Amyloids, brain fogs and possible treatment approaches.

My last post dealt with CFS and Alzheimer’s Disease. They are very similar in many aspects and if CFS lacks the physical fatigue symptom, then they can become very difficult to separate – especially in individuals over 60. Under 65, Alzheimer’s Disease will rarely be suspected (if it occurs, it is called Early Alzheimer — as in under 65, it does not mean early-stage of Alzheimer).

In this post I want to review the list of amyloids conditions and suggest that CFS may actually fall into this spectrum. The hyper-coagulation model for CFS results in fibrin deposits instead of amyloid deposits. What’s the difference? According to Wikipedia…

  • Amyloids are insoluble fibrous protein aggregates
  • Fibrin is a fibrous, non-globular protein involved in the clotting of blood

So both are fibrous, proteins and not dissolved normally by the body.

In treating CFS, there are often two modes of attack:

  • Break down the soluble fibrin monomers before they form deposits. Typically this is done with piracetam and / or turmeric.
  • Break down any existing fibrin deposits. Typically this is done with fibrinolytics (bromelain, serrapeptase, nattokinease and lubrokinease). This will typically exposed infections in tissue and allow up to 10x better antibiotic penetration.

The reason for doing this is that both CFS and Chronic Lyme Disease both present(80-90%)  with Antiphospholipid Antibody Syndrome aka Hughes Syndrome according to studies on PubMed.

I decided to hit pubmed to see if the second list also had impact on amyloids. Two of them are documents as degrading (breaking down amyloids

I strongly suspect that the others two fibrinolytics also degrades amyloids. This implies that these four fibrinolytics may be of significant benefit to all of the amyloids diseases (as well as CFS and related). I should mention that each of these fibrinolytics appear to work in slightly different ways, so taking all four may be needed.

Amyloids Diseases

Alzheimer’s disease
Diabetes mellitus type 2
Parkinson’s disease
Transmissible spongiform encephalopathye.g. Bovine spongiform encephalopathy
Huntington’s Disease
Medullary carcinoma of the thyroid
Cardiac arrhythmias, Isolated atrial amyloidosis
Rheumatoid arthritis
Aortic medial amyloid
Familial amyloid polyneuropathy
Hereditary non-neuropathic systemic amyloidosis
Dialysis related amyloidosis
Finnish amyloidosis
Lattice corneal dystrophy
Cerebral amyloid angiopathy
Cerebral amyloid angiopathy (Icelandic type)
systemic AL amyloidosis
Multiple Myeloma
Sporadic Inclusion Body Myositis

As a personal note, with my 2012 onset, I was able to keep working for many weeks by increasing the dosages of the fibrinolytics as symptoms worsen. Whether they were acting on fibrin alone or amyloids (or both) cannot be determined. My coagulation tests came back normal which suggests that fibrin may not be the sole issue. When I reached a dosage that resulted in easy bruising that did not go away, I was forced to stop the fibrinolytics. I went on a steep cognitive crash and went on sick leave within a few days.

Bacteria and Amyloid

The biggest quick decrease of neurological impairment that I observed in my treatment this time was when I started taking 3 herbs (Tulsi, Haritaki, Neem) that were reported on PubMed as being effective against Enterococcus. Enterococcus is a 24x overgrowth in CFS studies. So on speculation, I decided to see if Enterococcus is associated with Amyloids (or the above conditions). I found almost two dozen articles associating this bacteria with amyloid arthropathy in veterinary papers. It was also reported as an overgrowth seen with diabetic patient populations[1]. Improvement seen with supplementation of a specific species of Enterococcus in arthritis[2]. In general, there appear to be no studies done of the gut flora patterns for the above diseases 😦

A Science Daily article presented some interesting facts,
In bacteria, two proteins—CsgA and CsgB—are involved in the process, each with its own precise function. The job of CsgA is to build up amyloid fibers, but only after CsgB—dubbed “the nucleator”—has set the stage.

So bacteria produces the proteins, a shift in the bacteria may result in an imbalance and thus accumulation. The article further states

Having one protein in charge of nucleation and the other in charge of fiber elongation is a clever strategy that allows for control of a process that otherwise might occur unpredictably, as seems to happen with disease-associated amyloids.

What we need is studies of each amyloid-associated disease patient population to determine how gut bacteria is altered.

Until that time, patients (with an amyloid-associated condition) may wish to discuss taking Tulsi, Haritaki, Neem with their medical professionals. My own professional had no issues — these are all grandfathered (likely great grandfather 40x) herbs with centuries of use, making the benefit to risk very favorable. They had significant impact on neurological loss (after several days of headaches).