Showing posts with label Ketogenic diets are unhelpful and dangerous for managing mitochondrial diseases. Maybe (2). Show all posts
Showing posts with label Ketogenic diets are unhelpful and dangerous for managing mitochondrial diseases. Maybe (2). Show all posts

Sunday, October 20, 2019

Ketogenic diets are unhelpful and dangerous for managing mitochondrial diseases. Maybe (2)

I'm hoping we all remember Sauer. If not there's a post here:

Sauer vs Lisanti

And a brief summary at the start of this one:

Sauer and 13-HODE

Sauer demonstrated that food withdrawal from rats carrying tumour xenografts makes those tumours grow like wildfire. He went on to show that it was 13-HODE which made the tumours grow and that either linoleic acid or arachidonic acid (both 13-HODE precursors) were essential for tumour growth in his model. Fasting released these carcinogenic PUFA from adipocytes when the rats were starved.

You cannot make 13-HODE without linoleic acid. Or arachidonic acid if you prefer.

Do you want to make a tumour grow? Feed your model linoleic acid. It's easy. Or you could try using a Ketocal based ketogenic diet for glioblastoma multiforme management in real live humans. There was a trial doing this recently:

Ketogenic diet treatment as adjuvant to standard treatment of glioblastoma multiforme: a feasibility and safety study

which didn't really pick up any benefit, it was only a pilot study. Serious concern about the composition of the ketogenic diet was expressed in this letter to the editor:

Problems associated with a highly artificial ketogenic diet: Letter to the Editor Re: van der Louw EJTM, Olieman JF, van den Bemt PMLA, et al. ‘Ketogenic diet treatment as adjuvant to standard treatment of glioblastoma multiforme: a feasibility and safety study’

link tweeted by Miki Ben-Dor.

Much of the diet was Ketocal based "consisting of refined vegetable oils from sunflower, soy, and palm fruit..."

This looks like an excellent source of the 13-HODE precursor linoleic acid, which Sauer might have recognised as the growth promoter in his rat models.

I would suspect that the ketogenic diet supplied benefit from ketosis, but this was largely offset by tumour promotion from the linoleic acid content.

Is there any end to the damage done by the lipid hypothesis?

Probably not.

Peter