Green Smoothie Genes – Oxalates in Your Diet

Green Smoothie Genes for OxalatesGreen smoothies have been a health fad for quite a while now. Most people rave about the health benefits of sneaking lots of spinach and other leafy greens into a delicious tasting smoothie. But not all people benefit from large amounts of spinach due to its high oxalate content. Here is an interesting article on the drawbacks of too many oxalates for some people: The Green Smoothie Fad:  This Road to Health Hell is Paved with Toxic Oxalate Crystals

It turns out that genetics play a role in your body’s ability to handle oxalates, along with your gut microbiome.  Approximately 80% of kidney stones are composed of oxalates bound to calcium.  A study from 2005 states that “5% of American women and 12% of men will develop a kidney stone at some time in their life, and prevalence has been rising in both sexes.” [ref]

Foods high in oxalates include leafy greens such as spinach, swiss chard, certain types of kale, arugula, and fruits such as blackberries, blueberries, and raspberries.  Here is a more complete list: Foods that contain oxalates

Kidney Stone genes:

A 2009 study found that those with the A allele in rs1501899 were at a higher risk for calcium kidney stones.  rs1501899 is a SNP in the CaSR gene (calcium-sensing receptor gene).  [ref]  Another study on that same SNP (rs1501899 – A allele) found a higher risk for stones in those with hyperparathyroidism.[ref]

A 2014 Chinese study found that the rs4142110 T-allele “significantly decreased calcium oxalate stone risk”.  Note that the T allele is the most common for most populations.  [ref]

A 2013 study looked at the SPP1 gene and found that the GG genotype of rs2853744 was a risk factor for stones.  [ref]

Primary hyperoxaluria:
The disease associated with a metabolic defect causing too many oxalates to build up in the kidneys is called hyperoxaluria. It is caused by a deficiency in alanine-glyoxylate aminotransferase which can be caused by polymorphisms in several genes. [ref]  There are three types of primary hyperoxaluria.

Primary Hyperoxaluria Type 1

AGXT (alanine-glyoxylate aminotransferase) is a gene found only in the liver. The AGXT gene codes for an enzyme that is involved in the process of detoxification of glyoxylate. Insufficient enzyme production leads to too much oxalate for the kidneys to clear.  Primary Hyperoxaluria Type 1 is the name of the kidney disease caused by calcium oxalate deposition. [ref] Most of the genetic polymorphisms associated with hyperoxaluria are not sequenced by 23andMe.

rs34116584 (T is the risk allele) is one of the more common polymorphisms that is thought to contribute to hyperoxaluria and is found in over 10% of Caucasians. Also called P11L in studies, it is the polymorphism found in 50% of people who have hyperoxaluria. Most affected are those who are homozygous for the mutation. [ref] This SNP is thought to act in conjunction with other SNPs to cause hyperoxaluria.[ref]

rs34664134 (A is the minor allele) is another SNP tested by 23andMe for the AGXT gene.  It is rare to find the polymorphism, and right now there haven’t been any studies published on it.  But if you have the minor allele, you may want to check on this sometime down the road when more is known about its significance.

rs180177166 (Insertion would be the minor allele) is another fairly rare variant in the AGXT gene.  Again, there aren’t any studies, but it is listed as the insertion being a pathogenic allele.

Primary Hyperoxaluria Type 2

23andMe SNPs for hyperoxaluria include i5012629 and i5012628 on the GRHPR gene.

  • i5012629 (DD is Primary Hyperoxaluria type 2, DI is a carrier of the risk allele)  “I” is normal.  Some people may see it listed as AAGT instead of I.
  • i5012628 (DD is  Primary Hyperoxaluria type 2, DI is a carrier of the risk allele)  “I” (or G) is normal.  Also known as rs80356708.

This is by far not an exhaustive list of polymorphisms that can cause problems with too many oxalates.  I encourage you to continue researching if this topic is of interest to you.

More to read:


Updated 2/5/17

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