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Posted by Marnie (Member # 773) on :
 
It inhibits HMG CoA reductase!

http://ajpregu.physiology.org/content/300/3/R635.full

Researchers...try to stick with me on this.

Print the following out and go over and over it.

Insulin is produced by pancreatic B cells.

Insulin helps carry glucose into the cells.

Proinflammatory IL1B secretion ongoing -> insulin resistance.

Pancreatic b-cells require an optimal insulin content to allow instantaneous secretion of insulin.

This is maintained by insulin biosynthesis and intracellular degradation of insulin, i.e. make insulin or break it down.

Il 1-b causes an enhancement of islet intracellular insulin DEGRADATION.

With LESS insulin available, this impacts a gene celled INSIG (2 forms..1 and 2).

INSG = insulin I = induced G= gene, hence INSIG.

That gene (INSIG) is ***insulin induced.***
Without that gene being induced via insulin (level dropped), INSIG is deficient.

Cells deficient of Insig -> increase HMG CoA reductase!

HMG CoA reductase is a component in the cholesterol pathway. Bb is dependent on that pathway.

Statin drugs, BERBERINE, and Mg INHIBIT that enzyme, HMG CoA reductase.

That gene, INSIG �2 (if it WAS available � if there WAS enough insulin to activate it) binds to the RXR receptor and VDR receptor,

but TNFa (anti-inflammatory) blocks those receptors too!

So it would appear the body is keeping glucose out of the cells and they then must rely on an alternative fuel i.e., fatty acids.

That scenario would make Bb happy since he needs them to construct �his� cell wall and make �his� ATP.

Hyperhomocysteinemia also upregulates HMG Co A reductase. (Those with the �MTHFR gene problem have a harder time controlling homocysteine levels.)

High-methionine induces hyperhomocystenemia.


A folate deficiency (or those with the 5-MTHFR defect who can�t convert folic acid to 5-METHYL Folate) -> active folic acid deficiency which correlates to

DEPLETED phosphatidylcholine (without lowering plasma homocysteine).

Under conditions of folate deficiency,

brain membrane content of the ***methylated phospholipid phosphatidylcholine*** was significantly depleted,

which was reversed with supplemental methionine.

Bb has 2 lipoproteins..

methylated phospholipid phosphatidylcholine

and phosphatidylglycerol.

(Phosphatidylcholine can convert to Phosphatidylglycerol via Phospholipase D and Glycerol.)

Phospholipase A1 and A2 breaks apart phosphatidylcholine.

Phospholipase C acts on phosphatidylglycerol.

(There are many forms of Phospholipase C.)

Phospholipase C (originally called lecithinase and also referred to as ***α-toxin***) catalyzes the hydrolysis of the linkage between glycerol and phosphate in lecithin = trivial name for phosphatidylcholine) and other phosphatides.

(A deficiency of phospholipase C acting on phosphatidylglycerol is a factor in Niemann-Pick disease where fats accumulate in various organs�fatty liver, brain , etc.)

Phospholipase C (to break up phosphatidylglycerol) goes on to be broken down to make DAG which ***activates PKC*** (calcium activated protein transfer � the K = kinase = protein transfer) which alters cellular activity.

(Tamoxifen is a man-made PKC INHIBITOR.)

The many receptors that activate phospholipase C are mainly G � protein coupled receptors�

Guanine (an amino acid) nucleotide binding protein (G protein)

From modulatory neurotransmitter receptors (amine receptors belonging to

*** rhodopsin *** family),

Gq is usually coupled to e.g. the G-protein coupled receptors.

Because Bb�s proteins are so similar to our own, we end up attacking our own (brain et.al) membranes.

Bb not only triggers phospholipase A (1 and 2), but also, it appears phospholipase C.

I suspect the presence of rhodopsin in (I suspect photosynthetic) Bb as a �bacterial rhodopsin� is triggering phospholipase C.

It would appear Bb triggers us to do the messy work for him�to break apart OUR proteins (phosphatidyl choline and phosphatidyl glycerol in order to get the nutrients �he� needs to make �his� cell walls and to supply the nutrients �he� needs to make his ATP.

I think Bb especially needs rhodopsin (retinal+opsin). If we can impact that we just might win the fight.

In the meantime, worth considering: berberine or Zyflamend or

for kids with juvenile arthritis...Rx called Tocilizumab (IV) - the addition of methotrexate would be extremely hard to tolerate, IMO.

However, "Google": Zyflamend children.
 
Posted by lymielauren28 (Member # 13742) on :
 
Hmmm...my brain just exploded:)
 
Posted by Marnie (Member # 773) on :
 
Print it out...read it slowly over and over.

Eventually it will "click".

Bottom line...Bb triggers an immune response that is helpful to "him"...not us.
 
Posted by lymielauren28 (Member # 13742) on :
 
Will do. Thanks Marnie!
 


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