Did you know that oxalates can damage your heart and circulatory system, contributing to heart disease?
Our kidneys clean the blood. All of the oxalate that kidneys excrete every day gets there by traveling in our blood stream. The job of delivering toxic oxalate to the kidneys puts the arteries in harm’s way.
Researchers Don’t Expect Oxalate in Tissues
When oxalate deposits are found in tissues (other than the kidneys) doctors and researchers are surprised that the kidneys are working just fine. They believe that before oxalate collects in our bodies, the oxalate must first ruin the kidneys. This passage, below, from UCLA Pathologists Fishbein and Fishbein illustrates this conventional belief.
In a review of coronary arteries from 80 patients, we found 4 cases in which there were prominent oxalate deposits within the atherosclerotic plaques in coronary arteries. Oxalate deposits were also present in the media of arteries, the thyroid gland, and other organs, but not the kidneys, and the patients surprisingly did not have renal failure. (Fishbein and Fishbein 2009, p. 1315)
This expectation is based on the long-standing but unproven assertion that detectable (non-renal) oxalate deposits are a product of poor kidney function. In a previous report published by the journal Cardiovascular Pathology in 2008 they propose the new term “atherosclerotic oxalosis” to describe arterial plaque containing oxalate crystals.
This report was part of a study of coronary atherosclerosis in HIV infected patients, using atherosclerotic plaque samples from the National Neurologic AIDS Bank.
Whenever oxalate flows into the kidneys and other tissues in amounts beyond what they can handle (exceeding a capacity threshold), oxalate overload can occur. This can trigger accumulation of oxalate in the body. For some people this shows up as kidney deposits and kidney stones. But oxalate can encounter, be stashed, and be left behind in any susceptible tissue in the body, not just the kidneys.
Other Forms of Oxalate are Usually Overlooked
Note the use of the term prominent in the comment quoted above. The researchers do not mention trace deposits, nano-crystals, ionic oxalate, and other chemical forms of oxalate in the examined tissues as a possibility. Unexplored, no doubt.
There is also no mention of the age of the specimens at the time of examination. We know that oxalate deposits rapidly fade in biopsied tissue and cadavers. (It would be interesting to see a study specific to arteries and arterial plaque to investigate the durability of less prominent oxalate deposits in plaque.) To reliably find oxalate, living tissues need to be examined within two hours of death or excision, but often are not. This may help to explain why oxalate in the arterial plaque is assumed to be rare, it can be hard to detect.
Calcium oxalate may be a factor in “hardening arteries”. And it may be more common than this research suggests, given the crude detection methods we use. Artery plaque oxalosis is most likely in people with metabolic stress such as HIV, metabolic syndrome, chronic inflammation, diabetes, insulin resistance, chemical injury, poly-pharmacy, auto-immune conditions, and so on. We don’t know how oxalate may harm “healthy” people with “perfect” arteries.
Over and over, science has demonstrated that oxalate can collect in any tissue in the body—and not necessarily due to kidney problems.
Reason enough to become oxalate aware!
Here is an update: an 2017 report of an Italian study looking at heart artery plaque in 229 people, obtained through a tissue bank. They did a special microanalysis in 41 plaque samples to differentiate between two types of calcifications: calcium oxalate vs hydroxapatite. 37% of the plaques were primarily calcium oxalate and 63% were hydroxyapatite. Oxalate calcifications were detected mainly in unstable plaques in 27% of cases, whereas HA tended to dominate unstable plaques 60% of the time.
Of course, unstable plaques are the ones that tend to break loose and block fine capillaries, restricting blood flow to brain or heart tissues thus causing non-hemorrhagic stroke or heart attacks . https://www.ncbi.nlm.nih.gov/pubmed/28739184
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