Finally a hint at cause and cure.

So just after my last post came out this study came out. Study reveals how long-term infection and inflammation impairs immune response as we age. I have to admit this has me excited. 

First for the relatively long discussion of clonal hematopoiesis (creation of clonal cells). I mean I knew I had a clone but I wasn't aware that it was a "thing".  And it absolutely is a thing that is much more broad and effects far more people than just MGUS.

Clonal hematopoiesis is characterized by the overrepresentation of blood cells derived from a single clone. Clonal hematopoiesis of indeterminate potential, or CHIP, is a common aging-related phenomenon in which hematopoietic stem cells or other early blood cell progenitors contribute to the formation of a genetically distinct subpopulation of blood cells.

So is MGUS just another name for this "Clonal hematopoiesis" except that it is a type of clonal hematopoiesis that just limits the potential end results (MM or WM)? So accordingly it is taken out of the CHIP sub type and given its own name. 

Then there is this:

This common phenomenon known as clonal hematopoiesis (CH) is known to start in early fifties and is frequently associated with loss of function mutations in the DNMT3A gene.

Well that is bang on for me. With mine appearing to start at age 49 and 1/2.  

Then there is this:

CH is associated with a significantly higher risk of blood cancers, cardiovascular disease, stroke and all-cause mortality.

What... wait, my doctor says it is nothing to worry about ! Well, I am suspecting this is because of increased blood viscosity that comes along clonal cells.

But this is where I get excited.

shows for the first time that long-term infection and chronic inflammation drive CH (clonal cell creation) mediated by the loss of Dnmt3a function. . . HSCs (blood stem cells) in mice lacking Dnmt3a gene did not differentiate (form into proper normal cells) much . . . We undertook the current study to test our prediction that defective differentiation (defective normal cell creation) and increased duplication of Dnmt3a HSCs (blood stem cells) allows them to overtake and outcompete normal HSCs when fighting chronic infections or facing long-term inflammatory conditions.

So let's unpack this. Long term infection alone is probably not the precise issue it is only that long term infection causes "chronic inflammation".  It is chronic inflammation that causes Clonal hematopoiesis (creation of clone cells). This says, that in response to chronic inflammation.... it seems that it is your STEM CELLS hematopoietic stem cells (HSCs) break first.  So when your body calls them up to make a plasma cell they are already defective. 

Ok, it is me? This seems to be a MAJOR answer in what and how to prevent progression of MGUS.  And it brings it all together. 

Under the Umbrella of "CHRONIC INFLAMMATION" are many different things.

• Being overweight. 
• Having auto immune.
• Having long term infections.
• Metabolic Syndrome.
• Diabetes.

And we already know that things that reduce inflammation will assist with MGUS

• Tumeric
• Reduction in Auto Immune disease.
• Fasting 
• Keto / Carnivore
• Anti inflammatory foods.

So it appears to me that right now, today, anyone with MGUS should be getting inflammation biomarker tests and doing what they can to reduce inflammation. 

Blood Tests for Inflammation

• CRP blood test (C-reactive protein) - my last result was 5, it should be under 3.
• Plasma viscosity (PV) - never had this test hard to find.
• ESR blood test - my last result was 14, normal is  0-29 mm/hr for women