Why are oxalates a problem?
Oxalates serve no purpose in the body. However, they can cause serious problems and tend to do so in four ways:
- via crystal formation and subsequent interaction with immune cells, cause pronounced inflammation. This can result in irritation at the brain, dry skin, joint pain, bladder issues, etc. Both the scientific literature and clinical observations show that, while there are very common patterns in high-oxalate individuals, oxalate crystals can be found in almost all tissues.
- depletion of vitamins and minerals. In forming crystals, oxalates are also robbing your body of these minerals (the negative charge of oxalic acid makes postively charged ions, like Ca2+, Mg2+, Zn2+ and Fe2+, vulnerable). Individuals with oxalate issues often have unexplained anaemia or may struggle to increase mineral levels, regardless of how much they supplement.
- ‘crowding out’ of competitive molecules, such as sulphur, bicarbonate and chloride, that share transport channels. This can compromise a huge array of metabolic reactions.
- depleting glutathione. Oxalates cause huge oxidative stress, which depletes our antioxidant compounds like glutathione. Given how important glutathione is for regulating methylation, immune function, liver detoxification and controlling inflammation in the central nervous system, this can have devastating effects on your well-being.
What symptoms do oxalates cause?
Here’s the interesting part. There are no symptoms specific to oxalates. The symptoms will always depend on where the oxalate crystals are deposited. One of the many mysteries of oxalates is why some individuals store high concentrations of crystals beneath the skin (and therefore suffer from ‘mystery’ eczema) and others may store them in the joints (and therefore suffer from ‘mystery’ pain in the knees, hips, etc). Other may store them in the central nervous system, which is where they can cause all sort of symptoms (poor balance if they should cluster around the cerebellum, anxiety should they gather at the amygdala, and poor memory should they be located on the hippocampus).
In any cases, we will see signs of physical inflammation and neural agitation, which guarantees that energy will never optimal and sleep will never be as refreshing as it should be.
As you might imagine, all of these symptoms are attributable to other causes. And this is indeed how many end up being treated (doctors tend to prescribe ever-increasing amounts of steroids to control the inflammation or use psychotropic drugs to compensate for anxiety, while complementary therapists reach for an arsenal of fish oils, anti-microbials and ever-more-violent detox procedures).
Why do some people have problems with dietary oxalates and not others?
Healthy volunteers have been measured to absorb between 0.75 and 1.9% of oxalates they consume. Susan Owens, a prominent oxalate research, reports that this increases to 50% in some individuals. This all comes down to digestive function. Under ideal circumstances, the body is well-protected from oxalates through three mechanisms:
- oxalate degrading bacteria, such as oxalobacter formigenes. This is a bacterial species that is easily wiped out by antibiotics.
- mineral chelation. Around 80% of the calcium you consume will not be absorbed from the gut. It is deliberated left in the intestines, where it can bind free oxalic acid, and it does so easily (forming a calcium oxalate crystal). Calcium oxalate is not very soluble, thus cannot cross the intestinal barrier easily and therefore leaves the body in the stool. Problems occur when fat absorption is compromised. as this sees the undigested fats form complexes with the minerals; this reduces the amount of minerals left to chelate the oxalic acids.
- increased intestinal permeability. If the oxalic acid has not been degraded by bacteria or chelated by minerals, it can have a run at the intestinal lining. If the digestive lining is in a good state, minimal absorption of oxalates will occur. If it is inflamed and more permeable (‘leaky gut’), oxalates will cross the intestinal barrier easily via the paracellular route (between the junctions), leading to a massive build-up inside the body. Some individuals (with a SLC26A6 polymorphism) may be more suspectible to oxalate absorption via the transcellular route (though intestinal cells), although this needs further research.
The higher the accumulation of oxalates, the more likely that the individual has no oxalate-degrading bacteria, do es not digest fats properly and has inflamed/leaky gut lining. This is why dietary oxalates cause havoc in them and not others.
Are there other sources of oxalates?
Unfortunately so. Non-dietary oxalates can come from four sources:
- Intestinal infections. This can result in a huge amount of oxalate formation (as species such as candida and aspergillus have been shown to be prolific producers of oxalic acid). Candida also produces arabinose, which may impact on endogenous formation through anti-B6 effects, and all yeast produce erythroascorbic acid (discussed below). In my experience, intestinal infections and oxalate issues tend to go hand-in-hand.
- Endogenous production. A combination of genetic susceptibility and a lack of enzyme co-factors (eg. Vitamin A, B1, B6, Magnesium) can result in the mis-processing of amino acids and sees the liver form oxalates from ‘safe’ amino acids, like hydroxyproline (mainly found in collagen).
- Excess Vitamin C. A further way that oxalates accumulation can occur is from excess Vitamin C intake during periods of oxidative stress (once vitamin C, aka ascorbic acid, is oxidized into dihydroascorbic acid, it can then be further hydrolyzed into diketogulonic acid and then into oxalic acid). Microbial production of erthyroascobic acid, from intestinal pathogens, may also contribute to this pathway.
Suddenly, it’s no surprise that 91% of the individuals included in my 2017 Chronic Fatigue Survey showed raised urinary oxalates…
How are oxalates dealt with?
The first priority is determining why the oxalates are an issue. As mentioned above, these can be absorbed in the gut from dietary sources, produced by intestinal pathogens, formed from Vitamin C or manufactured within the body should metabolic pathways become deranged.
In most cases, we will avoid oxalates in the diet, while also adding Vitamin B6 to block conversion of dietary amino acids into oxalates (and compensate for the anti-B6 effects of arabinose). We will also consider steps required to repair the metabolic pathways involved in oxalate production. Vitamin A, Magnesium Biotin, Vitamin B1, Vitamin K and assessing redox balance feature heavily in this work. Obviously, considering the role of intestinal infections is very relevant, although practitioners may want to consider the likelihood of tolerance to this aggressive approach in the early stages of treatment.
Will I always have an issue with oxalates?
No. Only as long as your digestive tract is vulnerable, you are subject to chronic intestinal infections or your metabolic pathways are deranged. All are fixable, although it normally takes several months.
How long does Oxalate dumping last for?
When we stop the input of oxalates into the system, we expect the body to respond by ejecting these oxalates from the cells. This sees both oxalate crystals and free oxalic acid released into the system. The irritation that it causes is known as ‘oxalate dumping’, something that is acknowledged in the literature but largely unexplored. However, this can be explained by the movement of oxalates out of the cell, during which we can expect increased interaction with structures called inflammasomes (which, as the name suggests, initiate inflammation). My observations tie in exactly with those of other researchers; I see each dump lasting for 3-6 days, although there are many occasions where multiple dumps occur back-to-back, which can see ongoing dumping symptoms occur daily for a fortnight.
While there are the occasionally ‘quick responders’ that record huge improvements in short periods of time, it is always likely to be an up-and-down journey with both sustained spells of inflammation and glimpses of improved wellbeing. This tends to get slightly easier each week before it settles. We normally see things settle at some point between 8-20 weeks. Although oxalates will continue to be released after things settle, I would not expect them to disturb your wellbeing to the point that it will affect your day-to-day wellbeing or affect other therapeutic avenues we wish to explore.
If dumping symptoms are still highly evident at this point, I would be keen to look at ongoing accumulation from intestinal production (or endogenous production in the liver).
What can be done to ameliorate oxalate dumping?
During phases of oxalate dumping, symptoms tend to flare both at the cellular level (where the crystals are being released from) and also systemically (where both oxalates and free oxalic acid can now cause irritation).
There are two basic approaches (and one bonus approach) used to lessen the symptoms during these dumping phases:
- eat oxalate-rich food. This puts the body back into ‘storage mode’, stopping any further release of more oxalate crystals. This obviously means that we are storing up the problem for a later day, although sometimes this is necessary to reduce painful crystal formation.
- consume lots of ‘oxalate competitors’ such as sulphur, bicarbonate, chloride and Biotin. Due to a similar molecular shape, these agents occupy the pathways that oxalic acid would normally use to enter cells, crowding out the oxalate and stopping it from having such an impact at cellular level. The easiest ways to get the first three is through baths (Epsom salts, Bicarbonate of Soda and Magnesium Chloride, respectively) and Biotin is available in supplement form.
- Take Arginine, which is recommended to help deal with pain. I have seen largely disappointing responses to this, but I include it for consideration.
(additionally, should the stool turn grey or yellow during the oxalate dumping process, we should consider the use of Taurine).
How effective are these steps? Most individuals report feeling some relief, although generally this is a case of reducing the intensity of symptoms than eliminating them. The reality is that I don’t see them make that much of a difference, at best ‘taking the edge off’. For this reason, I try to avoid the first option as the small amount of relief rarely justifies extending the timescale required.
Where can I find more information on Oxalates?
There is a Trying Low Oxalates group on Facebook, which is maintained by Susan Owens. She is a biomedical researcher who has spent years studying the effects of oxalates in the body. For an accurate, up-to-date oxalate calculator that measures both soluble and insoluble oxalates, try my Sensible Oxalate Calculator here.