2.3.1 Herxheimer / die-off / acetaldehyde support

Acetaldehyde is one of the primary toxins released during microbial die-off events and also in smaller amounts, multiple times per day, in response to normal dietary intake of nutrients. Our food intake also feeds our resident microorganisms – including the pathogenic species – which allows them to produce (toxic) metabolites and poison us following each meal.

Acetaldehyde potentially places a difficult burden on our metabolism in key places – histamine degradation, neurotransmitter degradation, collagen synthesis, carnitine synthesis (needed to transport longer chain fatty acids), fatty acid degradation, glucose transport and glycolysis, GABA metabolism, choline metabolism, methylation, vitamin B6 degradation, vitamin A degradation, lysine degradation, pyruvate metabolism and other pathways. Aldehyde dehydrogenase enzymes (ALDH2, 1A1, 1A2, etc.) detoxify acetaldehyde into acetate as a priority over their normal substrates. Having low NAD⁺ as a result of chronic IFN-γ activity exacerbates this problem significantly, as ALDH normally requires NAD⁺, magnesium and zinc.

Taurine, NAD⁺, magnesium, zinc and molybdenum help promote ALDH activity and restore normal metabolism. Cultivating acetaldehyde metabolising probiotic species like bifidobacterium and reducing acetaldehyde producing species is the long-term goal, however using one of these short-term interventions can be very helpful pre-meal and during die-off:

Kislip - https://ase-onlinestore.com/products-list/asetablet-1box/, worldwide shipping from Japan

Acetium - https://www.biohitshop.com/product/3/acetium-capsules-3-x-60-pcs, EU shipping only
ZBiotics - https://zbiotics.com/products/zbiotics, too expensive for daily use
NAC - small amounts after meals are now included in the DIY Sipper recipe.
DHM - now included in Stage 1, though additional amounts can be taken