The esophagus is a closed and collapsed tube, and continuous flow of gas or putrid substances from the stomach indicates a health problem—such as reflux serious enough to be bringing up stomach contents or a fistula between the stomach and the esophagus—which will demonstrate more serious manifestations than just foul odour.In the case of allyl methyl sulfide (the byproduct of garlics digestion), odour does not come from the stomach, since it does not get metabolized there. Systemic diseases
There are a few systemic (non-oral) medical conditions that may cause foul breath odour, but these are infrequent in the general population. Such conditions are:
Fetor hepaticus: an example of a rare type of bad breath caused by chronic liver failure. Lower respiratory tract infections (bronchial and lung infections). Kidney infections and kidney failure. Carcinoma. Trimethylaminuria ("fish odour syndrome"). Diabetes mellitus. Metabolic conditions, e.g. resulting in elevated blood dimethyl sulfide.Individuals affected by the above conditions often show additional, more diagnostically conclusive symptoms than bad breath alone. Delusional halitosis
One quarter of the people seeking professional advice on bad breath have an exaggerated concern of having bad breath, known as halitophobia, delusional halitosis, or as a manifestation of olfactory reference syndrome. They are sure that they have bad breath, although many have not asked anyone for an objective opinion. Bad breath may severely affect the lives of some 0.5–1.0% of the adult population.
Genetic testing can also confirm the disease, as mutations in the AGPAT2 gene is indicative of CGL1, a mutation in the BSCL2 gene is indicative of CGL2, and mutations in the CAV1 and PTRF genes are indicative of CGL3 and CGL4 respectively. Physical diagnosis of CGL is easier, as CGL patients are recognizable from birth, due to their extreme muscular appearance, which is caused by the absence of subcutaneous fat.CGL3 patients have serum creatine kinase concentrations much higher than normal (2.5 to 10 times the normal limit). This can be used to diagnose type 3 patients and differentiate them from CGL 1 and 2 without mapping their genes. Additionally, CGL3 patients have low muscle tone when compared with other CGL patients. Treatment
Metformin is the main drug used for treatment, as it is normally used for patients with hyperglycemia. Metformin reduces appetite and improves symptoms of hepatic steatosis and polycystic ovary syndrome. Leptin can also be used to reverse insulin resistance and hepatic steatosis, to cause reduced food intake, and decrease blood glucose levels. Diet
CGL patients have to maintain a strict diet for life, as their excess appetite will cause them to overeat. Carbohydrate intake should be restricted in these patients. To avoid chylomicronemia, CGL patients with hypertriglyceridemia need to have a diet very low in fat. CGL patients also need to avoid total proteins, trans fats, and eat high amounts of soluble fiber to avoid getting high levels of cholesterol in the blood.