Oxalates and Cancer

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If we can get cancer cells to die faster than they grow, we can shrink cancer tumours, and even – eventually – fully cure them. And a shrinking or vanishing tumour can't kill us. This is plain logic and the aim of our Mosaic Method.

It's of course far harder to do than say. How do we increase the death rate of cancer cells? How do we decrease their growth rate? The Mosaic Method uses multiple attack points to try and achieve both at the same time.

Today, we'll zoom in on a part of step six of the method – namely, the elimination of oxalate from the diet. In the Mosaic Method Guide (which you can get for free under https://www.marchward.com/mosaic), we've only barely touched on why oxalates are so counterproductive, when trying to outlive cancer.

So, I want to expand on that.

Oxalate is a compound commonly found in plant foods. It's also made by our own bodies – primarily by the liver. We can influence both sources of oxalate, but why would we want to? What makes oxalate harmful to cancer patients?

For cancer patients oxalate is mainly of interest in its role as a substance causing inflammation and mitochondrial dysfunction (1–5). Chronic inflammation and mitochondrial dysfunction stand on two spots of a vicious cycle promoting one another (6–7). Mitochondrial dysfunction is the primary cause in the development of cancer and restoring mitochondrial metabolism through various means has been shown to reduce cancer growth and thus patient mortality (8–13).

Though I've written on this at length in the prior post 'How Our Dad Is Outliving Cancer', it bears repeating, what mitochondria are and how they influence cells and consequently how their disruption can cause cancer.

Mitochondria (Fig. 1 – 3) are small compartments within cells, which primarily handle energy metabolism and various quality control measures (15–17). There exists an alternative energy metabolism in the cytosol (Fig. 1 – 2) – namely sugar fermentation (technically known as 'glycolysis') –, but this alternative energy metabolism is highly inefficient, both in terms of energy produced and waste generated. The most potent of the quality control measures – the so-termed apoptosis, a cell suicide – can only be initiated in two ways: The mitochondria can determine the cell they reside in to be too damaged and then initiate apoptosis, or specialised cells of the immune system can detect infected or defective cells and kill them.

As this post is on oxalates and they seem to not have a whole lot to do with immune evasion, we'll focus on the mitochondria. Since mitochondria are the primary cause of cancer and since they can kill defective cells, logic dictates, that if we can restore mitochondrial function, the restored mitochondria will either enable the cancer cell to heal or kill it outright, if it's too damaged. And indeed this logic is reflected in the research (5, 8–10).

As I've already mentioned, oxalates cause both inflammation and disrupt mitochondrial function. It would thus stand to reason, that oxalates can directly cause cancer, when found in appropriate concentrations. And wouldn't you know it, this is absolutely the case.

It's long since been established, that some types of breast cancer – specifically the highly aggressive HER2-positive breast cancers – are correlated with deposits of insoluble oxalates (18). Now, correlation isn't enough as evidence, but it was enough of an indication to leave further research wished for.

And so, Castellaro et al. studied oxalates in the context of breast tissue cells and breast cancer cells. Causation was studied more directly by exposing mice to oxalates and checking for breast cancer development.

They found, that 3 weeks of exposure to oxalate of healthy breast tissue cells led to about an 8-times greater growth rate over non-exposed cells. What's worse, is that injection of calcium oxalate (an insoluble oxalate) into the breast led to cancer development also in mice and to a 100% mortality rate within 90 days. Injection of the same amount of oxalate in the form of the soluble potassium oxalate lead to far quicker 100% mortality within 30 days. Interestingly, however, injection of the same soluble oxalate into the back of the mice led to no fatalities within the studied time-frame.

To me this seems to indicate, that oxalates made by our own body are hardly an issue, as they are primarily produced by liver and oxalates seem to be cancer-promoting in a tissue-specific way. There's more research needed on the effect upon other cells, although it is known, that oxalates trigger and promote cancer-like behaviour in other tissues, such as kidneys and lungs. This seems to indicate a broader potential in causing cancer development – and thus also stopping the healing of cancer (18–19).

Mind, that the research on the interactions of oxalates and cancer has been most heavily focused on study in breast cancer. Nonetheless, it's known, that oxalate has negative consequences for certain immune cells and inflammatory signalling (3–4). This has also been shown to follow dietary consumption of oxalates specifically, thus bringing me back to the importance of abstaining from dietary oxalates (20).

It seems, that the liver has some way of coping with oxalate, and indeed the liver is incredibly apt at handling toxins in general – given the fact, that handling toxins is one of its primary roles, this is hardly surprising. Still, the liver can have too much oxalate and inhibition of oxalate production then improves liver health (21).

Since modulating oxalate production pharmacologically is beyond my pay grade, we'll focus on dietary oxalate – as it's absorbed into the blood in the small intestine and then distributed throughout the body without much control over tissue-specific distribution – and on dietary factors, which promote oxalate production.

So let's look at that.

Where do we find oxalates in food stuffs? We find oxalates almost exclusively in plant foods. Now, it would be simplest to just abstain entirely from plant foods. But, but, I know. It's simple, but not necessarily easy. So, here's something interesting: processing of oxalate-rich food by way of steeping and boiling and consumption of oxalate-rich food together with calcium-rich food significantly lowers oxalate content in and absorption from the food (23–24).

So, if I were you, I'd abstain as best as possible from plant food stuffs, but if you then do eat them, eat them with dairy or egg shells and only after long (48+ hours) steeping in water. If you like coffee or tea, for example, I'd highly recommend to use some milk in both or perhaps sprinkle some powdered egg shells in there. The latter won't really affect the taste, but if you find it unconscionable to treat your tea or coffee to powdered egg shells, consider just taking a tipfull of a teaspoon with water before hand.

Now, what foods promote oxalate production and what foods inhibit it? Well, the evidence for this is indirect. Studies looking at the influence of diet on oxalate metabolism tend to focus on urinary oxalate load, not body-internal oxalate load, as they mostly concern themselves with kidney stone disease, for which urinary oxalate is causally implied (25–27). Urinary oxalate secretion does however seem to be influenced by gelatine, fructose (fruit sugar), and vitamin B6 deficiency. As vitamin B6 is found in large enough quantities and high bioavailability in meat and even some plant foods, I don't think vitamin B6 is an issue (28). You may find a personal deficiency upon blood imaging.

All in all, I think it's wisest to stay away from dietary oxalates as best as is possible. I don't necessarily think other measures are necessary with regard to body-internal oxalates and their potential influence on cancer.

Health and healing to you,

Merlin.

P.S.: You can get the full Mosaic Method Guide for free under https://www.marchward.com/mosaic.

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