above and below the normal range are known as, respectively, hyperuricemia and hypouricemia. Likewise, uric acid concentrations in urine above and below normal are known as hyperuricosuria and hypouricosuria. Uric acid levels in saliva may be associated with blood uric acid levels. High uric acid Hyperuricemia (high levels of uric acid), which induces gout, has various potential origins: Diet may be a factor. High intake of dietary purine, high-fructose corn syrup, and sucrose can increase levels of uric acid. Serum uric acid can be elevated by reduced excretion via the kidneys. Fasting or rapid weight loss can temporarily elevate uric acid levels. Certain drugs, such as thiazide diuretics, can increase blood uric acid levels by interfering with renal clearance. Tumor lysis syndrome, a metabolic complication of certain cancers or chemotherapy, due to nucleobase and potassium release into the plasma. Low ATP (energy) reservoirs activating the Purine Nucleotide Cycle to produce ATP from adenine nucleotides (AMP, IMP, and S-AMP). Low ATP reservoirs can be due to strenuous exercise, fasting or starvation, or impairment of ATP production such as metabolic myopathies, diabetes, scurvy (Vitamin C deficiency), and excessive alcohol consumption. Excess IMP (inosine monophosphate) is converted into uric acid. IMP → Inosine → Hypoxanthine → Xanthine → Uric Acid Gout A 2011 survey in the United States indicated that 3.9% of the population had gout, whereas 21.4% had hyperuricemia without having symptoms. Excess blood uric acid (serum urate) can induce gout, a painful condition resulting from needle-like crystals of uric acid termed monosodium urate crystals precipitating in joints, capillaries, skin, and other tissues. Gout can occur where serum uric acid levels are as low as 6 mg per 100 mL (357 μmol/L), but an individual can have serum values as high as 9.6 mg per 100 mL (565 μmol/L) and not have gout. In humans, purines are metabolized into uric acid, which is then excreted in the urine. Consumption of large amounts of some types of purine-rich foods, particularly meat and seafood, increases gout risk. Purine-rich foods include liver, kidney, and sweetbreads, and certain types of seafood, including anchovies, herring, sardines, mussels, scallops, trout, haddock, mackerel, and tuna. Moderate intake of purine-rich vegetables, however, is not associated with an increased risk of gout. One treatment for gout in the 19th century was administration of lithium salts; lithium urate is more soluble. Today, inflammation during attacks is more commonly treated with NSAIDs, colchicine,