A brand new diet is being extensively used to treat children with autism and other disorders. Researcher named Susan Owens discovered that the use of a diet low in oxalates markedly reduced symptoms in children with autism and PDD. For example, a mother with a son with autism reported that he became more focused and calm, that he played better, that he walked better, and had a reduction in leg and feet pain after being on a low oxalate diet. Prior to the low oxalate diet, her child could hardly walk up the stairs. After the diet, he walked up the stairs very easily. Many hundreds of children with autism throughout the world are now being placed on this diet with good results.

Benefits Reported By Parents Using Low Oxalate Diet

Improvements in gross and fine motor skills

Improvements in expressive speech

Better counting ability

Better receptive and expressive language

Increased imitation skills

Increased sociability

Speaking in longer sentences

Decreased rigidity

Better sleep

Reduced self-abusive behavior

Increased imaginary play

Improved cognition

Loss of bed wetting

Loss of frequent urination

Improved handwriting

Improved fine motor skills

Improvement in anemia

... and many others

How Can High Oxalates Be Treated?

Use antifungal drugs to reduce yeast and fungi that may be causing high oxalate. Children with autism frequently require years of antifungal treatment. I have noticed that arabinose, a marker used for years for yeast/fungal overgrowth on the Organic Acids Test (OAT) at The Great Plains Laboratory, is correlated with high amounts of oxalates (Table 2 and Figure 2) and arabinose has been found to be an important fuel for fungal oxalate production (5). Candida organisms have been found surrounding oxalate stones in the kidney (9).

Give supplements of calcium citrate to reduce oxalate absorption from the intestine. Citrate is the preferred calcium form to reduce oxalate because citrate also inhibits oxalate absorption from the intestinal tract. The best way to administer calcium citrate would be to give it with each meal. Children over the age of 2 need about 1000 mg of calcium per day. Of course, calcium supplementation may need to be increased if the child is on a milk-free diet. The most serious error in adopting the gluten-free, casein-free diet is the failure to adequately supplement with calcium.

Try N-Acetyl glucosamine to stimulate the production of the intercellular cement hyaluronic acid to reduce pain caused by oxalates (16).

Give chondroitin sulfate to prevent the formation of calcium oxalate crystals (17).

Vitamin B6 is a cofactor for one of the enzymes that degrade oxalate in the body and has been shown to reduce oxalate production (18).

Increase water intake to help to eliminate oxalates.

Excessive fats in the diet may cause elevated oxalate if the fatty acids are poorly absorbed because of bile salt deficiency. Non-absorbed free fatty acids bind calcium to form insoluble soaps, reducing calcium’s ability to bind oxalate and reduce oxalate absorption (19). If taurine is low in the Amino Acids Test, supplementation with taurine may help stimulate bile salt production (taurocholic acid), leading to better fatty acid absorption and diminished oxalate absorption.

Probiotics may be very helpful in degrading oxalates in the intestine. Individuals with low amounts of oxalate-degrading bacteria are much more susceptible to kidney stones (20). Both Lactobacillus acidophilus and Bifidobacterium lactis have enzymes that degrade oxalates (21).

Increase intake of essential omega-3 fatty acids, commonly found in fish oil and cod liver oil, which reduces oxalate problems (22). High amounts of the omega-6 fatty acid, arachidonic acid, are associated with increased oxalate problems (23). Meat from grain fed animals is high in arachidonic acid.

Take supplements of vitamin E, selenium, and arginine which have been shown to reduce oxalate damage (24, 25).

Undertake a low oxalate diet. This may be especially important if the individual has had Candida for long periods of time and there is high tissue oxalate buildup. There may be an initial bad reaction lasting several days to a week after starting the diet since oxalates deposited in the bones may begin to be eliminated as oxalates in the diet are reduced.

Evaluate vitamin C intake. Vitamin C can break down to form oxalates. However, in adults, the amount of oxalate formed did not increase until the amount exceeded 4 g of vitamin C per day (26). A large study of more than 85,000 women found no relation between vitamin C intake and kidney stones (27). In addition, an evaluation of 100 children on the autistic spectrum at The Great Plains Laboratory revealed that there was nearly zero correlation between vitamin C and oxalates in the urine (Table 2). Megadoses (more than 100 mg/Kg body weight per day) of vitamin C were shown to markedly reduce autistic symptoms in a double blind placebo controlled study (28) so any restriction of vitamin C needs to be carefully weighed against its significant benefits.

Oxalate Metabolism

In the genetic disease hyperoxaluria type I and in vitamin B-6 deficiency, there is a deficiency in the enzyme activity of alanine glyoxylate amino transferase (AGT), leading to the accumulation of glyoxylic acid. The high glyoxylic acid can then be converted to glycolate by the enzyme GRHPR or to oxalate by the enzyme LDH. Thus, glycolate, glyoxylate, and oxalate are the metabolites that are then elevated in the Organic Acids Test (OAT) in hyperoxaluria type I and in vitamin B-6 deficiency.

In the genetic disease hyperoxaluria type II, there is a deficiency in an enzyme (GRHPR) that has two biochemical activities: glyoxylate reductase and hydroxypyruvic reductase. This enzyme converts glyoxylate to glycolate and glycerate to hydroxypyruvate. When this enzyme is deficient, glycerate cannot be converted to hydroxypyruvate and glyoxylate cannot be converted to glycolate. In this disease, glyoxylate is increasingly converted to oxalate and glycerate is also very elevated.

External sources of oxalates include ethylene glycol, the main component of antifreeze. Antifreeze is toxic mainly because of the oxalates formed from it. In addition, some foods also contain small amounts of ethylene glycol. Vitamin C (ascorbic acid or ascorbate) can be converted to oxalates but apparently the biochemical conversion system is saturated at low levels of vitamin C so that no additional oxalate is formed until very large doses (greater than 4 g per day) are consumed. It is interesting that fungi can also produce vitamin C which may explain why many children with autism have high vitamin C even though they do not take supplements containing vitamin C. The high correlation between arabinose and oxalates indicate that intestinal yeast/fungal overgrowth is likely the main cause for elevated oxalates in the autistic spectrum population. The deposition of oxalates in critical tissues such as brain and blood vessels, the oxidative damage caused by oxalate salts, and the deposition of oxalate mercury complexes in the tissues may all be important factors in the core etiology of autism.

[Insert OAT Sample Test Result – Oxalate Section]



Oxalate Interconversions

Oxalic acid undergoes many conversions depending on the acidity of the environment in which it is present. The acidity of a water solution is usually indicated by a value called the pH. A very low pH like 0 or 1 indicates a very acidic solution while a pH of 13 or 14 would represent a very alkaline solution. A pH of 7 indicates a condition of neutrality. Blood has a pH of 7.4 which is very slightly alkaline. The pH of urine varies between 4.5 to 8 with an average of 6. Oxalic acid can lose a positively charged hydrogen ion or proton at a very low pH. The first pK value for oxalic acid (1.27) indicates the pH in which there are equal amounts of oxalic acid and its form missing a proton called monobasic oxalate. At a higher pH, the monobasic oxalate converts to a dibasic oxalate form with two negative charges. The second pK value for oxalate (4.28) indicates the pH at which there are equal values of monobasic and dibasic oxalates. At the pH of blood, which is extremely constant, virtually all oxalate is in the dibasic form. Because the pH of urine varies greatly, oxalate is mainly in the dibasic form in average urine while it is in both the monobasic and dibasic form in very acidic urine samples. When oxalates are tested, they are all converted to the same form before testing so they may be termed oxalates, oxalate, or oxalic acid.

Insolubility is a Key Factor in Oxalate Toxicity

Solubility of oxalate at body temperature is only approximately 5 mg/L at a pH of 7.0. The solubility of oxalic acid in water, in contrast, is approximately 106,000 mg/L. Thus, the oxalate form of oxalic acid is extremely insoluble. At most physiological pH values, oxalate salts are predominant. Oxalate has the ability to form salts with a wide variety of metals but each of these salts has a different solubility. A yardstick for measuring solubilities of different salts is called the solubility product constant or Ksp. The smaller the value of the Ksp, the greater the insolubility of a salt. Another way to express this is that the lower the Ksp, the greater the tendency of that salt to form insoluble crystals that may form in tissues. The table below lists the Ksp salts of oxalic acid in their order of solubility with the most insoluble salts listed at the top.

What is the importance of these solubility product numbers?