So i had treated an b12-deficiency and experienced the "worse before better" situation. To make a long story short, this actually turned out to be an induced copper deficiency as my body rapidly started producing new red blood cells to correct the macrocytic anemia. This required increased mobilization of iron from ferritin, which is handled by the copper dependent protein ceruplasmin; thus copper levels dropped.
Might be something to look in to for anyone else that's also having the "worse before better" respons.
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SebastianB
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Very interesting, thank you so much for posting! It makes sense.
Copper is very rarely low, unless locked up by something like high iron or molybdenum and when that's the case other micro nutrients like cobalt can be unavailable too. In animals the easy way to tell is their coat (hair) goes a sort of coppery/ginger colour and they just don't "do" well - and it seriously comprises fertility.
What were your symptoms, please? Did you have any other micronutrients checked?
Symptoms were pretty much the same as b12-deficiency: Tired, weak, nerv problems (pins and needles), anemia, dry flacky skin. My doctor prescribed a supplement to get my levels back up, and i'm doing much better. Besides b12 and copper i've been checked for zink and iron. They were good. Was only tested for copper because my plasma iron and transferrin saturation got low after b12-treatment, and my doctor wanted to see if this was the cause (since other explanations were unlikely).
Edit: She also advised me to avoid consuming to much iron (like large servings of liver or blackpudding, smaller amounts is fine) since this could potentially elevate the hepcidin respons and decrease iron utilization.
This is very interesting and important. There is a wierd stigma towards copper in iron and b12 boards but it is well evidenced to be lowered by both iron b12 and vitamin c supplementation too. People hanging on to the hope b12 will ‘keep improving’ things after years of injections need perhaps to expand their thinking and listen to their body. It is all so interrelated. What am I formed doctor you have though. Amazing. I hope you feel better!
Thank you for sharing this information . I will now start looking at my copper levels. I did read somewhere else to not start B12 treatment unless you have good levels of selenium, iron or molybdenum, they are requested to activated vitamin B2 ( without these …co-factors you are most likely also deficient in vitamin B2 ). So you need to supplement those first if you are deficient in these. To start with very small doses increasing every day. I think this information is found on a closed Facebook group … understanding B12 deficiency… you have to ask to become a member answering questions etc. it’s a study group etc …..with notes of a Dr. Gregory Russell Jones PhD, biochemist . You can find information if you put his name in Google. Also his treatment for Autism using B12( oils) very interesting. I am not medical trained but active in finding as much information to understand vitamin deficiencies like B12, actually all of B vitamins and Vitamin D .
True, we require iron and selenium for proper thyroid function to convert riboflavins, and molybdenum as it's serves as an co-factor for this enzymatic production as well. Similarly, other nutrients are needed in other aspects for this to go smoothly; like iodine for thyroid function, b6/pyridoxine for folate recycling etc.. But, don't forget that we should get these nutrients trough our diet, and not unnecessarily rely on supplements to much.
I didn't save most of what i read when i researched it, and some is just what my doctor told me. However, this article explain ceruplasmin and the role of it in iron metabolism quite well in my opinion (I am of course not an expert).
Thanks for sharing, definitely useful information. I imagine this is because -
"According to the currently accepted view, ferrous iron transported out of the cell by ferroportin would be safely oxidized by ceruloplasmin to facilitate loading on transferrin. Therefore, the ceruloplasmin-ferroportin system represents the main pathway for cellular iron egress and it is responsible for physiological regulation of cellular iron levels."
-Thus iron wont be extracted from gastrointestinal cells if ceruplasmin is to low, as to avoid the poisonous effect of un-oxidized iron.
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