My ears pricked up (metaphorically) when he mentioned myositis ossificans, about which he comments "This does not end well".
I have spent some time in the past thinking about pathological arterial calcification, as applied to the aorta of of patients with familial hypercholesterolaemia. Bear in mind that the dietary advice for patients with FH is about the worst you could possibly imagine and, of course, has no evidence base. My thoughts and assorted links are in an old blog post here. At the time I had never heard of Sci-hub so was unable to access this rather neat diagram of the mechanism of action of insulin, Pi and pyrophosphate:
Back to pathological soft tissue calcification. Clearly the obvious question about myositis ossificans has to be to ask whether it is in part driven by hyperinsulinaemia/hyperglycaemia or both.
As far as I am aware this is not a question which had been asked. It is simply genetic and that's it.
However, a similar question has already been answered in relationship to a serious generalised soft tissue mineralisation condition described as "calcinosis and scleroderma", back in a publication from 1932 (apologies to the person who tweeted the link, I didn't note their name to acknowledge. And twitter is ephemeral). That is too long ago to be listed on Pubmed so if you would like to read it you can go and ask Elsevier how much they would like to charge you for a peek in to the past or you can go to that awful place that none of use ever use to download any paper for free.
CALCINOSIS AND SCLERODERMA: TREATMENT OF A CASE BY USE OF THE KETOGENIC DIET
"Calcinosis and scleroderm" looks to be one of a family of soft tissue calcification diseases. The case report from 1932 describes the complete remission of this extremely unpleasant condition in a child following a period of time on ketogenic diet of the type used at the start of the last century, before dieticians were invented/summoned from Hades.
Did the ketogenic diet resolve this child's pathological calcification by suppressing insulin levels, glucose levels or both? Does it work by lowering alkaline phosphatase production by cells in/around inflammatory lesions? Or by some other mechanism?
Would it do the same for pathological arterial calcification? Given a tool like the ketogenic diet, perhaps there is some logic to CAC testing?
Unless you feel that tissue calcification is an appropriate part of healing until it gets to scleroderma levels...
Peter
