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Oxalates and Chronic Disease

New science and clinical experience reveal concerns about oxalates that far exceed traditional kidney stone pathology. In order to best support their patients and clients, integrative practitioners, and especially diet and nutrition specialists, would benefit from greater understanding of their influence.
Oxalates present in our bodies as sharp crystals or crystalline structures with jagged edges that cause pain, irritation, and distress. They are highly reactive molecules that can bind with certain minerals, particularly calcium and magnesium, as well as iron and copper. Having high oxalate levels in the body (hyperoxaluria) can be problematic, and not giving proper consideration to one’s oxalate intake can impede the effectiveness of even the best healing diet protocol.
High oxalate levels can be a factor in many chronic conditions, including digestive issues, autoimmune diseases, and neurological disorders. Oxalates affect mitochondrial function and can create inflammation, thus influencing every system in the body.
Understanding oxalates
Although most commonly identified with the formation of calcium oxalate kidney stones (composed of oxalate bound to calcium), free (unbound) oxalate can interfere with cellular functions, affecting health on a broader, systemic level. Clinical studies and anecdotal evidence indicate that oxidative stress, mitochondrial disruption and damage, and nutrient depletion – all of which can be caused by high oxalate levels – trigger widely varied symptoms, including fatigue, inflammatory cascades, joint pain, or pain elsewhere in the body. Chronic low energy is very common because of a reduction in adenosine triphosphate (ATP, which stores and transports chemical energy) in the mitochondria of the cells.
Oxalates can be a hidden source of headaches, urinary pain, genital irritation, and joint, muscle, intestinal, or eye pain. Other common oxalate-caused symptoms include mood disorders, anxiety, sleep problems, weakness, and burning feet. Indicators of oxalate problems can also include digestive or respiratory issues, or even bedwetting for children.
It’s important to note that oxalates can inhibit the absorption of calcium, magnesium, and other minerals, which actually makes oxalates an “anti-nutrient.” When minerals from our food become bound by oxalate – for instance, calcium (thereby forming insoluble calcium oxalate) – they cannot be absorbed properly by the intestinal tract. This can lead to deficiencies of these minerals.
In the gut of a healthy person, oxalates typically bind with these minerals and are then eliminated in the stool. While this inhibits absorption of these nutrients, it beneficially ensures that the oxalates are excreted rather than crossing the intestinal barrier into the bloodstream and causing cellular distress and damage.
If oxalate gets into cells, it can disrupt mitochondrial function and cause a variety of systemic disturbances. Here are some of the varied effects of high oxalate in the cells and tissues:
- Disrupts mineral absorption and usage
- Impairs cellular energy
- Depletes nutrients such as glutathione and interferes with biotin
- Creates oxidative stress[1]
- Activates the immune system to trigger inflammatory cascades
- Interferes with and damages mitochondrial function[2]
- Induces seizures (during toxic exposure to oxalate)[3,4,5]
- Causes faulty sulfation
- Triggers histamine release
Types and sources of oxalates
Oxalates can be divided into two types: exogenous (produced outside the body and acquired through dietary intake) and endogenous (produced within the body by liver cells).
Exogenous oxalate can accumulate from a diet that is high in spinach, nuts, beans, or other high-oxalate foods. Individualizing therapeutic diets is essential, because “by the book,” some well-known special diets strongly rely on higher-oxalate foods (especially almonds/almond flour). Diets that are often heavy on nut flours include the Specific Carbohydrate Diet, GAPS, and Paleo. Vegetarian diets are also often high in oxalate, since they usually include many beans, grains, nuts, and seeds, as well as high-oxalate greens and starchy vegetables, such as spinach and sweet potatoes.
High-Oxalate FoodsSpinach Swiss chard Almonds and almond flour All other nuts Chia seeds Sesame seeds Buckwheat Quinoa Most legumes Potatoes Sweet potatoes Chocolate Beets |
Practitioners should be aware that diets high in oxalate can create a wide variety of problems for some people. Modifying the diet can make a dramatic difference in lowering the oxalate load. (Note: it is important to reduce oxalates in the diet very slowly to avoid a detox reaction.) However, most of our body’s total oxalate content is created during normal body metabolism. It is generally accepted that 80-90 percent of urinary oxalate is produced endogenously,[6] within the cells, and this can wreak havoc in the body.
The origin of oxalate issues
Deficiencies and endogenous production
Each person’s ability to process oxalate varies, based on certain deficiencies, metabolic pathways, or genetic factors. Some nutrient deficiencies, including that of vitamins B6 and B1, can cause the body to produce oxalate in problematic amounts. Others, such as vitamin A deficiency, can cause the body to absorb excess oxalate through the gut.
Further, because some substances – such as ascorbic acid or the amino acid glycine (a key component inbone broth) – can be converted into oxalate in the body, complications can arise. Thus, certain supplements or a diet too high in meat can be a problem for some people. Fructose, xylitol, and other sugar alcohols may also be converted to oxalate.
When the gut is unhealthy
The health of the gut and its microbiome influence whether or not a person will have an issue with oxalates. A problem with oxalates can occur when the gut is inflamed and hyperpermeable (i.e., leaky gut) and there is fat maldigestion and malabsorption, or when there are not enough good bacteria (especially particular forms) to break down the oxalate in the gastrointestinal tract. Developing problems with oxalate is also more likely if there aren’t enough minerals in the gut to bind it.
Oxalobacter formigenes is a strain of beneficial bacteria that degrade oxalate. Unfortunately, a few – or sometimes even one – courses of antibiotics can wipe out our oxalobacter colonies for months, if not indefinitely. Certain other probiotic bacteria also break down oxalate. If there’s a history of antibiotic use or other causes of gut dysbiosis, one should work on correcting the microflora balance.
Excess undigested fat compounds matters. The extra fat floating around in the gut can bind calcium, making the calcium unavailable for oxalate binding and thus allowing free oxalate to pass through the gut barrier and enter the bloodstream.
For people with oxalate issues, it is important to know whether fat malabsorption is at play. A stool analysis can help you determine this. Some individuals may have symptoms indicative of fat digestion issues, such as floating or greasy stools. Gastroenterologists can often see signs of fat malabsorption during an upper GI endoscopy. Once it is determined that fat is not being digested and absorbed properly, an individual may need to restrict fat intake to avoid the further complication of oxalate issues, particularly in the short run, as they work on their digestion, whether with enzymes, support of bile production, or other means.
Sulfate, poor sulfation, and mitochondrial dysfunction
In addition to gut issues, sulfate and sulfation (a metabolic pathway involved in detoxification) can be underlying factors in oxalate issues. When sulfate is low and sulfation biochemistry is poor, oxalate problems can arise. Sulfate is very important in the body; it’s needed for processing phenolic foods (such as fruits, vegetables, and nuts) and for dozens of bodily processes, including digestion, intestinal barrier regulation, and neurodevelopment.
There is a two-way relationship between oxalate and sulfate: oxalates can cause low sulfate, and low sulfate can cause oxalate problems. Excess oxalates can interfere with the body’s ability to allow sulfate into the cell, thus inhibiting sulfation. On the other hand, with poor sulfation from low sulfate levels, oxalate is more readily carried into cells on (unoccupied) sulfate transporters.
Another way that low sulfate can cause problems with oxalates involves the kidneys. Susan Owens, who heads the Autism Oxalate Project at the Autism Research Institute, has said that insufficient sulfate inside the kidney tubule cells would interfere with the ability of the kidneys to remove oxalate from the blood and deliver it to the urine. This could cause higher levels of oxalate in the system.
Faulty sulfation plays a role in many chronic health conditions, of which autism,[7,8] food sensitivity,[9] Alzheimer’s disease, chronic fatigue syndrome,[10] inflammatory bowel disease,[10] and asthma[10] are only a few. Because there are so many conditions that have poor sulfation underlying them, it’s sensible to consider a low-oxalate diet and nutritional support for a variety of chronic healthissues.
Furthermore, when sulfate is low, intolerances to phenols can occur. Therefore, those who have low sulfate may also have an issue with both phenols and oxalates in food. People with depleted sulfate frequently do well on a low-phenol and low-oxalate diet.
Effects of high oxalate in the body
Mitochondrial dysfunction
As previously noted, oxalates that enter the cells can damage the mitochondria,[11] potentially affecting every organ and system of the body. This is a primary reason that oxalates can become problematic. It’s also why oxalate’s effect on chronic disease can be difficult to study through association. Some of the conditions that can involve mitochondrial dysfunction are autism, Alzheimer’s, Parkinson’s, multiple sclerosis, neurodevelopmental disorders, retinopathy, and cancer. While high oxalate may or may not provide the initial impetus for mitochondrial conditions, it is an important factor to consider for those with mitochondrial issues.
Oxidative stress, inflammation, and glutathione
There are even more pieces to this puzzle. High oxalate levels can lead to oxidative stress and subsequent inflammation and oxidative injury.[12,13] High oxalate can elevate superoxide (which has a proinflammatory role in many diseases) and deplete glutathione and other antioxidants.[14] Oxidative stress, inflammation, and low glutathione status are common manifestations in many chronic diseases. Understanding this relationship can help practitioners appropriately address the triggers that can be causing problems. In dealing with conditions involving oxidative stress and inflammation, it’s important to consider oxalate’s potential systemic implications when devising therapeutic interventions.
Conclusion
Extensive research indicates a multitude of chronic health conditions in which oxalate is implicated. These include:
- Asthma
- Autism[15]
- Autoimmune thyroiditis and other autoimmune conditions
- Chronic fatigue syndrome
- Cystic fibrosis[16]
- Fibromyalgia
- Hypothyroidism[17]
- Inflammatory bowel disease[18]
- Interstitial cystitis
- Kidney stones
- Low muscle tone
- Migraines and headaches
- Mitochondrial damage and dysfunction
- Rett syndrome[19]
- Seizures
- Vulvodynia
For 15 years, I’ve done research and educated parents and clinicians about therapeutic diets and nutrition for autism. It’s a very complex chronic disorder, and studying its intricacies provides great insight into addressing a wide variety of health conditions. Autism and many other disorders share underlying mechanisms of inflammation, mitochondrial dysfunction, and faulty sulfation, as well as digestive issues, leaky gut, and dysbiosis.
As we continue to survey these underlying factors and consider how oxalate may play a role, it’s easy to appreciate – and not particularly surprising – that there are so many chronic disorders that may be affected by oxalate. The degree of overlap in those conditions is significant and worth exploring more deeply.
Adapted from “Oxalates & Chronic Disease: How the Healthy Foods You Love May Be Making You Sick,” by Julie Matthews. See the full article at BioIndividualNutrition.com.
About the Author
Julie Matthews is a Certified Nutrition Consultant specializing in autism and BioIndividual Nutrition® for fifteen years. She provides dietary guidance backed by scientific research and applied clinical experience. Her award-winning book, Nourishing Hope for Autism, has helped people around the world to make food and nutrition choices that aid the health, learning, and behavior of those with autism, ADHD, and other developmental delays. She presents at leading conferences in the US and abroad and sits on several scientific advisory boards. Visit NourishingHope.com and BioIndividualNutrition.com.
REFERENCES
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- Veena CK, et al. Mitochondrial dysfunction in an animal model of hyperoxaluria: a prophylactic approach with fucoidan. European Journal of Pharmacology. 2008; 579(1):330-336.
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- Pfeiffer H, et al. Fatal cerebro-renal oxalosis after appendectomy. International Journal of Legal Medicine. 2004; 118(2):98-100.
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- Conyers RA, Bais R, Rofe AM. The relation of clinical catastrophes, endogenous oxalate production, and urolithiasis. Clinical Chemistry. 1990; 36(10):1717-1730.
- Waring RH, Klovrza LV. Sulphur metabolism in autism. Journal of Nutritional and Environmental Medicine. 2000; 10(1):25-32
- Alberti A, et al. Sulphation deficit in “low-functioning” autistic children: a pilot study. Biological Psychiatry. 1999; 46(3):420-424.
- Scadding GK, et al. Poor sulphoxidation ability in patients with food sensitivity. British Medical Journal. 1988; 297(6641):105-107.
- Moss M, Waring RH. The plasma cysteine/sulphate ratio: A possible clinical biomarker. Journal of Nutritional and Environmental Medicine. 2003; 13(4):215-229.
- Veena CK, et al. Mitochondrial dysfunction in an animal model of hyperoxaluria: a prophylactic approach with fucoidan. European Journal of Pharmacology. 2008; 579(1):330-336.
- Biswas SK, de Faria JB. Which comes first: renal inflammation or oxidative stress in spontaneously hypertensive rats? Free Radical Research. 2007; 41(2):216-224.
- Khan SR. Hyperoxaluria-induced oxidative stress and antioxidants for renal protection. Urological Research. 2005; 33(5):349-357.
- Khand FD, et al. Mitochondrial superoxide production during oxalate-mediated oxidative stress in renal epithelial cells. Free Radical Biology and Medicine. 2002; 32(12):1339-1350.
- Konstantynowicz J, et al. A potential pathogenic role of oxalate in autism. European Journal of Paediatric Neurology. 2012; 16(5):485-491.
- Terribile M, et al. Factors increasing the risk for stone formation in adult patients with cystic fibrosis. Nephrology Dialysis Transplantation. 2006; 21(7);1870-1875.
- Goldman M, Doering GJ. The effect of dietary ingestion of oxalic acid on thyroid function in male and female Long-Evans rats. Toxicology and Applied Pharmacology. 1979; 48(3):409-414.
- Danese S, et al. Extraintestinal manifestations in inflammatory bowel disease. World Journal of Gastroenterology. 2005; 11(46):7227-7236.
- Motil KJ, et al. Fractional calcium absorption is increased in girls with Rett syndrome. Journal of Pediatric Gastroenterology and Nutrition. 2006; 42(4):419-426.
Published in the Price-Pottenger Journal of Health & Healing
Winter 2017 – 2018 Volume 41 Number 4
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