Oxalate Article

May Be Misleading

Kudos to the Townsend Letter for publishing the January 2015 piece by William Shaw titled “The Green Smoothie Fad: This Road to Health Hell is Paved with Toxic Oxalate Crystals.”¹ This is a valuable and timely warning about serious problems caused by excessive oxalate consumption. Oxalates that are not excreted may accumulate in the body and cause systemic inflammation, oxidative stress, and a wide variety of potentially debilitating health problems.^2–6 A state of chronic (mild) poisoning by oxalates may negatively affect the health of a lot of people, yet it is generally unrecognized.

To remain credible, writers discussing this topic must strive to convey the most accurate knowledge available. Dr. Shaw’s article included several potentially misleading assertions that merit clarification for readers interested in understanding this complex issue and in preventing or reducing excessive oxalate consumption.

Dr. Shaw states in his steps for the control of excessive oxalate that the body has “enzymes that degrade oxalate” and that B6 supports this process. The body does not degrade oxalate. Oxalate is a terminal metabolite that must be excreted, primarily by the kidneys. The only mechanism mammals have to degrade oxalate is via the actions of a few varieties of microorganisms often present in healthy intestinal flora.⁷ The body can excrete some oxalate into the intestinal tract (and skin), especially when the kidneys are not fully functioning.⁸ Unfortunately, the gut microorganisms that degrade oxalate are easily destroyed by antibiotic drugs (such as erythromycin, doxycycline, or flagyl), other pharmaceutical drugs, and by excessive oxalate consumption.^9,10 Thus, this microbial protection is lacking in many people. Antifungal drugs may cause additional microflora disruption and further strain the kidneys whose job it is to excrete oxalate, and prudence suggests that they be used with caution only when fungal infection is clearly evident. Gut health is indeed critical to reducing susceptibility to oxalate, as absorption of oxalate is higher when the gut is inflamed or otherwise disturbed.^11,12 Dietary and accumulated oxalates exasperate the difficulties of restoring gut health.

Although vitamin B6 does not help the body degrade oxalate, Dr. Shaw is correct in asserting that B6 (pyridoxine) supplementation is an important therapy for reducing internal oxalate production. The body produces oxalate from glyoxylate, especially so when vitamin B6 is deficient.¹³ B6 is a coenzyme that, among its many other metabolic functions, helps the AGT enzyme to detoxify glyoxylate by converting it to glycine rather than oxalate. Oxalate overload can also cause B6 deficiency, leading to a vicious cycle of overproduction of oxalate by the body. Pharmacologic doses of vitamin B6 reduce internal production of oxalate.¹⁴ Simply taking vitamin B6 will not in itself lower health risks from excessive oxalate consumption in the diet, or from insufficient excretion of oxalate.¹⁵

There is no direct evidence that the body’s ability to handle oxalate is improved by increased water intake, although dilute urine is easier on the urinary tract generally. Drinking copious amounts of water may improve oxalate elimination for kidney stone forming patients, but water taken with food may increase the intestinal absorption of oxalate from foods, regardless of kidney function.¹⁶

Dr. Shaw’s article also adds to the widespread confusion over what foods are truly high in oxalate. For instance the article states that arugula is high in oxalate. Yet according to expert testing done on behalf of the VP Foundation, 1 cup of arugula contains less than 2 mg total oxalate and about 0.5 mg of soluble oxalate, which is quite low.¹⁷ Compare that with raw baby spinach, which contains 320 mg total oxalate and 230 mg of soluble oxalate per cup.¹⁸ Foods with less than 5.0 mg of oxalate per serving are considered low in oxalate, while foods over 10 (Harvard University) or 14.9 (VP Foundation) are considered high in oxalate.^19,20 The resource offered by Dr. Shaw for learning about oxalate content of foods (UPMC) is of limited value, as are many similar online lists hosted by academic medical centers.^19,21 Like other lists, it is not fully up to date, is limited in the number of foods listed, ignores supplements completely, and contains errors.

To date, no mainstream nutrition, public health, or medical agency has compiled a comprehensive and up-to-date database of the oxalate content of foods in a consumer-accessible form. However, there are two peer-to-peer educational organizations that are helping people obtain accurate information about oxalates in foods, the VP Foundation (http://www.thevpfoundation.org) and the Autism Oxalate Project, (http://www.lowoxalate.info). Since 2002, the VP Foundation has engaged Michael Liebman, PhD, as scientific adviser and head of the foundation’s food testing program. Dr. Liebman is an international expert on the methodology for measuring food oxalate and oxalate bioavailability, and the VP Foundation is an established leader helping low-oxalate dieters obtain accurate data about oxalates in food. Unfortunately, due to a lack of funds, its carefully compiled data have not been issued in one convenient reference document, but are scattered throughout its newsletters. Dr. Shaw, like low-oxalate dieters, is understandably confused about what foods and supplements are low in oxalate.

Current estimates of how much oxalate people are eating and how much of it is absorbed are not reliable, nor are they reflective of current dietary trends. However, recent studies found that dietary oxalate contributes 24% to 67% to urinary oxalate excretion.^22,23 Oxalate intake has been underestimated because of inaccurate techniques used to assay food oxalate, and absorption has also been difficult to assess.²⁴ Our rudimentary understanding of how the body stores oxalate in tissues, and metabolic conditions that favor mobilization and excretion of sequestered oxalates complicates estimates of oxalate absorbtion.²²

To fully make sense of this complex and fascinating topic we need a lot more research. Still, the low-oxalate, adequate calcium, diet with, combined with appropriate supplements, offers a powerful therapeutic option for willing clinicians and patients.²⁵ I found this diet to be the only way for me to recover from a sleep disorder, arthritis, muscle pains, headaches, and fatigue. I have assisted a number of clients in reversing their chronic health problems including irritable bowel syndrome, hand and wrist pain, pain of incomplete healing from injury, back pain, poor quality sleep, and other brain function issues using the low-oxalate diet and supportive supplements. Anyone interested in trying this therapy should seek guidance from qualified persons who have experience with the diet and be sure to obtain accurate information about the oxalate content of foods. The VP Foundation and the Autism Oxalate Project have both helped thousands improve their health and well-being with the low-oxalate diet.

Thank you for raising awareness of the problems with dietary oxalate. I hope you will continue to cover this topic and help to clear up the confusion and generate more demand for and interest in filling the gaps in our knowledge about oxalates and health.

Respectfully,

Sally K. Norton, MPH

Vitality Coach, Speaker & Health Consultant

Richmond, Virginia

https://sallyknorton.com

sally@sallyknorton.com

Notes

1. William Shaw. The green smoothie fad. Townsend Lett. 2015;(378). http://www.townsendletter.com/Jan2015/green0115.html.

2. Marengo SR, Romani AMP. Oxalate in renal stone disease: the terminal metabolite that just won’t go away. Nat Clin Pract Nephrol. 2008;4(7):368–377. doi:10.1038/ncpneph0845.

3. Lorenz EC, Michet CJ, Milliner DS, Lieske JC. Update on oxalate crystal disease. Curr Rheumatol Rep. 2013;15(7):340. doi:10.1007/s11926-013-0340-4.

4. Knauf F, Asplin JR, Granja I, et al. NALP3-mediated inflammation is a principal cause of progressive renal failure in oxalate nephropathy. Kidney Int. 2013;84(5). doi:10.1038/ki.2013.207.

5. Getting JE, Gregoire JR, Phul A, Kasten MJ. Oxalate nephropathy due to “juicing”: case report and review. Am J Med. 2013;126(9):768–772. doi:10.1016/j.amjmed.2013.03.019.

6. Khan SR. Reactive oxygen species, inflammation and calcium oxalate nephrolithiasis. Transl Androl Urol. 2014;3(3):256–276. doi:10.3978/j.issn.2223-4683.2014.06.04.

7. Allison MJ, Cook HM, Milne DB, Gallagher S, Clayman RV. Oxalate degradation by gastrointestinal bacteria from humans. J Nutr. 1986;116(3):455–460.

8. Hatch M, Gjymishka A, Salido EC, Allison MJ, Freel RW. Enteric oxalate elimination is induced and oxalate is normalized in a mouse model of primary hyperoxaluria following intestinal colonization with Oxalobacter. Am J Physiol Gastrointest Liver Physiol. 2011;300(3):G461–G469. doi:10.1152/ajpgi.00434.2010.

9. Choudhury D, Ahmed Z. Drug-associated renal dysfunction and injury. Nat Clin Pract Nephrol. 2006;2(2):80–91. doi:10.1038/ncpneph0076.

10. Sostres C, Gargallo CJ, Lanas A. Nonsteroidal anti-inflammatory drugs and upper and lower gastrointestinal mucosal damage. Arthritis Res Ther. 2013;15(Suppl 3):S3. doi:10.1186/ar4175.

11. Theka T, Rodgers A, Ravenscroft N, Lewandowski S. Intestinal permeability in subjects from two different race groups with diverse stone-risk profiles. Urolithiasis. 2013;41(2):111–117. doi:10.1007/s00240-013-0543-1.

12. Pang R, Linnes M, O’Connor HM, Li X, Bergstralh E, Lieske JC. A controlled metabolic diet reduces calcium oxalate supersaturation but not oxalate excretion after bariatric surgery. Urology. 2012;80(2):250–254. doi:10.1016/j.urology.2012.02.052.

13. Hagler L, Herman RH. Oxalate metabolism. I. Am J Clin Nutr. 1973;26(7):758–765.

14. Curhan GC, Willett WC, Speizer FE, Stampfer MJ. Intake of vitamins B6 and C and the risk of kidney stones in women. J Am Soc Nephrol JASN. 1999;10(4):840–845.

15. Mitwalli A, Ayiomamitis A, Grass L, Oreopoulos DG. Control of hyperoxaluria with large doses of pyridoxine in patients with kidney stones. Int Urol Nephrol. 1988;20(4):353–359.

16. Lien Y-HH. Juicing Is Not All Juicy. Am J Med. 2013;126(9):755–756. doi:10.1016/j.amjmed.2013.04.007.

17. The low oxalate diet addendum. Fall 2007– numerical values table. VP Found Newsl. 2007;(29):8–10.

18. The low oxalate diet addendum. Winter 2010 – numerical values table. VP Found Newsl. 2010;(33):18–23.

19. Oxalate content of foods [online document]. 2008. Harvard T. H. Chan School of Public Health Nutrition Department. Available at https://regepi.bwh.harvard.edu/health/Oxalate/files. Accessed October 2, 2014.

20. Yount J, Gottlieb A. The Low Oxalate Cookbook, Book Two. Graham, NC: Vulvar Pain Foundation; 2005.

21. Low oxalate diet [Web page]. University of Pittsburgh Medical Centers Nutrition Services. http://www.upmc.com/patients-visitors/education/nutrition/pages/low-oxalate-diet.aspx. Accessed February 18, 2015.

22. Holmes RP, Goodman HO, Assimos DG. Dietary oxalate and its intestinal absorption. Scanning Microsc. 1995;9(4):1109–1118; discussion 1118–1120.

23. Holmes RP, Goodman HO, Assimos DG. Contribution of dietary oxalate to urinary oxalate excretion. Kidney Int. 2001;59(1):270–276. doi:10.1046/j.1523-1755.2001.00488.x.

24. Ismail A. al-Wahsh. A comparison of two extraction methods for food oxalate assessment. J Food Res. 2012;1(2). doi:10.5539/jfr.v1n2p23.

25. Lieske JC, Tremaine WJ, De Simone C, et al. Diet, but not oral probiotics, effectively reduces urinary oxalate excretion and calcium-oxalate supersaturation. Kidney Int. 2010;78(11):1178–1185. doi:10.1038/ki.2010.310.