THE MANIFESTO

metabolism diagram that I came up with.
Yes I did this in my free time.

Finding the answers was A LOT more fun than putting the diagram together.
Thankyou Google, at least I know this much.

Patients with rheumatoid arthritis have B12 levels higher than normal subjects.
http://www.researchgate.net/publication/21094210_Plasma_vitamin_B12_binding_proteins_correlate_with_disease_activity_in_patients_with_rheumatoid_arthritis
http://onlinelibrary.wiley.com/doi/10.1002/art.20636/pdf
IL-6 regulates metallothionein-1.
http://www.pnas.org/content/87/8/3137.full.pdf

The “causation” or “cause and effect” sequence of events is very tricky and sometimes hard to follow.   This is why I tried different things to see what happened to my own body and kept reading until I found something that made sense, like a thorough explanation as to why things happen.

Google is great for making this accessible to us, but there’s so much to vet?  Not all of the research is purely unbiased or straight forward.   But after reading some, it started to come together.  And yes this took a while.

The Metallothionein business is a big dead give away to rheumatoid arthritis and metabolism.

Metallothionein-1 (MT-1) detoxes metals from the body and goes up with zinc.  Without MT-1, MEST is exposed and the body gains weight very fast on a high fat diet.(MEST is also known as MIR-133-from the immune system that tells mesenchymal stem cells to create adipose tissue with nutrients instead of muscle, skin, tissue, bone or cartilage repair).

When the body is stressed, the Parathyroid tells the body to release calcium from the bones.

When it does that, it also releases Zinc from the bones.  (Important minerals are released from the body when the body burns off fuel, ie. Magnesium drops when ATP is burned off-or something like that.  Phosphates drop when the body releases carbon ie. Carbon dioxide.  Fructose causes phosphate trapping which causes problems with metabolism.  High fructose corn syrup does mess up the metabolism and liver which might cause the high B12 levels that are associated with rheumatoid arthritis)…anyways.

When the body releases zinc from the bones from ANY stress, it binds with Metallothionein and goes into the liver as Zinc Metallothionein or Zn-MT.  This reduces the Zn-MT from the body and exposes MEST.

VITAMIN C “DETOXES” Zn-MT.
Selenium recycles Vitamin C, it also drops cysteine that naturally binds unsaturated fatty acids together that riboflavin kinase created enzymes from FAD that breaks apart to release energy.
ZINC INCREASES MT.

MT is positively correlated with ESTROGEN RECEPTORS.
Cortisol triggers stress reactions- it is said that ZINC DROPS CORTISOL LEVELS?
ASPIRIN and of course ethanol increases TNF-alpha and drops IL-6. http://www.sciencedirect.com/science/article/pii/S0006291X09013552

http://www.ncbi.nlm.nih.gov/pubmed/11330422

Carnosine drops all of them.
http://www.ncbi.nlm.nih.gov/pubmed/18222027

Anyways... it's been said that insulin blocks leptin.  The body is supposed to balance insulin levels out on it's own.  Without adequate T3 activity with riboflavin conversion to FAD and FMN in the cells....(AND WATER)-the body can't make enzymes necessary to break down the short and mid chained fatty acids (that cysteine binds together) to stop UNNECESSARY insulin production by the body.

Hexosamine biosynthesis impairs insulin action via a cholesterolgenic response.

Plasma membrane cholesterol accumulation has been implicated in cellular insulin resistance. Given the role of the hexosamine biosynthesis pathway (HBP) as a sensor of nutrient excess, coupled to its involvement in the development of insulin resistance, we delineated whether excess glucose flux through this pathway provokes a cholesterolgenic response induced by hyperinsulinemia.

EXPOSING 3T3-L1 ADIPOCYTES TO PHYSIOLOGICALLY RELEVANT DOSES OF HYPERINSULINEMIA (250PM-5000PM) INDUCED A DOSE-DEPENDENT GAIN IN THE MRNA/PROTEIN LEVELS OF 3-HYDROXY-3-METHYL-GLUTARYL-COENZYME A REDUCTASE (HMGR). THESE ELEVATIONS WERE ASSOCIATED WITH ELEVATED PLASMA MEMBRANE CHOLESTEROL.  

 Mechanistically, hyperinsulinemia increased glucose flux through the HBP and O-linked β-N-acetylglucosamine (O-GlcNAc) modification of specificity protein 1 (Sp1), known to activate cholesterolgenic gene products such as the sterol response element-binding protein (SREBP1) and HMGR. Chromatin immunoprecipitation demonstrated that increased O-GlcNAc modification of Sp1 resulted in a higher binding affinity of Sp1 to the promoter regions of SREBP1 and HMGR. Luciferase assays confirmed that HMGR promoter activity was elevated under these conditions and that inhibition of the HBP with 6-diazo-5-oxo-l-norleucine (DON) prevented hyperinsulinemia-induced activation of the HMGR promoter. In addition, both DON and the Sp1 DNA-binding inhibitor mithramycin prevented the hyperinsulinemia-induced increases in HMGR mRNA/protein and plasma membrane cholesterol. In these mithramycin-treated cells, both cortical filamentous actin structure and insulin-stimulated glucose transport were restored. Together, these data suggest a novel mechanism whereby increased HBP activity increases Sp1 transcriptional activation of a cholesterolgenic program, thereby elevating plasma membrane cholesterol and compromising cytoskeletal structure essential for insulin action.

http://www.ncbi.nlm.nih.gov/pubmed/23315940

Zinc is also needed by the body to make insulin degrading enzyme....
http://www.academia.edu/1798332/Formation_of_insulin_fragments_by_insulin-degrading_enzyme_the_role_of_zinc_II_and_cystine_bridges

But too much of insulin makes problems (THYMUS GLAND HAS INSULIN RECEPTORS!!!)


Leptin is the hormone that regulates appetite and mimics insulin to cause weight loss, and people with more adipose tissue have more leptin than skinnier people.

But “naturally skinny people” ie. “subjects of constitutional thinness” had high leptin levels although they were skinny. http://www.ajcn.org/content/85/4/967.full

Anyways, high leptin was blocked when MEST was exposed.   I came to the suspicion that this was technically called “leptin resistance”.  

TNF-alpha is blocked by ZN-MT.
IL-6 blocks TNF-alpha.

Well TNF-alpha 2R (TNFR2) is a “proliferative” cytokine that tells the body to repair itself and not put fat on the body with calories.

TNF-alpha receptor 2 protects IGF-1 from PPAR-alpha/FGF-21.

Igf-1 protects the NADPH which is the lipid carrier that carries iodotyrosine dehydrogenase in the liver to break down old T3 so the thyroid can release new T3 to speed up the thyroid which both creates “fat burning” carnitine and riboflavin kinase that converts riboflavin into FAD and FMN.
FAD breaks down unsaturated fatty acids to NATURALLY sort out insulin levels (body can’t burn fat with high basal insulin levels and high insulin causes high LDL- which is how riboflavin stimulates the metabolism and reduces heart disease risk big time).  Thymus gland has high insulin receptor.

Now remember, IL-6 regulates metallothionein-1.  http://www.pnas.org/content/87/8/3137.full.pdf
High B12 results in IL-6.  (I think this has something to do with a messed up liver)   There was a medication for rheumatoid arthritis that blocks IL-6.  IT’s called Tocilizumab.

The other interesting factor is that estrogen is a blocker of IL-6, so they say.  

Estrogen has been paraded in the medical community because it's quite the bread basket but results say otherwise.

That research doesn’t make sense to me so I’m just looking for their explanation as to why it does that, again, the “causation” can be tricky. There are lots of details!  

So the answer might be Zinc which increases metallothionein-1 and Vitamin C that drops Zn-MT.

AGAIN:



And of course ... blood work testing menu sample:
http://www.theranos.com/test-menu?ref=our_solution
You can get a LOT of perameters from bloodwork on this for less than $70.