Methylene Blue Inhibition Of Oestradiol-induced Increase Of Ceruloplasmin Serum Levels In Rats

haidut

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gbolduev said:
http://www.ncbi.nlm.nih.gov/pubmed/7841167

It stops production of ceruloplasmin even with estrogen application.What?

I though Peat wanted to raise ceruloplasmin))

GBolduev, is it possible that the decrease of ceruloplasmin is adaptive? One of the main functions of ceruloplasmin is to inhibit nitric oxide synthase (NOS) and also oxidize NO to nitrites. Since methylene blue itself inhibits NOS and lowers levels of NO maybe the body sees this as a sign of reduced need for ceruloplasmin.
http://www.enzolifesciences.com/ALX-200 ... an-plasma/
"...Has previously been considered a target for nitric oxide (NO) and an inhibitor of endothelial nitric oxide synthase (eNOS/NOS III). Catalyzes S-nitrosothiol formation in cell culture media. Is a NO oxidase and nitrite synthase that determines endocrine NO homeostasis."

Estrogen stimulates NOS and increases NO levels. Methylene blue is an aromatase inhibitor and estrogen receptor antagonist, so in general things that lower estrogen levels would be expected to lower ceruloplasmin as well, right? May be that is another reason it lowers ceruloplasmin.
http://www.ncbi.nlm.nih.gov/pubmed/2467322
viewtopic.php?t=6736

But you are right about Peat mentioning ceruloplasmin. I have always wondered what is his position on this. I could not find anything specific from him whether we should raise ceruloplasmin or lower it. He just said he would like to see nutrition based on how it affects ceruloplasmin. Do you have some quotes from him saying we should be raising ceruloplasmin?
 
Joined
Nov 26, 2013
Messages
7,367
https://en.wikipedia.org/wiki/Ceruloplasmin said:
Excess[edit]
Greater-than-normal ceruloplasmin levels may indicate or be noticed in:


acute and chronic inflammation (it is an acute-phase reactant)
rheumatoid arthritis
Angina[13]
Alzheimer's disease[14]
Schizophrenia[15]
Obsessive-compulsive disorder[16]
 

narouz

Member
Joined
Jul 22, 2012
Messages
4,429
haidut said:
https://raypeatforum.com/forums/posts/94459/
gbolduev said:
http://www.ncbi.nlm.nih.gov/pubmed/7841167

It stops production of ceruloplasmin even with estrogen application.What?

I though Peat wanted to raise ceruloplasmin))

GBolduev, is it possible that the decrease of ceruloplasmin is adaptive? One of the main functions of ceruloplasmin is to inhibit nitric oxide synthase (NOS) and also oxidize NO to nitrites. Since methylene blue itself inhibits NOS and lowers levels of NO maybe the body sees this as a sign of reduced need for ceruloplasmin.
http://www.enzolifesciences.com/ALX-200 ... an-plasma/
"...Has previously been considered a target for nitric oxide (NO) and an inhibitor of endothelial nitric oxide synthase (eNOS/NOS III). Catalyzes S-nitrosothiol formation in cell culture media. Is a NO oxidase and nitrite synthase that determines endocrine NO homeostasis."

Estrogen stimulates NOS and increases NO levels. Methylene blue is an aromatase inhibitor and estrogen receptor antagonist, so in general things that lower estrogen levels would be expected to lower ceruloplasmin as well, right? May be that is another reason it lowers ceruloplasmin.
http://www.ncbi.nlm.nih.gov/pubmed/2467322
viewtopic.php?t=6736

But you are right about Peat mentioning ceruloplasmin. I have always wondered what is his position on this. I could not find anything specific from him whether we should raise ceruloplasmin or lower it. He just said he would like to see nutrition based on how it affects ceruloplasmin. Do you have some quotes from him saying we should be raising ceruloplasmin?

...and...

Such_Saturation said:
https://raypeatforum.com/forums/posts/94461/
https://en.wikipedia.org/wiki/Ceruloplasmin said:
Excess[edit]
Greater-than-normal ceruloplasmin levels may indicate or be noticed in:
acute and chronic inflammation (it is an acute-phase reactant)
rheumatoid arthritis
Angina[13]
Alzheimer's disease[14]
Schizophrenia[15]
Obsessive-compulsive disorder[16]

haidut, and Such...
In another thread gbolduev brought ceruloplasmin into discussion
in relation to possible iron storage problems.
This is a cropped version of his response.
I'd be interested in how you guys would try to unpack his Eckian? perspective on this stuff:


gbolduev said:
Basically if you are stressed you will use a lot of pregnenolone to make progesterone for cortisol and aldo pathway and will have very little DHEA. That will put your testosterone and estradiol into the lower part of the range. And you will start accumulating iron and copper in the liver. The mechanism how it works is this.

To release iron from the liver you need xanthine oxidase which runs on vitamin B2 and molybdenum, then you need ceruloplasmin to oxidize iron and put it on transferrin.

SO here we can possibly have 2 problems , lack of B2 or molybdenum , and lack of DHEA from stress so there is very little estrogen made.LOW estrogen equals low ceruloplasmin which equals no iron on transferrin and tons of it in ferritin.
...
Also iron chelation is good, but dont forget we have low iron in tissues but some free iron in the organs and also tons of iron in the liver. SO I think proper iron chelation would be by making iron bioavailable so it does not spill from the liver and making sure you have proper ceruloplasmin levels to make iron work.
 
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Joined
Nov 26, 2013
Messages
7,367
I'm not necessarily fond of debating with people who might not or cannot answer. But you can see very well here how the situation is:

Such_Saturation said:
https://raypeatforum.com/forums/posts/94461/
https://en.wikipedia.org/wiki/Ceruloplasmin said:
Excess[edit]
Greater-than-normal ceruloplasmin levels may indicate or be noticed in:


acute and chronic inflammation (it is an acute-phase reactant)
rheumatoid arthritis
Angina[13]
Alzheimer's disease[14]
Schizophrenia[15]
Obsessive-compulsive disorder[16]

Gbolduev seems confused that methylene blue stops the stuff even with estrogen administration. Perhaps we should be thinking of the fact that this is why we enjoy all methylene blue's benefits in the first place. There is the underlying process descibed on raypeat.com that makes it useless to engage Ray Peat's opinions if we do not actually go read what that process is (nitric oxide to waste respiration, etc.). In the case of this user this is very clear when he talks about carbon dioxide somehow leaching minerals into the cell, and then fails to explain why this would happen. That explanation could be easily, if given, seen to contradict the one given by Ray Peat concerning the carbon dioxide stream, and this would lead to actual progress in the discussion.

Furthermore, I personally can't find anything Ray Peat wrote about ceruloplasmin, much less concerning bringing it to any extreme level up or down. There seems to be a continuous unintentional strawman fallacy from many people in this aspect. But on Tuesday I will check my ceruloplasmin and my iron levels with the ratio that haidut found.
 
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narouz

Member
Joined
Jul 22, 2012
Messages
4,429
Such_Saturation said:
https://raypeatforum.com/forums/posts/97298/ I'm not necessarily fond of debating with people who might not or cannot answer.

To the best of my knowledge he is welcome here.
The moderator known as 4peats has said he is.
I, narouz, have sent him a personal email saying
come on back it's safe. :lol:

So...I think he will come back soon.
Oh wait! I forgot...




Such_Saturation said:
There is the underlying process descibed on raypeat.com that makes it useless to engage Ray Peat's opinions if we do not actually go read what that process is (nitric oxide to waste respiration, etc.). In the case of this user this is very clear when he talks about carbon dioxide somehow leaching minerals into the cell, and then fails to explain why this would happen.

gbolduev's nutritional views would seem to be fundamentally upside down from Peat's in many respects.
And, yes, it's true: he obviously doesn't care to study Peat's oeuvre.
I'm not gonna make the guy pass an entrance exam. :lol:

I just like to see what he thinks about these matters.
I'm curious.
 

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It is difficult to "see what he thinks" if there is not a line of communication, it's just two different levels.
 

haidut

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Such_Saturation said:
https://raypeatforum.com/forums/posts/97298/ I'm not necessarily fond of debating with people who might not or cannot answer. But you can see very well here how the situation is:

Such_Saturation said:
https://raypeatforum.com/forums/posts/94461/
https://en.wikipedia.org/wiki/Ceruloplasmin said:
Excess[edit]
Greater-than-normal ceruloplasmin levels may indicate or be noticed in:


acute and chronic inflammation (it is an acute-phase reactant)
rheumatoid arthritis
Angina[13]
Alzheimer's disease[14]
Schizophrenia[15]
Obsessive-compulsive disorder[16]

Gbolduev seems confused that methylene blue stops the stuff even with estrogen administration. Perhaps we should be thinking of the fact that this is why we enjoy all methylene blue's benefits in the first place. There is the underlying process descibed on raypeat.com that makes it useless to engage Ray Peat's opinions if we do not actually go read what that process is (nitric oxide to waste respiration, etc.). In the case of this user this is very clear when he talks about carbon dioxide somehow leaching minerals into the cell, and then fails to explain why this would happen. That explanation could be easily, if given, seen to contradict the one given by Ray Peat concerning the carbon dioxide stream, and this would lead to actual progress in the discussion.

Furthermore, I personally can't find anything Ray Peat wrote about ceruloplasmin, much less concerning bringing it to any extreme level up or down. There seems to be a continuous unintentional strawman fallacy from many people in this aspect. But on Tuesday I will check my ceruloplasmin and my iron levels with the ratio that haidut found.

Here is where I got the quote on Ray and ceruloplasmin:
http://www.dannyroddy.com/weblog/ironov ... eserotonin
"...I think the copper/iron ratio is under hormonal-developmental control, and I have never seen an attempt to use ceruloplasmin to guide nutrition. Regular good light exposure is probably important for preventing the displacement of copper by iron."

In one interview he also said that official nutritional guidance would be a lot more reliable if it used as a guide relevant metabolic indicators such as proper copper/iron ratio manifested by "higher" ceruloplasmin. Unfortunately, neither the interviewer nor the listeners asked him to extrapolate on that ceruloplasmin reference. So, I don't know what he meant by "higher" - i.e. upper ranges of the "normal" range or above the limit...If someone has talked to him about it or knows of another reference please share.
Gbolduev says that you can be both deficient and toxic on copper. The way I understand it, is that if your plasma copper is within range and ceruloplasmin is also within range (or even above range) then your copper status is fine and it is doing its job without being toxic. It is only when plasma copper is high-normal and ceruloplasmin is in the bottom 25% (or lower) of the range when copper starts to become an issue. But these conditions are rare - i.e. being copper toxic. Most people are actually iron toxic and ceruloplasmin plays a role there. Ceruloplasmin's main purpose if to deplete iron from the tissues and in the process replace iron with copper. That's why it is elevated in acute inflammatory reactions - i.e. if the liver is working well it is producing more ceruloplasmin and the body uses it to pull iron out of the inflamed tissue. I don't think ceruloplasmin itself is pathological. Quite the opposite. It CAN be a sign of trouble but not a cause.
This may be why Peat talks about ceruloplasmin - i.e. as a way to lower iron/copper ratio IN TISSUES.
 
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Blossom

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Great explanation Haidut, thanks.
 

haidut

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narouz said:
post 97294
haidut said:
post 94459
gbolduev said:
http://www.ncbi.nlm.nih.gov/pubmed/7841167

It stops production of ceruloplasmin even with estrogen application.What?

I though Peat wanted to raise ceruloplasmin))

GBolduev, is it possible that the decrease of ceruloplasmin is adaptive? One of the main functions of ceruloplasmin is to inhibit nitric oxide synthase (NOS) and also oxidize NO to nitrites. Since methylene blue itself inhibits NOS and lowers levels of NO maybe the body sees this as a sign of reduced need for ceruloplasmin.
http://www.enzolifesciences.com/ALX-200 ... an-plasma/
"...Has previously been considered a target for nitric oxide (NO) and an inhibitor of endothelial nitric oxide synthase (eNOS/NOS III). Catalyzes S-nitrosothiol formation in cell culture media. Is a NO oxidase and nitrite synthase that determines endocrine NO homeostasis."

Estrogen stimulates NOS and increases NO levels. Methylene blue is an aromatase inhibitor and estrogen receptor antagonist, so in general things that lower estrogen levels would be expected to lower ceruloplasmin as well, right? May be that is another reason it lowers ceruloplasmin.
http://www.ncbi.nlm.nih.gov/pubmed/2467322
http://www.raypeatforum.com/forum/viewtopic.php?t=6736

But you are right about Peat mentioning ceruloplasmin. I have always wondered what is his position on this. I could not find anything specific from him whether we should raise ceruloplasmin or lower it. He just said he would like to see nutrition based on how it affects ceruloplasmin. Do you have some quotes from him saying we should be raising ceruloplasmin?

...and...

Such_Saturation said:
post 94461
https://en.wikipedia.org/wiki/Ceruloplasmin said:
Excess[edit]
Greater-than-normal ceruloplasmin levels may indicate or be noticed in:
acute and chronic inflammation (it is an acute-phase reactant)
rheumatoid arthritis
Angina[13]
Alzheimer's disease[14]
Schizophrenia[15]
Obsessive-compulsive disorder[16]

haidut, and Such...
In another thread gbolduev brought ceruloplasmin into discussion
in relation to possible iron storage problems.
This is a cropped version of his response.
I'd be interested in how you guys would try to unpack his Eckian? perspective on this stuff:


gbolduev said:
Basically if you are stressed you will use a lot of pregnenolone to make progesterone for cortisol and aldo pathway and will have very little DHEA. That will put your testosterone and estradiol into the lower part of the range. And you will start accumulating iron and copper in the liver. The mechanism how it works is this.

To release iron from the liver you need xanthine oxidase which runs on vitamin B2 and molybdenum, then you need ceruloplasmin to oxidize iron and put it on transferrin.

SO here we can possibly have 2 problems , lack of B2 or molybdenum , and lack of DHEA from stress so there is very little estrogen made.LOW estrogen equals low ceruloplasmin which equals no iron on transferrin and tons of it in ferritin.
...
Also iron chelation is good, but dont forget we have low iron in tissues but some free iron in the organs and also tons of iron in the liver. SO I think proper iron chelation would be by making iron bioavailable so it does not spill from the liver and making sure you have proper ceruloplasmin levels to make iron work.

My own blood tests do not confirm his views on iron and copper in liver, at least for me. I posted a study that uses the ferritin/AST ratio as indication of liver iron burden and my is below 2. The study said no issues with liver iron overload were seen until the ratio hits 17. Also Peat said that xantine oxidase is not something you want to enhance and the studies I have seen support that view. Also, my serum copper is normal and ceruloplasmin is in the upper ranges of normal. So, my copper should be bioavailable and not toxic. However, I would certainly like to hear Peat's opinion on ceruloplasmin. He has referenced it several times rather mysteriously and not expanded more on how to modify it and what levels are optimal.
Here is some info on xanthine oxidase.
http://raypeat.com/articles/articles/caffeine.shtml
"...Caffeine stops production of free radicals by inhibiting xanthine oxidase, an important factor in tissue stress."
"...One of the ways in which uric acid functions as an “antioxidant” is by modifying the activity of the enzyme xanthine oxidase, which in stress can become a dangerous source of free radicals. Caffeine also restrains this enzyme. There are several other ways in which uric acid and caffeine (and a variety of intermediate xanthines) protect against oxidative damage. Coffee drinkers, for example, have been found to have lower levels of cadmium in their kidneys than people who don’t use coffee, and coffee is known to inhibit the absorption of iron by the intestine, helping to prevent iron overload."
 
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Regina

Member
Joined
Aug 17, 2016
Messages
3,549
Location
Chicago
Here is where I got the quote on Ray and ceruloplasmin:
http://www.dannyroddy.com/weblog/ironov ... eserotonin
"...I think the copper/iron ratio is under hormonal-developmental control, and I have never seen an attempt to use ceruloplasmin to guide nutrition. Regular good light exposure is probably important for preventing the displacement of copper by iron."

In one interview he also said that official nutritional guidance would be a lot more reliable if it used as a guide relevant metabolic indicators such as proper copper/iron ratio manifested by "higher" ceruloplasmin. Unfortunately, neither the interviewer nor the listeners asked him to extrapolate on that ceruloplasmin reference. So, I don't know what he meant by "higher" - i.e. upper ranges of the "normal" range or above the limit...If someone has talked to him about it or knows of another reference please share.
Gbolduev says that you can be both deficient and toxic on copper. The way I understand it, is that if your plasma copper is within range and ceruloplasmin is also within range (or even above range) then your copper status is fine and it is doing its job without being toxic. It is only when plasma copper is high-normal and ceruloplasmin is in the bottom 25% (or lower) of the range when copper starts to become an issue. But these conditions are rare - i.e. being copper toxic. Most people are actually iron toxic and ceruloplasmin plays a role there. Ceruloplasmin's main purpose if to deplete iron from the tissues and in the process replace iron with copper. That's why it is elevated in acute inflammatory reactions - i.e. if the liver is working well it is producing more ceruloplasmin and the body uses it to pull iron out of the inflamed tissue. I don't think ceruloplasmin itself is pathological. Quite the opposite. It CAN be a sign of trouble but not a cause.
This may be why Peat talks about ceruloplasmin - i.e. as a way to lower iron/copper ratio IN TISSUES.
Thank you Haidut. It is great to get referred back to superb posts/threads such as this. The iron/glycolysis article at DannyRoddy is nice and simple. Enough to cause me night sweats over the amount of people in this vicious circle state. In combination with the thread on Nitric Oxide Theory of Aging, the processes toward my mom's Alzheimer's become quite clear. It just took a few iron pills for the straw to break the camel's back.
I hope I will learn more from my iron/copper tests. I know I have the HFE gene (from 23andMe), fwiw. But, as RP in the article says, "copper/iron ratio is under hormonal-developmental control.
Well, you've presented us with quite the arsenal of ways to thwart the path of dysregulation. Once again, carbon dioxide, aspirin, caffeine, tetracyclines, MB, vitamin E, niacinamide, progesterone, pregnenolone, red light, mildronate?, agmatine?, famotidine?, glycine, cyproheptadine, emodin, magnesium, zinc, DHEA, red light, lots of light, activated charcoal and everybody's favorite NO PUFA. Avoid stress. Enough thyroid.
I wonder if it is possible to reverse the damage done by past infections/NO.
Thanks so much!!
 
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Dante

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Joined
Sep 9, 2016
Messages
459
In one interview he also said that official nutritional guidance would be a lot more reliable if it used as a guide relevant metabolic indicators such as proper copper/iron ratio manifested by "higher" ceruloplasmin. Unfortunately, neither the interviewer nor the listeners asked him to extrapolate on that ceruloplasmin reference. So, I don't know what he meant by "higher" - i.e. upper ranges of the "normal" range or above the limit...If someone has talked to him about it or knows of another reference please share.
Gbolduev says that you can be both deficient and toxic on copper. The way I understand it, is that if your plasma copper is within range and ceruloplasmin is also within range (or even above range) then your copper status is fine and it is doing its job without being toxic. It is only when plasma copper is high-normal and ceruloplasmin is in the bottom 25% (or lower) of the range when copper starts to become an issue. But these conditions are rare - i.e. being copper toxic. Most people are actually iron toxic and ceruloplasmin plays a role there. Ceruloplasmin's main purpose if to deplete iron from the tissues and in the process replace iron with copper. That's why it is elevated in acute inflammatory reactions - i.e. if the liver is working well it is producing more ceruloplasmin and the body uses it to pull iron out of the inflamed tissue. I don't think ceruloplasmin itself is pathological. Quite the opposite. It CAN be a sign of trouble but not a cause.
This may be why Peat talks about ceruloplasmin - i.e. as a way to lower iron/copper ratio IN TISSUES.
Guess i am one of those rare ones since my serum copper is high end of the normal while ceruloplasmin is very low at 20.7 (normal range -> 20 - 60) My LFT and iron function tests are normal.
. Besides, though it's rare one could have low serum copper and low ceruloplasmin and still have accumulated copper in tissues .
See this paper
Lingual Dyskinesia and Tics: A Novel Presentation of Copper-Metabolism Disorder
So, its a n=1 case study of a 16 year old who exhibited acute severe hemilingual dyskinesia and prominent tics with ballismus of the upper limbs and normal brain and spinal MRI results. He was put under a battery of tests (vitamins, electrolytes, ANA, acute phase reactants , genetic test etc) all of which were normal except
his ceruloplasmin and copper levels were low: 0.13 g/L (normal range: 0.17– 0.66 g/L) and 8 mol/L (normal range: 11–28 mol/L), respectively.
However, a penicillamine challenge revealed increased urinary copper levels of 6.2 mol/day (normal range: 0.1– 0.8 mol/day). These increased values were much higher than the norm but still lower than the diagnostic value for Wilson disease, which is 25 mol/day.
So, at the end, he was treated with zinc gluconate(lol here) as tetrathiomolybdate is not commercially available in Canada and trienthine has been reported to cause irreversible worsening of neurologic symptoms. Eight weeks after initiation of treatment, the movements disappeared, although his copper and ceruloplasmin levels had not yet been normalized
Conclusion -> despite the low serum levels of copper, the urinary levels after penicillamine challenge were high, which suggested a storage disorder and low serum copper is not always indicative of copper deficiency and that urinary copper levels should be taken into account when planning therapy
 

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haidut

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Guess i am one of those rare ones since my serum copper is high end of the normal while ceruloplasmin is very low at 20.7 (normal range -> 20 - 60) My LFT and iron function tests are normal.
. Besides, though it's rare one could have low serum copper and low ceruloplasmin and still have accumulated copper in tissues .
See this paper
Lingual Dyskinesia and Tics: A Novel Presentation of Copper-Metabolism Disorder
So, its a n=1 case study of a 16 year old who exhibited acute severe hemilingual dyskinesia and prominent tics with ballismus of the upper limbs and normal brain and spinal MRI results. He was put under a battery of tests (vitamins, electrolytes, ANA, acute phase reactants , genetic test etc) all of which were normal except
his ceruloplasmin and copper levels were low: 0.13 g/L (normal range: 0.17– 0.66 g/L) and 8 mol/L (normal range: 11–28 mol/L), respectively.
However, a penicillamine challenge revealed increased urinary copper levels of 6.2 mol/day (normal range: 0.1– 0.8 mol/day). These increased values were much higher than the norm but still lower than the diagnostic value for Wilson disease, which is 25 mol/day.
So, at the end, he was treated with zinc gluconate(lol here) as tetrathiomolybdate is not commercially available in Canada and trienthine has been reported to cause irreversible worsening of neurologic symptoms. Eight weeks after initiation of treatment, the movements disappeared, although his copper and ceruloplasmin levels had not yet been normalized
Conclusion -> despite the low serum levels of copper, the urinary levels after penicillamine challenge were high, which suggested a storage disorder and low serum copper is not always indicative of copper deficiency and that urinary copper levels should be taken into account when planning therapy

Have you done iron saturation, transferrin, ferritin, etc? It would be unusual to have high copper without some signs of iron deficiency. High serum copper is usually due to excess estrogen, as Peat said in one interview. Vitamin E and aspirin lower serum copper, as does zinc (as the study above mentions).
 

encerent

Member
Joined
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Messages
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Have you done iron saturation, transferrin, ferritin, etc? It would be unusual to have high copper without some signs of iron deficiency. High serum copper is usually due to excess estrogen, as Peat said in one interview. Vitamin E and aspirin lower serum copper, as does zinc (as the study above mentions).

Do they measure anything useful when you donate blood that I should ask them to provide me?"
 

haidut

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Location
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Do they measure anything useful when you donate blood that I should ask them to provide me?"

I think they do a CBC and iron panel to rule out anemia. They may also test for HIV and other infections but that varies. You can ask for the results of whatever they test for.
 

Dante

Member
Joined
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Messages
459
Have you done iron saturation, transferrin, ferritin, etc? It would be unusual to have high copper without some signs of iron deficiency. High serum copper is usually due to excess estrogen, as Peat said in one interview. Vitamin E and aspirin lower serum copper, as does zinc (as the study above mentions).
No iron deficiency. Ferritin was 80 (normal was 30-300). Transferrin and Iron saturation were also within range(somewhere in the middle).Serum copper is 130(normal was 70-140) , what i am worried about is the low ceruloplasmin.
 
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