And now it's Schizophrenia

https://www.ncbi.nlm.nih.gov/pubmed/28256360<

Only an abstract but the full free is available to medical people or those registered with Elsevier.  Just the abstract is interesting enough though. I might try to register somewhere tomorrow............... Sarah

Actually, I just went to Elsevier from the abstract and straight away got the full text!  I forget, but maybe I am registered already..................Sarah

Completed Stratton/Wheldon regime for aggressive secondary progressive MSi in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

CPNi is taking over the world!

Seems to be!

Completed Stratton/Wheldon regime for aggressive secondary progressive MSi in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

Schizophrenia: I have just had time to read this paper and think it might be interesting for many people...............Sarah

Completed Stratton/Wheldon regime for aggressive secondary progressive MSi in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

Minocycline is already an accepted (but unused!) treatment for some types of schizophrenia:

https://slatestarcodex.com/2013/09/12/the-life-cycle-of-medical-ideas/<

Still, my guess is that schizophrenia is mostly something other than Cpni: there is a change of mentality associated with MSi, but it's very different from the sort of craziness that schizophrenics exhibit.  MS patients don't go around hearing voices and being actively dangerous to themselves and others.  Also, schizophrenics don't typically experience attacks of numbness and other such MS symptoms.

Norman, schizophrenia is as likely to be not just cpni as MSi or cardiac problems or rheumatoid arthritis or many other things.  I was genetially predisposed to get MS but David fell prey to both cardiac problems and bad myalgia.  David treated us both for our own individual diseasesi and we are now both recovered.  Maybe the same could happen with some types of schizophrenia...............Sarah

Completed Stratton/Wheldon regime for aggressive secondary progressive MSi in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

When you have an infection of the same area (the brain), but with two very different sets of symptoms, it's natural to expect two different causal agents.  For schizophrenia, perhaps it's Toxoplasma gondii, which is known to mess with the sanity of rats that it infects, and for which there are suggestions that it does likewise for humans.  Yes, one can suppose host factors make all the difference -- that's more or less what conventional medicine supposes, except with them thinking that there are zero pathogens driving things -- but really there are a lot of germs out there to choose from.

Still, yes, there is a reason that I didn't state my opinion as being anything stronger than a "guess".

As an impoverished medical student I once lived in a secure mental hospital for three months. (I was given free accommodation in return for getting up at night to suture injuries.) I found schizophrenia to have a vast spectrum of  presentations, courses and outcomes. Still, it is human nature to try to neaten and codify. I noticed that juveniles with schizophrenia often had livido reticularis, which can indicate vasculitisi, often found in C. pneumoniae infectionsi<. (The above hospital achieved the singular distinction of being called “the dirtiest hospital in England” during a visit by an inspection team. It is now demolished.)

 

I think that C. pneumoniae may have an input into a number of diverse brain disorders. MSi, certainly, and chronic fatigue, but Brian Balin’s team have found evidence of C. pneumoniae infection in Alzheimer’s disease, the organism being found maximally in the most damaged areas, the hippocampi, responsible for the apportionment of memory. The germ may play a part in fronto-temporal dementiai (Pick’s Disease).

 

D W - [Myalgia and hypertension">i (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazolei. No medication now. Morning BP typically 110/75]

Indeed David, as I can testify.  Here is more on the link between CPni and central nervous system disorders, but also including body manifestations of vasculitisi and diabetes (common with MSi an AD). There are a couple of good diagrams about how the bacteria evade the host's defences if you click on the link.

https://www.ncbi.nlm.nih.gov/pubmed/26961231<

"Strong epidemiologic evidence and common molecular mechanisms support an association between Alzheimer's disease (AD) and type 2-diabetes. Local inflammationi and amyloidosis occur in both diseasesi and are associated with periodontitis and various infectious agents. This article reviews the evidence for the presence of local inflammation and bacteria in type 2 diabetes and discusses host pathogen interactions in chronic inflammatory disorders. Chlamydophyla pneumoniae, Helicobacter pylori and spirochetes are demonstrated in association with dementiai and brain lesions in AD and islet lesions in type 2 diabetes. The presence of pathogens in host tissues activates immunei responses through Toll-like receptor signaling pathways. Evasion of pathogens from complement-mediated attack results in persistent infection, inflammation and amyloidosis. Amyloid beta and the pancreatic amyloid called amylin bind to lipid bilayers and produce Ca(2+) influx and bacteriolysis. Similarly to AD, accumulation of amylin deposits in type 2 diabetes may result from an innate immune response to chronic bacterial infectionsi, which are known to be associated with amyloidosis. Further research based on an infectious origin of both AD and type 2 diabetes may lead to novel treatment strategies."

To me the Alzheimers link coexists nicely with the MSi link: as people age their immunei systems weaken, so what had been an "autoimmune disease" in younger people becomes a "degenerative disorder" in the elderly: instead of the immune system fighting back being the main feature of the disease, it's just a slow decline.  (Likewise, there is probably some name or set of names that today's medicine has for children with a Cpni brain infection, since like the elderly they are seldom diagnosed with MS, yet it is most implausible that they are all immune to Cpn.  "Autism" seems like a possibility.)

I've never regarded psychiatrists as being people who really knew what they were doing, but from reading "The Center Cannot Hold", by a lady who herself has schizophrenia and describes living with it, it's clear that at least with some of these patients something is going on that is very different than is experienced by MS patients.

There is a quote I like from my favorite historian, Macaulay:

"That Walpole had foul play is almost certain, but to what extent it is difficult to say. Lord Islay was suspected; the Duke of Newcastle something more than suspected. It would have been strange, indeed, if his Grace had been idle when treason was hatching."

Something similar can be said of Cpn, with its tendency to infect white blood cells and thereby travel to any part of the body that is already infected and add to the disease.  Still, with schizophrenia, I would suspect that some other germ is the cause of some of the more distinctive features of the disorder.

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