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There Is No Role for a Low Oxalate Diet in Current Era Stone Management
By: Kristina L. Penniston, PhD, RDN, FAND | Posted on: 01 Feb 2022
Introduction
Patients depend on us to prescribe tested and effective treatments. In the current era, as public skepticism about science and medicine is rising, patients’ trust in us is more important than ever. This applies to medical and nutritional management of kidney stone disease. Therapeutic dietary changes may reduce stone recurrence risk provided they 1) address (an) identified etiological factor(s) contributing to the patient’s stone disease, 2) are achievable and sustainable over time, 3) cause no or limited unwanted side effects and 4) have ample evidence to support their use. A low oxalate diet, including when prescribed within a blanket regimen of dietary therapies to all patients with stones, fails these tests and is thus not appropriate in the current era stone management.
What Is a Low Oxalate Diet?
There is no consensus definition. In theory, it limits oxalate-rich foods to below some cutoff expressed in mg per day. This cutoff is variable, depending on providers’ beliefs, but is typically 50–100 mg per day. There are problems with this approach. For example, it is possible for individuals to consume the same foods but to calculate different oxalate content. Factors related to this variability are shown in table 1.1–3 For these reasons, cutoffs for a low oxalate diet are practically meaningless. The low oxalate diet is a treatment with no standard definition and varies widely in its application and practice.
Table 1. Factors related to variability and inconsistency in the reported oxalate content of foods
Factor | Reason for Variability |
---|---|
All foods have not been assessed for oxalate | Nutrient analysis techniques and food lists miss the true oxalate content of foods |
Interregional geographic variability | Differences in soil acidity and calcium exchangeability affect oxalate content1 |
Intra-plant variability | Oxalate content varies by plant maturity at harvest and also within the plant itself (eg leaves vs roots vs stems)2 |
Postharvest processing | Oxalate content for some foods differs when boiled vs steamed vs prepared in some other way3 |
Reported information varies widely | Leads to exclusion of some foods low for oxalate and vice versa |
Etiology
Determining the etiological factor(s) in any disease is the first step in medical management. While patients with kidney stones may present with similar physical symptoms and renal imaging (flank pain, lower urinary tract symptoms, visualized calculi in kidneys or lower urinary tract), causative factors can differ. This is not unique among medical conditions. In anemia, for instance, the etiology for the generally shared sequelae (fatigue, shortness of breath, low hemoglobin or hematocrit, low red blood cells) must be correctly identified in order to develop an effective response—iron supplementation does not address anemia caused by vitamin B12 or folate deficiency. Similarly, patients whose calcium oxalate (CaOx) stone disease is not caused by high urine oxalate will not be helped by a low oxalate diet. There are many potential contributors to hyperoxaluria; oxalate intake is not always primary. Consider the patient who consumes virtually no or only a little plant material. Recommending a low oxalate diet to this patient, whose oxalate intake is already low, is meaningless therapy. Moreover, in such a case, the recommendation of a more appropriate strategy, ie one that correctly addresses the etiology, is obviated.
Achievability and Sustainability
To be successful, nutrition therapy must be achievable. Challenges in undertaking a specifically defined low oxalate diet were already addressed. Very diligent patients frequently end up eliminating more foods than necessary in pursuit of the goal: “I haven’t eaten a tomato in 20 years.” This patient did not believe me when I told her that available evidence suggests that tomatoes are not actually high for oxalate. But she was given the information decades ago by her urologist (“He has treated all my stones,” she said), who she insisted knew more about nutrition than I. Even after pointing out she had continued to form primarily CaOx stones all these 20 years and that her 24-hour urine results demonstrated other treatable risk factors (low citrate and magnesium), she could not be convinced to eat a tomato. By avoiding tomatoes all these years, not to mention many other fruits and vegetables, the patient had not achieved a lower oxalate diet.
What about sustainability? Patients who don’t like to eat fruits, vegetables and whole grains find a low oxalate diet quite sustainable. But if you’ve ever heard a patient ask, “What can I eat?” or express some other frustration about following dietary recommendations, sustainability must be questioned. Dietary restrictions of any kind have a poor history of sustainability.4 For those who want to incorporate a healthy variety of plant-based foods into their diets, a low oxalate diet is not sustainable.
Side Effects
A diet low in plant-based foods, particularly when practiced zealously, is insufficient for antioxidants, which are primarily plant-derived phytochemicals conferring many health benefits, including those related to cardiovascular disease, inflammation, degenerative diseases and many cancers. The benefits of fiber, nearly exclusively provided by foods of plant origin, are lost. Potential digestive tract effects of low fiber consumption include altered bowel function (eg constipation, diarrhea, loss of colonic lubrication) and dysbiosis. Patients with diabetes on a lower fiber diet sacrifice a dietary strategy to control blood glucose. Table 2 lists other side effects. In sum, the risk-to-benefit ratio for a low oxalate is high, rendering it of questionable therapeutic value.
Table 2. Potential side effects of a low oxalate diet
Restricted Foods | Dietary Effect of Restriction | Specific Stone Risk | Mechanism for Stone Risk |
---|---|---|---|
Most all fruits and vegetables | Lower intake of bicarbonate precursors | Calcium (all types), uric acid | Lower urine citrate, lower urine pH |
Leafy green vegetables, beans, nuts, seeds, whole grains, chocolate | Lower magnesium intake | Calcium oxalate | Lower urine magnesium |
Whole grains, nuts, seeds, some fruits and vegetables | Lower consumption of prebiotics from fiber | Calcium oxalate | Higher urine oxalate due to lower oxalate degrading capacity of gut microbes |
Nuts, seeds, tubers, some whole grains | Lower phytate intake | Calcium (all types) | Lower urine phytate |
Evidence
The kind of evidence we typically require prior to implementing a clinical therapy is lacking for a low oxalate diet. One controlled nutrition study among CaOx stone formers demonstrated a reduction in urinary oxalate excretion on a low oxalate diet.5 However, this same study revealed higher CaOx stone risk due to lower urine citrate and magnesium and higher urinary CaOx supersaturation. A short-term study demonstrated lower urine oxalate6 and a longer-term study demonstrated lower recurrence rates7 among CaOx stone formers on low oxalate diets, but there are no high-quality, well-designed, appropriately controlled, long-term trials to confirm these findings. In contrast, evidence for reducing the bioavailability (absorption) of dietary oxalate is robust.2,8,9 In clinical nutrition, the bioavailability of nutrients and other food-derived components is frequently manipulated. While the aim is usually to enhance bioavailability (eg by pairing consumption of nonheme iron with ascorbic acid, dietary fat with carotenoids and fat-soluble vitamins), the opposite can be accomplished, such as by pairing fat, fiber and/or protein with meals to reduce glucose absorption.
Few other widely practiced “therapies” in medicine have so little evidence as the low oxalate diet for stone prevention. In patients whose CaOx stone risk is diet-related, evidence supports 1) balanced dietary patterns that are ample for fruits, vegetables and fiber,10 and, if needed, 2) calcium consumption sufficient to reduce oxalate bioavailability.
- Dauer JM and Perakis SS: Contribution of calcium oxalate to soil-exchangeable calcium. Soil Science 2013; 178: 671.
- Massey LK, Roman-Smith H and Sutton RA: Effect of dietary oxalate and calcium on urinary oxalate and risk of formation of calcium oxalate kidney stones. J Am Diet Assoc 1993; 93: 901.
- Chai W and Liebman M: Effect of different cooking methods on vegetable oxalate content. J Agric Food Chem 2005; 53: 3027.
- Vadiveloo MK and Parekh N: Dietary variety: an overlooked strategy for obesity and chronic disease control. Am J Prev Med 2015; 49: 974.
- Noori N, Honarkar E, Goldfarb DS et al: Urinary lithogenic risk profile in recurrent stone formers with hyperoxaluria: a randomized controlled trial comparing DASH (Dietary Approaches to Stop Hypertension)-style and low-oxalate diets. Am J Kidney Dis 2014; 63: 456.
- Gupta M, Gallante B, Bamberger JN et al: Prospective randomized evaluation of idiopathic hyperoxaluria treatments. J Endourol 2021; https://doi.org/10.1089/end.2021.0122.
- Borghi L, Schianchi T, Meschi T et al: Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria. N Engl J Med 2002; 346: 77.
- von Unruh GE, Voss S, Sauerbruch T et al: Dependence of oxalate absorption on the daily calcium intake. J Am Soc Nephrol 2004; 15: 1567.
- Brinkley L, McGuire J, Gregory J et al: Bioavailability of oxalate in foods. Urology 1981; 17: 534.
- Lin B-B, Lin M-E, Huang R-H et al: Dietary and lifestyle factors for primary prevention of nephrolithiasis: a systematic review and meta-analysis. BMC Nephrol 2020; 21: 267.