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Fat and ferroptosis – it’s just not that simple!

Hi Gang!

I was made aware of posts in FB groups suggesting that because ferroptosis is strongly linked to fat ‘peroxidation’ of cell membranes by free radicals (ROS or reactive oxygen species) that you don’t need to bother with blocking fat pathways.

Not so. There are fat pathways that absolutely should be blocked, e.g. the mevalonate (cholesterol) pathway which produces CoQ10, a potent inhibitor of ferroptosis, which I hope by now you know is blocked by statins.  The main inhibitor of ferroptosis is called the ferroptosis suppressor protein 1 pathway (FSP1)which runs in parallel to the GPX4 membrane repair enzyme, and this suppressive pathway is active in hundreds of cancers to prevent ferroptosis taking place. It promotes production of CoQ10 and I would love to recommend a natural alternative to statins here, but nothing else really cuts the mustard like these drugs. If you are serious about ferroptosis (and many of you should be considering it) then you need to ignore the media slaying the use of statins, as the majority of patients take them with no side effects at all. They really are invaluable to this process.

SCD-1 (Stearoyl CoA Desaturase) is another important fat pathway which transforms saturated fat to monounsaturated fat (MUFA) e.g. oleic acid which the cancer cell can incorporate into its membrane as part of its armour to prevent it from degradation and ferroptosis. It is the polyunsaturated fats (PUFAs) that are needed to trigger ferroptosis. Niacin is part of my ferroptosis protocol for blocking the SCD-1 pathway. Read how blocking this pathway is especially important for ovarian cancer:

Stearoyl-CoA Desaturase 1 Protects Ovarian Cancer Cells from Ferroptotic Cell Death – PubMed (

Blocking the CD36 fat transporter on cancer cells by taking danshen will help prevent the uptake of oleic acid as mentioned above, so another thumbs up for one of my favourite supplements. Danshen has also shown another ability to trigger ferroptosis in breast cancer by stopping the action of the glutathione peroxidase(GPX4) membrane repair enzyme.

Avoiding high lipid and cholesterol levels in the blood stream is important because raised levels create metabolic stress which then triggers the sustained action of the membrane repair enzyme GPX4, which in turn inhibits ferroptosis.

The following article on lung adenoma and dietary modifications shows that a high fat diet will interfere with ferroptosis and drive cancer metastases:

In addition, the cancer cells make fat from scratch (de novo) through the fatty acid synthesis pathway which leads to a subsequent decrease in poly-unsaturation which then protects them from the ROS and lipid peroxidation caused by ferroptosis.  Fatty acid oxidation may also protect from ferroptosis by producing NADH which is involved in ‘redox’ balancing – producing glutathione to protect the cancer cells with antioxidant.

I realise I might have lost many of you at this point… (if I have please consider my online course!)… but to summarise…

Which fats should you ingest and which should you avoid?

Polyunsaturated fats (PUFAs) like walnut oil, flaxseed DHA, EPA and GLA are good for activating ferroptosis as they are sensitive to oxidation, whereas saturated fat and monounsaturated fat can stimulate progression. Saturated fats are less sensitive to the effects of ROS, making the cell membranes resistant to treatment. Don’t forget coconut oil contains a lot of saturated fat.

And yes I know I previously said olive oil was okay, which it is if you are starving cancer using high quality extra virgin olive oil (EVOO), but since doing a deep dive into ferroptosis, you need a different profile of oils to take for this phase, or at the very least take danshen.

As for how long you try the Kill Phase with ferroptosis? It could be a few days, a week or even longer (e.g. for pancreatic cancer) depending on the severity of your disease. You will need to discuss this with your physician.  There are no hard and fast rules, everyone is different.

If you want further clarification, I have a whole chapter on ferroptosis in the latest edition of How To Starve Cancer.  It is critical you understand which pathways can lead to treatment resistance, how to block these and the supplements and drugs to activate this exciting new treatment option for best effects. I also have a video in my online course so check my website for details of how to obtain both if you haven’t already:

(N.B. Beware of scammers out there using the same/similar names/websites to mine to sell you products. They are not me! They have bogus scientific information and some are phishing sites).

Rather than leaving fat pathways open, in my latest book I suggested that you could leave glutaminolysis unblocked as during ferroptosis both glutamine and glutamate play important roles.

To understand this you need to understand how the xCT antiporter functions on the surface of the cell; it pulls cystine molecules into the cell cytoplasm while at the same time exchanging it and pumping out glutamatemolecules (I have some videos in my online course). A high concentration of glutamate on the outside of the cell will prevent the cyst(e)ine entering, thereby starving the cell of this amino acid which depletes intracellular glutathione, which in turn helps activate ferroptosis. Alongside this, another important feature of  glutaminolysis is the production of alpha ketoglutarate, which can replace the glutamine required for activating ferroptosis.  Autophagy is another pathway that you can leave open as you need ‘ferritinophagy’ (breakdown of ferritin in the lysosome) to occur.

As many cancers are addicted to glutaminolysis and autophagy, like their addiction to iron, you can take advantage of all of this to make them more susceptible to ferroptosis. But please don’t go leaving fat unblocked!

Blocking fat pathways is not just important, it is essential!

Hope that clears that up!


Jane xx