Tuesday, August 7, 2018

CHINESE RESTAURANT SYNDROME: WHAT ACTUALLY HAPPENS?

Chinese restaurant syndrome (CRS) is a kind of hypersensitivity reaction in response to a MSG (mono sodium glutamate) containing meal. Common clinical features that were reported from suspected CRS patients include flushing, headache, chest pain, nausea, vomiting, diarrhea, facial pressure and burning sensation. In addition to these mild features, occasional angioedema and bronchospasm associated with life threatening anaphylaxis were also reported. A number of mechanisms has been proposed to explain this phenomenon.

1. When MSG is consumed in large doses, excess glutamate is converted to acetylcholine through     Kreb's cycle. This suggestion was made on three facts. First, there is an astounding similarity   between  symptoms of CRS and those produced by an acetylcholine injection. Second, it was noted   that approximately one fourth of human cholinesterase being depleted following a MSG containing   meal. Third, CRS symptoms could be modulated using drugs that work on cholinergic systems.   (Ghadimi et. al., 1971)

2. Folkers and the team could prevent development of CRS symptoms by preadministering vitamin   B6. So, they suggested CRS as a manifestation of vitamin B6 defficiency. (1984)

3. In 1986, Kennedy suggested that CRS results due to irritative action of MSG on esophagus. This   theory was supported by two findings; first, Price and team (1978) had already demonstrated CRS   like symptoms using esophageal infusions of coffee, orange juice and tomato juice. Second,   previous researchers had shown to reduce CRS symptoms in MSG sensitive individuals by   administering MSG in capsular form.

4. Chin and team in 1989 pointed out the striking similarity of CRS symptoms with that of scramboid poisoning. Hence, they proposed CRS symptoms occur due to naturally occurring histamine in foods.

5. Xeon and team (2009), carrying out an experiment on mouse cortical neurons, illustrated the capability of inducing swelling and injury of mature neurons at clinically relevant concentrations (53 micM), at which headache occurs.

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