Quote from Dr. Garrett Smith on February 13, 2019, 12:08 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 copper-related issues are directly related to different bodily responses to Poison/"Vitamin A" toxicity.

It will be difficult to suss out completely, as none of the 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, a paper linking major depression to higher ceruloplasmin (the main copper-binding protein, can indicate copper toxicity) and lower retinol-binding protein (RBP, when it is too low and Poison/"Vitamin A" is too high and free to run around unbound, that is one definition of Poison/"Vitamin A" toxicity):

Higher alpha 1-antitrypsin, haptoglobin, ceruloplasmin and lower retinol binding protein plasma levels during depression: further evidence for the existence of an inflammatory response during that illness.

Recently, a few reports have shown that severe depression may be associated with higher levels of positive acute phase proteins (APPs), such as haptoglobin (Hp), alpha 1-acid glycoprotein (alpha 1S) and lower levels of negative APPs (visceral proteins), such as albumin (Alb) and transferrin (Tf). In order to reassess whether depression is related to alterations in the expression of plasma APP concentrations, we measured in 84 normal controls and depressed inpatients positive APPs such as Hp, alpha 1-antitrypsin (alpha 1AT), hemopexin (Hpx), ceruloplasmin (Cp), complement component C3C and one visceral protein, i.e., retinol binding protein (RBP). We found increased plasma concentrations of Hp, alpha 1AT, and Cp in major depressed subjects as compared with healthy controls, with minor depressives exhibiting an intermediate position. RBP was significantly lower in minor and major depressives than in normal controls. The disorders in these proteins were rather sensitive (62%) for major depression, with a specificity equalling 96%. Our findings are compatible with the hypothesis that major depression may be accompanied by inflammatory changes with higher levels of positive APPs (i.e., alpha 1AT, Hp, Cp, alpha 1S) and lower levels of visceral proteins (i.e., RBP, Tf, Alb).