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 due to the kinetics involved. This means that these enzymes are the primarily affected reactions by chronic acetaldehyde and this will initially create a number of metabolic impairments to important pathways. This may be observed as eg. elevated LDL cholesterol, elevated serum vitamin B6, elevated histamine, elevated retinol / beta-carotene and an array of symptoms.