If this thread hasn’t given you a headache yet, perhaps this post will.
The main points that sulfites are not typically the cause of headaches, and that true life-threatening sulfite allergies are very rare, have been known for many years but bear repeating periodically because the public misperception is tough to shake. Here’s an abstract from a 20-year-old review article which nicely summarizes the salient points.
J Am Coll Nutr. 1995 Jun;14(3):229-32.
Sulfite sensitivity: significance in human health.
Lester MR.
Abstract
Endogenous sulfite is generated as a consequence of the body’s normal processing of sulfur-containing amino acids. Sulfites occur as a consequence of fermentation and also occur naturally in a number of foods and beverages. As food additives, sulfiting agents were first used in 1664 and approved in the United States as long ago as the 1800s. With such long experience with their use, it is easy to understand why these substances have been regarded as safe. They are currently used for a variety of preservative properties, including controlling microbial growth, preventing browning and spoilage, and bleaching some foods. It is estimated that up to 500,000 (< .05% of the population) sulfite-sensitive individuals live in the United States. Sulfite sensitivity occurs most often in asthmatic adults–predominantly women; it is uncommonly reported in preschool children. Adverse reactions to sulfites in nonasthmatics are extremely rare. Asthmatics who are steroid-dependent or who have a higher degree of airway hyperreactivity may be at greater risk of experiencing a reaction to sulfite-containing foods. Even within this limited population, sulfite sensitivity reactions vary widely, ranging from no reaction to severe. The majority of reactions are mild. These manifestations may include dermatologic, respiratory, or gastrointestinal signs and symptoms. Severe nonspecific signs and symptoms occur less commonly. Broncho-constriction is the most common sensitivity response in asthmatics. The precise mechanisms of the sensitivity responses have not been completely elucidated. Inhalation of sulfur dioxide (SO2) generated in the stomach following ingestion of sulfite-containing foods or beverages, a deficiency in a mitochondrial enzyme, and an IgE-mediated immune response have all been implicated.(ABSTRACT TRUNCATED AT 250 WORDS)
As for the bare bone basics of ethanol metabolism…
Alcohol dehydrogenase (ADH) comes in various forms (isozymes), but it’s main job is to convert alcohol into acetaldehyde, not acetaldehyde into acetate. Aldehyde dehydrogenase converts acetaldehyde into acetate.
Alcohol makes you drunk. It also causes diuresis by inhibiting antidiuretic hormone, leading to dehydration which is one of the causes of hangover symptoms. Acetaldehyde is a toxin that also gives rise to a number of hangover symptoms. Acetate is non-toxic.
Problems can arise from under- or over-activity of alcohol dehydrogenase.
People with low alcohol dehydrogenase activity don’t break down alcohol in the stomach as rapidly as normals and therefore absorb more alcohol, making them more easily inebriated after ingesting relatively low doses of alcohol. This is common in women, especially young women. There are also racial variances in alcohol dehydrogenase activity.
Some people carry a mutated version of alcohol dehydrogenase in which the enzyme is more efficient at converting ethanol to acetaldehye. Since their acetaldehyde dehydrogenase works at normal efficiency breaking down the acetaldehyde, they develop higher levels of that metabolite and are more prone to suffering its toxic effects.