Dysregulated oxalate metabolism is a therapeutic target in atherosclerosis | Hacker News Reader

Dysregulated oxalate metabolism is a therapeutic target in atherosclerosis

cell.com

81 pointsvoisin19 comments

Can anyone in the medical/nutrition/research field talk about the practicality of this finding (if any) on how people should moderate oxalate in their diet? Some of the healthiest foods have high oxalate levels, but I was under the impression it was one of those dietary fat != blood/bodily fat type things. Or how oxidants actually can help (in the right levels) by assisting in killing off errant and cancerous cells (which is why extreme over consumption of anti oxidants can hurt you)

I study medical and nutritional research for fun. Papers like these are always interesting to me.

Oxalates are a mixed bag, and are considered an "anti-nutrient", by binding nutrients and preventing absorption during digestion. Ex: Spinach has loads of calcium, but raw, is a poor source of calcium due to oxalate content. However, cooking foods with oxalates in them breaks down the oxalates and frees up the nutrients and partially prevents the anti-nutrient effect.

Excessively high Vitamin C diets (don't supplement to ridiculous amounts, some people do), possibly in combination with low calcium diets (calcium in the body is used to flush oxalates out), can lead to increased risk of kidney stones in diets with high oxalate content. Having a genetic mutation that leads to increased risk of kidney stones can add to this. Please note, there is a lot of ifs in that statement I just said, each one of them independently increases risk, but generally do not reach problematic levels unless you do (or have) more than one.

You shouldn't really worry about oxalates, just don't consume oxalate containing foods in absurd amounts, unless you already are at risk of forming the kind of kidney stones effected by oxalates, then you probably should switch to a low oxalate diet. As usual, talk to your doctor if you think you might be at risk.

Drinking iced (black) tea is potentially deadly in quantities that some southerners might not see as absurd. https://healthcare.utah.edu/healthfeed/postings/2015/04/0423...

This is a great example of a myth in the making due to poor reporting and science-by-case-report.

The report in question is just that-- a case report. It is not scientific in any sense. There's no way to establish causality here. All we can tell is this guy had oxalate kidney stones, and he also drank a lot of tea. That's it.

Controlled studies have found lower rates of kidney stones in tea drinkers:

- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6412450/ - Daily Green Tea Infusions in Hypercalciuric Renal Stone Patients: No Evidence for Increased Stone Risk Factors or Oxalate-Dependent Stones

- https://www.acpjournals.org/doi/10.7326/0003-4819-128-7-1998... - Beverage Use and Risk for Kidney Stones in Women

- https://academic.oup.com/aje/article/143/3/240/77956 - Prospective Study of Beverage Use and the Risk of Kidney Stones

- https://pubmed.ncbi.nlm.nih.gov/23676355/ - Soda and other beverages and the risk of kidney stones

And why iced tea in particular? That idea seems to have come from one single doctor, who said in an interview once that cold tea encourages people to drink more of it, versus hot tea. Again, no evidence, just cuz he thinks so:

https://www.medicalnewstoday.com/articles/248633#2

EDIT:

The authors of that case report somehow miscalculated the oxlate content of tea by a factor of ten. They claim that tea contains 50-100mg of oxalate per 100 ml. The actual content is about a tenth of that. Much less than a host of other common foods. And of course their report makes attempt to ascertain the rest of his diet.

This is essentially fake health news.

Is that reversible, that is did that man recover his kidney function after treatment?

Their letter claims that he underwent dialysis. But it doesn't matter; as I said in my other comment, this is fake health news.

> However, cooking foods with oxalates in them breaks down the oxalates and frees up the nutrients and partially prevents the anti-nutrient effect.

This advice should be taken very carefully. The amount of oxalate removed is highly dependent on the cooking method and the food in question. Furthermore, some foods like spinach remain very high in oxalates in comparison to other foods even after preparation. Finally, cooking is not effective at reducing insoluble oxalates. It's probable that insoluble oxalates are less problematic, but I don't know of any good data showing they are harmless.

I'd assume this article hints at the potential of using mRNA to treat arteriosclerosis.

I'd be interesting to learn how fasting affects the expression of said gene. Thats the easiest intervention anyone can take. (FWIW, I've been treated with a 12 day supervised waterfasting therapy for NAFLD and it reduced the volume of my liver by nearly 20%).

From my understanding, the main issue is impaired synthesis of glycine due to impaired/suppressed? genes. if you have that, you'd have to dramatically reduce oxalates to the point where it causes other problems. smarter to supplement glycine.

> supplement glycine

From the looks of it, the increased consumption of glycine supplements won't affect oxalate. Yes, glycine/oxalate ratio would be improved, but this would not decrease the amounts of oxalate. So the associated problems related to the excess of oxalate would persist.

For people with a predisposition to kidney stone this is already recommended (along with an increase in calcium intake).

https://kidneystones.uchicago.edu/how-to-eat-a-low-oxalate-d...

Someone correct me if I'm wrong, but, Oxalates aren't particularly high in the Western Diet.

Cruciferous vegetables seem more a feature of the Mediterranean diet or standard diet?

So I am assuming that the WD is lower in the necessary precursors for glycine production.

Also, I'm assuming that glycine ingested directly would just be metabolized before being used in the liver.

So the best actionable advice I can come up with is probably: "Eat more collagen"

> one of those dietary fat != blood/bodily fat type things.

What is meant by that though? Radio-labelling experiments do show that some dietary fat ends up as stored in fat cells.

https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2362....

https://en.wikipedia.org/wiki/Isotopic_labeling

Well the only human data is in figure 1, and it doesn't look that convincing. There seems to be a small difference in oxalate metabolism between people with/without coronary disease. They do a bunch of comparisons which aren't corrected for multiple testing, and then claim it is of some relevance which is the 'most significant' based on the lowest p.value. This is poor statistical practice if you ask me, such language should not be permitted in an academic paper, although this is utterly typical of nutritional science and life sciences in general. In any case, I think it is crazy to test the association between some nutritional/metabolic factor and a disease outcome in just 48 humans, the results are almost certainly bunk.

The translation is that in actual humans, oxalate metabolism possibly isn't that important to cardiovascular outcomes on average. But it is probably important for some people.

fwiw, high amounts of taurine is one of the few (only?) substances shown to slow/reverse atherosclerosis, at least in animals, a fascinating substance

In their extreme, oxalates can lead to oxalate nephropathy, a major affliction if kidneys. That can happen when Oxalobacter fermigenes is depleted in microbiome.

This comes as very worrisome news as a heavy peanut consumer.

A cousin of the Warburg effect?

Dysregulated oxalate metabolism is claimed to be just a dysfunctional metabolic pathway that leads to excess of oxalates.

Warburg effect is a bit different. While the author Otto Warburg believed that cancer cells preferred anaerobic (oxygen-less) glycolysis pathway, the modern view on this topic has evolved. Now we tend to believe that cancer cells maximize and exhaust all energy sources available to them. This includes a normal aerobic pathway. Once the mitochondria is stressed out and broken, it no longer is able to support the adequate levels of aerobic glycolysis. The host cell begins to starve in ATP and this is where the anaerobic pathway kicks in. So it is not that a cell has a specific preference; it is just a matter of survival and chemical auto-regulation.

So no, Warburg effect is not really a cousin as far as I can see.

Reply on news.ycombinator.com