I first met Stephen Fry M.D.  a couple of years ago at his booth at the ACAM meeting at the Diplomat Hotel in Hollywood, and enjoyed an interesting conversation about his work.  We met a second time last month again at his booth at a medical meeting.  Dr. Stephen Fry runs his own microbiology lab where he examines high powered views of biofilms in atherosclerotic plaque material obtained from surgical specimens. (1-2) These biofilms are colonized by multiple bacterial, fungal and protozoal organisms identified by DNA and  ribosomal RNA sequencing.  A true pioneer in the field, Dr Fry has identified a new organism not listed in the gene databank, which he named “Protomyxzoa Rheumatica”.   Left image courtesy of Stephen Fry MD Web site.

Leaky Gut and LPS

With the recent revelations of Allesio Fasano et al about the increased permeability of the gut wall called “Leaky Gut” which allows bacterial organisms, and undigested food particles into the blood stream, the next logical thought in this sequence is: What happens to all these micro-organisms which are leaking into the blood stream? 

Undoubtedly there is an immune response with release of inflammatory markers cytokines, myeloperoxidase etc.  In addition, this may trigger autoimmune disease through the wonders of “molecular mimicry”.  Some of these microbial organisms possess similar amino acid sequences shared by our own tissues, thereby creating autoimmune disease.  However, my question is : What happens when these microrganisms set up house ?  Where do they go and what do they do?   Left Image from Stephen Fry Lab showing bright staining of micro-organism identified as Protomyxzoa in Biofilm background.Courtesy of Music of the Spheres.

The Endothelium as the Innocent Bystander

Of course, all the blood from the gut enters the portal venous system which goes directly to the liver and spleen.  The reticuloendothelial system of the liver and spleen serve as a giant filtering system for all this “goop” leaking into the blood stream from our permeable small bowels.   This is protective.  However, assuming this filtering system has been overwhelmed allowing a bolus of slimy micro-organisms to gain entry to circulation, where does it go ?  Setting up house in the endothelium is not difficult to imagine.  The endothelium is the inner lining of our blood vessels and this layer is in direct contact our evil bolus of micro-organisms. Left image portal venous system showing splenic vein thrombosis courtesy of Internet J Surg.

Injury Leading to Infection

If one pauses for a minute to think about skin infections in kids,  the skin seems immune to infection until there is an injury, a scrape, laceration  or  some break in the dermal barrier.   This injury allows entry of micro-organisms which then form an infection with the usual hallmarks of pus and inflammation.  Same can be said for the vascular system.  Formation of atherosclerotic plaque tends to occur at sites of injury, such as at bifurcations where shear forces are maximal, and at sites of movement such as the coronary arteries imbedded in the moving surface of the left ventricle.  So, the idea of atherosclerotic plaque as infected biofilm certainly fits the pattern of commonly affected sites in the arterial tree.  Left Image Carotid Plaque courtesy of wikimedia commons.

Uffe Ravnskov and Killmer McKully

Uffe Ravnskov and Killmer McKully have been writing about this for at least 8 years now.(5-6)  In multiple publications listed below, the two doctors list research studies clearly  falsifying the cholesterol theory of atherosclerotic disease, while at the same time massing evidence that atherosclerotic plaque is an infected biofilm colonized with a diverse flora of bacterial, fungal and protozoal organisms.  Left Image Courtesy of Uffe Ravnskov MD

The End For Statins ?

If this is true, then this represents a paradigm shift our thinking about the etiology of atherosclerotic vascular disease, and the end of the anti-cholesterol statin drug era.   OOPS ! The drug industry is not going to be happy about this one.

Left image: Tight stenosis of internal carotid origin. Carotid  angiogram courtesy of jeffrey dach md.

Jeffrey Dach MD
7450 Griffin Road Suite 180
Davie, Florida 33314
954-792-4663

Articles with Related interest:

Biofilms in Chronic Sinusitis

Preventing Heart Attacks with Ouabain

Does High Cholesterol Cause Heart Disease?

Links and References:

1) Putative biofilm-forming organisms in the human vasculature: expanded case reports and review of the literature. Stephen Eugene Fry, Jeremy Eugene Ellis, Matthew Andrew Shabilla, Delyn Lorene Martinez, Renatta Schwarz, Richard Heuser, Constantine Moschonas . Phlebological Review 2014; 22, 1: 24–37 Biofilm_forming organisms human vasculature Stephen Eugene Fry Phlebological Review 2014

2) Stephen Fry Interview on Biofilms and Protomyxzoa Rheumatica Marc Braman

3) Lanter, Bernard B., Karin Sauer, and David G. Davies. “Bacteria present in carotid arterial plaques are found as biofilm deposits which may contribute to enhanced risk of plaque rupture.” MBio 5.3 (2014): e01206-14.

4) Bacterial Growth in Arteries Implicated in Heart Attacks Stress, biofilms, and cardiovascular disease By Jacob Schor, ND, FABNO, and Lise Alschuler, ND, FABNO

5) http://mbio.asm.org/content/5/5/e01717-14.full.pdf
Ravnskov, Uffe, and Kilmer S. McCully. “Biofilms, Lipoprotein Aggregates, Homocysteine, and Arterial Plaque Rupture.” mBio 5.5 (2014): e01717-14.
Biofilms Arterial Plaque Rupture Ravnskov Uffe Kilmer McCully 2014

6)  Ravnskov, U., and K. S. McCully. “Infections may be causal in the pathogenesis of atherosclerosis.” The American journal of the medical sciences 344.5 (2012): 391.  Infections May be Causal in the Pathogenesis of Atherosclerosis Ravnskov McCully 2012

7)  Ott, Stephan J., et al. “Detection of diverse bacterial signatures in atherosclerotic lesions of patients with coronary heart disease.” Circulation 113.7 (2006): 929-937.

8) Ott, S. J., et al. “Fungal rDNA signatures in coronary atherosclerotic_Ott_2007_Athrosclerosis  Fungal rDNA signatures in coronary atherosclerotic plaques.” Environmental microbiology 9.12 (2007): 3035-3045.

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