Does Vitamin A increase Ceruloplasmin?

And I will also consider the related question, do we need Vitamin A to load copper into Ceruloplasmin?

The answer to both of these questions is no. Yet this is an effect apparently seen, so how do we explain this apparent contradiction?

I liken this to the broken window theory as explained in economics. Yes, breaking windows can lead to increased economic activity, but breaking windows is not an efficient way to do things economically.

Vitamin A increases inflammation. That’s bad. Ceruloplasmin increases in response to inflammation. Vitamin A causes osteoporosis and arthritis. Ceruloplasmin is increased in arthritis. Arthritis literally means “joint inflammation”.

We also know that copper is acknowledged as a cure for osteoporosis, and that copper deficiency is a cause of osteoporosis. We also know that copper is anti inflammatory. So it makes logical sense that the body would increase ceruloplasmin to help heal inflammation and osteoporosis.

But there is no need to cause inflammation and osteoporosis to get the body to start using copper.

There are many other ways to increase ceruloplasmin: boron, copper, and exercise will all increase ceruloplasmin. Bodybuilding is naturally going to be inflammatory; it both stirs up toxins, helping the body to detox them, and it also creates that “pump”, which is inflammation. And while lifting weights is also a process of destruction, it stimulates re-growth in a good way.

Vitamin A for ceruloplasmin… is like saying throwing rocks at windows helps to create new window installations. The body’s default mechanism is to heal, such as increasing ceruloplasmin. Increasing ceruloplasmin is the healing process that is triggered by the destruction caused by Vitamin A.

Ceruloplasmin is a key copper transport and carrying protein. But Vitamin A’s effect on increasing ceruloplasmin is incidental and natural. It does not mean that Vitamin A is vital or essential to the process. It’s incidental. Incidental, definition: 1. accompanying, but not a major part of something. 2. liable to happen as a consequence of (an activity).

Isn’t Vitamin A necessary to absorb copper through ceruloplasmin? No. Albumin absorbs copper independently of ceruloplasmin. And many other proteins both bind to, and carry copper through the body, including the family of metallothioneins.

So, in sum, Vitamin A is not exclusively needed to boost ceruloplasmin, which is boosted by boron, copper and exercise. And ceruloplasmin is not exclusively needed to absorb copper, as we also have albumin, metallothioneins, and many other copper transport enzymes in the body.

Vitamin A DEFICIENCY also increases ceruloplasmin!

Vitamin A and ceruloplasmin:

[Relation between ceruloplasmin and vitamin A in Sprague-Dawley rats]

“An average increase between 22 and 33% was observed in the animals with vitamin A deficiency, the highest levels being observed in the females. These results are in agreement with Peterson’s previous work.”

Therefore, since Ceruloplasmin increases without Vitamin A, then Vitamin A is not necessary for the process.

Final question: “Morley Robbins says Vitamin A is required for the loading of copper onto ceruloplasmin. Is it?”

I have held off commenting on this for about 1 year, in part because Morley might know of a study I have not read. However, I don’t see how or why the “vitamin A toxin” would be necessary for this, in part, because toxins are not necessary, and in part, because of my research above. Also, first of all, the vast majority of people have utterly no problem loading copper into ceruloplasmin, so this is never a problem that needs to be solved. Second of all, people on extremely low vitamin A diets, who don’t even take any copper at all, also don’t have any clear indications that they have trouble with this as a problem. Third, the people who do have problems with loading copper into ceruloplasmin have what is called “Wilson’s” Disease, which is a super rare 1 in 200,000 disease, and is inapplicable to 199,999 people out of 200,000. The problems in Wilson’s appear to be caused by unknown toxins because they have both liver disease and nerve problems. Fourth, this problem in Wilson’s disease might be healed simply by taking enough copper to work, which studies show should work.

And finally, these three things all greatly differ in size, and cannot be seen “acting” upon one another in real time, because they are all too small. Copper is atomic in size. Retinol is a tiny molecule. Ceruloplasmin is a huge and very complex molecule. It is simply absurd to think that a tiny atom (copper) cannot enter a mammoth size protein (ceruloplasmin) without Vitamin A (a tiny molecule), because copper can simply diffuse into the molecule easily, and likely does and research shows that is likely, as the body makes more ceruloplasmin in response to copper supplementation.

In a related issue, Copper and Vitamin A have an inverse relationship in the liver. As Vitamin A increases, copper goes down. As copper increases, Vitamin A goes down. Vitamin A is the toxin, and copper is the anti-toxin.

Modification of vitamin A metabolism in rats fed a copper-deficient diet