Quote from Dr. Garrett Smith on February 13, 2019, 1:18 pm

Different people have different physiological reactions to Poison/"Vitamin A", just as different people can have wildly different responses to the same types of stress.

I do believe that many iron-related issues are directly related to different bodily responses to Poison/"Vitamin A" toxicity.

It will be difficult to suss out completely, as very few researchers are looking at this connection.  I'm accumulating the evidence here, and I see the effectiveness of this theory in my Nutritional Restoration clients already.

First, Non-Alcoholic Fatty Liver Disease is a problem that is absolutely related to Poison/"Vitamin A" toxicity.  In the next paper, you'll see many markers related to Poison/"Vitamin A" mentioned (they are connected), except that the authors only mention "may lead to a shortage of retinoid", which they don't even look for.  They don't measure any direct Poison/"Vitamin A" levels (see towards the bottom for the list of things they didn't test for).  It's hard to find problems if you don't look in all the places a problem might show up.  What I'm using this paper for is to show that iron metabolism and Poison/"Vitamin A" are absolutely connected.

Iron state in association with retinoid metabolism in non‐alcoholic fatty liver disease

Aim: We have recently reported that hyperdynamic state of retinoid metabolism, which may lead to the shortage of retinoid, is observed in patients with non‐alcoholic fatty liver disease (NAFLD). Hepatic iron overload, which causes production of reactive oxygen species (ROS), is also frequently seen in NAFLD patients.

Hyperdynamic means "characterized by great or heightened activity or change".  You must ask yourself, why would the body increase its Poison/"Vitamin A" metabolism in a state of disease?  Maybe it is to get rid of too much Poison/"Vitamin A", maybe?

The aim of the study is to examine iron state and retinoid metabolic state simultaneously, and to clarify the relationship between two disorders.

Methods: Thirty‐six persons, comprising 17 patients with simple steatosis (SS), 11 with NASH, and 8 normal controls (N), were examined on hepatic expression of iron metabolism‐related genes including hemojuvelin (HJV), hepcidin (HEPC), transferrin receptor 1 and 2 (TfR1, TfR2), ferroportin (FPN), neogenin (NEO) and ferritin heavy chain (FtH) and hepatic iron contents in addition to expression 51 genes which is involved in retinoid metabolism and antioxidative action.

Results: In patients with NAFLD, expression of HJV, TfR2, FPN, TfR1, FtH, SOD and catalase was increased, compared with that in N. In addition, hepatic iron content, which was increased in NASH, was correlated with expression level of TfR2. Expression of cellular retinoid binding protein (CRBP1), alcohol dehydrogenase 1 (ADH1) and cytochrome P450 26A1(CYP26A1) was significantly correlated with that of HJV, TfR2 and FPN, respectively.

So they're seeing that nearly all the genes associated with iron metabolism are elevated, and they already stated that iron overload in the liver is commonly associated with NASH (Non-Alcoholic SteatoHepatitis, another term for NAFLD).

Cellular Retinol-Binding Protein (CRBP) is elevated and is one of the proteins that the body makes to bind to and protect itself from Poison/"Vitamin A". It is also used in many studies as a surrogate marker for retinol levels in the blood.  Why would the body be making this if it didn't need to?

Alcohol dehydrogenase is elevated, and alcohol dehydrogenase is a major part of the breakdown process of Poison/"Vitamin A".  Alcohol dehydrogenase 2 is a major hepatic enzyme for human retinol metabolism.  Why would the body be ramping this up if it didn't need to?

Cytochrome P450 26A1 (CYP26A1) is also elevated, and the CYP26 family is another major part of the breakdown process of Poison/"Vitamin A".  The role of CYP26 enzymes in retinoic acid clearance.  Again, why would the body be ramping this up if it didn't need to?

Why would the body be ramping up:

• CRBP, a protective molecule against Poison/"Vitamin A"
• Alcohol dehydrogenase, a critical enzyme system in the breakdown of Poison/"Vitamin A"
• CYP26A1, critical pathways through the liver for the breakdown of Poison/"Vitamin A"

Obviously, the above things are of critical importance in retinoid metabolism, that's why the authors studied them!

Does it make sense that if genes associated with iron metabolism are ELEVATED in conjunction with IRON OVERLOAD, that if markers associated with Poison/"Vitamin A" are ELEVATED at the same time, then that would likely suggest some form of Poison/"Vitamin A" TOXICITY?

Conclusion: The results of the present study suggest that the reasons responsible for iron accumulation in NASH in the present study may partly be due to enhanced expression of TfRs, especially TfR2, and hyperdynamic state of retinoid metabolism is closely related to iron metabolism in the disease.

So the authors measured markers of Poison/"Vitamin A" metabolism, which were all elevated.

What they didn't measure:

• Serum retinol, the Poison/"Vitamin A" floating around the blood
• Serum retinyl esters, a marker of how much Poison/"Vitamin A" is stored in the liver
• Serum retinoic acid(s), the most damaging form of Poison/"Vitamin A"
• Liver biopsy, the gold standard of assessing actual Poison/"Vitamin A" toxicity in the liver

Look again at how many things they actually DID measure and assess.  Then, think about how they didn't actually look at Poison/"Vitamin A" levels in the system at all, they looked at all sorts of tangential measures of Poison/"Vitamin A", which were ALL ELEVATED.  Then they have the gall to suggest that all this extra breakdown/detoxification activity is causing a retinoid deficiency...which they didn't even look for!!!

The question becomes, do you believe that the body is INTELLIGENT,  or do you believe that the body is DUMB AND WASTEFUL?