Take‐home messages
Investigation of copper status can be a diagnostic challenge.
The non‐caeruloplasmin‐bound copper has deficiencies.
The copper:caeruloplasmin ratio should produce values that are independent of gender and age.
The copper:caeruloplasmin ratio, unlike non‐caeruloplasin‐bound copper, does not suffer from negative values; however, the other deficiencies of non‐caeruloplasmin‐bound copper also apply to the copper: caeruloplasmin ratio.
So we may need this?
(copper:caeruloplasmin):zinc
The paper is getting old and nothing really in the way of 'cited by' papers to reference, other than this article suggesting 24-h urinary copper (big pain) works in Wilson's Disease.
For some reason I got the idea when ordering my copper recently that ceruloplasmin wasn't important except with copper excess. It's cheap anyway, $20.70, at Life Extension. I sound like a LE commercial lately. I promise I am not an investor and don't know anyone's name there! They just happen to be so easy to work with and use labcorps that all my doc ordered labs go through too.
Last edited by circular on Fri Jun 10, 2016 9:46 pm, edited 1 time in total.
ApoE 3/4 > Thanks in advance for any responses made to my posts.
Circular, I would love more info about this too! Just yesterday I got back some lab tests after approximately 9 months of supplements and food/water recommendations to reduce a high serum copper level per the Walsh protocol. Last August, my serum copper was 134 ug/dL, which according to the Walsh worldview is high and could be causing/contributing to my mood issues. Now my serum copper is 75 ug/dL, which is near the bottom of the Walsh functional range, and should be "good". And although finding out about my 4/4 did knock me back a bit, I *have* been feeling better in many ways, so that's great.
But on the suggestion of a nutritional therapist I had consulted with for low copper food recommendations, I had also thrown in a test for ceruloplasmin, and apparently it is too low according to Lab Corp at 16.4 mg/dL. And according to one online calculator I found, perhaps this means I have too much free copper, but I am math-challenged and frankly out of my league in all this. Googling to try to get a grip on it seemed to quickly lead to nowhere and so I have booked another consult with the doctor I originally consulted by phone with to get more clarity.
To add to the confusion, now my plasma zinc is too high: it is now 164 ug/dL, which is too high both in the Lab Corp and Walsh ranges. So I've stopped zinc supplementation for now (and also the molybdenum I had been instructed to take to help reduce the copper) until I can talk to the doctor...
It depends. You need to test your levels, although there is some question if this is accurate, and supplement if needed. Studies have shown as you age, zinc levels tend to fall and are associated with all cause mortality, mainly because the immune system doesn't work as well. Makes sense that you need good zinc levels when you see how many enzymatic processes depend on zinc as a co-factor.
Ruth I'll be curious what your doctor says. WRT zinc perhaps you're just finding your supplemental sweet spot. It's great your copper has come down so far! Dr. Bredesen wants us to have a 1:1 ratio copper:zinc. I think you'll get there because you're working on it.
Now the low ceruplasmin could be a problem. I don't know anything about it really, but just found this interesting paper suggesting it inhibits myeloperoxidase, and inflammation marker, which I've been running somewhat high in for about three years. I have ceruplasmin in my cart for the next lab order, along with zinc and copper for an update after starting zinc to raise that and get my copper down (zinc was 82, copper 121 but didn't test ceruloplasmin). No doubt I'll be sitting in a new puddle of confusion alongside you.
I also need to go back and dig for what the ceruplasmin:copper ratio should be, ostensibly … for another day.
ApoE 3/4 > Thanks in advance for any responses made to my posts.
Testing blood levels of zinc seems to be tricky, especially when you look at the how zinc is used during inflammation.
“When a pathogen is recognized, a series of molecules wake up from dormancy to create a process that activates the innate immune response. A major part of this process involves the NF-κB pathway, named for a highly active protein that is known to play an important role in the immune response to infection. Once NF-κB is activated and enters the nucleus, a gene is expressed that produces a zinc transporter called ZIP8. The transporter then rapidly mobilizes to the cell's wall, where it can then shuttle zinc from the bloodstream into the cell.
After cell entry, zinc is then directed to and binds to a different protein in the NF-κB pathway. When this happens, it halts any further activity in that process. The cumulative impact of this feedback loop is that it prevents excessive inflammation, which can be damaging to cells and the body.
"There are certainly other zinc targets in the cell, but we found evidence that zinc is brought in by ZIP8 to turn the pathway off by interacting with this protein at a specific region," Knoell said.”
