Oxalate and its acid form oxalic acid are organic acids that are primarily from three sources:
- the diet,
- from fungus such as Aspergillus, Penicillium, and possibly Candida,
- and also from human metabolism.
Oxalic acid is the most acidic organic acid in body fluids and is used commercially to remove rust from car radiators. Antifreeze (ethylene glycol) is toxic primarily because it is converted to oxalate. Two different types of genetic diseases are known in which oxalates are high in the urine. The genetic types of hyperoxalurias (type I and type II).
Foods especially high in oxalates include spinach, beets, chocolate, peanuts, wheat bran, tea, cashews, pecans, almonds, berries, and many others. Oxalates are not found in meat or fish at significant concentrations. Daily adult oxalate intake is usually 80-120 mg/d; it can range from 44-1000 mg/d in individuals who eat a typical Western diet.
High oxalic with or without elevated glyceric or glycolic acids may be associated with the genetic hyperoxalurias, autism, women with vulvar pain, fibromyalgia, and may also be due to high vitamin C intake. However, kidney stone formation from oxalic acid was not correlated with vitamin C intake in a very large study.
Besides being present in varying concentrations in most vegetables and fruits, oxalates, the mineral conjugate base forms of oxalic acid, are also byproducts of molds such as Aspergillus and Penicillium and probably Candida.
If yeast or fungal markers are elevated, antifungal therapy may reduce excess oxalates.
High oxalates may cause anemia that is difficult to treat, skin ulcers, muscles pains, and heart abnormalities. Elevated oxalic acid is also the result of anti-freeze (ethylene glycol) poisoning. Oxalic acid is a toxic metabolite of trichloroacetic acid and other environmental pollutants. In addition, decomposing vitamin C may form oxalates during transport or storage.
When glycolic acid is also increased:
Elevated oxalate values with an associated increase in glycolic acid may indicate genetic hyperoxaluria (type I).
When glyceric acid is also increased:
Increased glyceric acid may indicate a genetic hyperoxaluria (type II).
When both glyceric and glycolic acid levels are normal:
Elevated oxalic acid with normal levels of glyceric or glycolic metabolites rules out a genetic cause for high oxalate. However, elevated oxalates may be due to a new genetic disorder, hyperoxaluria type III.
Regardless of its source, high oxalic acid may contribute to kidney stones and may also reduce ionized calcium.
Oxalic acid absorption from the GI tract may be reduced by calcium citrate supplementation before meals. Vitamin B6, arginine, vitamin E, chondroitin sulfate, taurine, selenium, omega-3 fatty acids and/or N-acetyl glucosamine supplements may also reduce oxalates and/or their toxicity.
Excessive fats in the diet may cause elevated oxalate if fatty acids are poorly absorbed because of bile salt deficiency. Unabsorbed free fatty acids bind calcium to form insoluble soaps, reducing calcium's ability to bind oxalate and increase its absorption. If taurine is low in a plasma amino acid profile, supplementation with taurine (1000 mg/day) may help stimulate bile salt production (taurocholic acid), leading to better fatty acid absorption and diminished oxalate absorption.
High levels of oxalates are common in autism. Malabsorption of fat and intestinal Candida overgrowth are probably the major causes for elevated oxalates in this disorder. Even individuals with elevated glyceric or glycolic acids may not have a genetic disease.
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