that current evidence supports cautious experimentation rather than definitive clinical recommendations.