gbold and mattyb disagree about things?
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This is not a protocol yet, this is a discussion. This is why I encourage @mattyb to stay in it and keep digging for the truth. I can admit that I dont have all the answers and I could be wrong, and I do apologise to Matty for may be being overly aggressive. Please don't take it personal, it is a russian thing I guess.
I'm sorry, you are a good guy and i want to keep discussing things with you.
Lets discuss this we need to dig out why this histidine is low in all those conditions.
@mattyb Here is a study about hairloss , since we mentioned it here. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5596642/
90% had low histidine.
I agree with you that low histidine can be regulatory . And I also mentioned it in UC thread .You say that UC has high histamine levels. Question is how do we know if UC has high histamine levels. I would assume it has high histamine activation, like in histapenia ( which is low histamine levels) and only in histapenia you get food allergies. IN histadelia ( high histamine) you dont get any food reactions it seems.
Histapenia is copper toxic people. they have low systemic histamine production. But have high mast cell activation problem with very sensitive receptors. And high release of CRH, since cortisol is not sensitive.
Also if low histidine is regulatory, then why taking histidine fixes everything. If the body keep histidine low on purpose . then it should get worse if you take it. But it does not. It gets better and it stops all histamine reactions. Is this because cortisol become more sensitive and CRH is not released. since CRH increases histamine release from the mast cells.
I'm sorry, you are a good guy and i want to keep discussing things with you.
Lets discuss this we need to dig out why this histidine is low in all those conditions.
@mattyb Here is a study about hairloss , since we mentioned it here. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5596642/
90% had low histidine.
I agree with you that low histidine can be regulatory . And I also mentioned it in UC thread .You say that UC has high histamine levels. Question is how do we know if UC has high histamine levels. I would assume it has high histamine activation, like in histapenia ( which is low histamine levels) and only in histapenia you get food allergies. IN histadelia ( high histamine) you dont get any food reactions it seems.
Histapenia is copper toxic people. they have low systemic histamine production. But have high mast cell activation problem with very sensitive receptors. And high release of CRH, since cortisol is not sensitive.
Also if low histidine is regulatory, then why taking histidine fixes everything. If the body keep histidine low on purpose . then it should get worse if you take it. But it does not. It gets better and it stops all histamine reactions. Is this because cortisol become more sensitive and CRH is not released. since CRH increases histamine release from the mast cells.
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It seems many of the participants had deficiencies in several of all the tested amino acids, right? So maybe it could be related to poor protein assimilation in general which would affect hair production negatively. I dont know what would be the driver for poor protein assimilation but could probably have different reasons...
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That is exactly what I was writting before. if you have lower stomach acid release like in histidine deficiency you would get. Then you slowly start losing other aminos also. And zinc, and iron , and calcium. and folate. and b12.
And then you get a dead end situation. Where there is not enough histidine, this causes high CRH, and very sensitive histamine even after the allergic irritant is gone. SO this can happen
1) overmasturbation. over sex. ( that is why masturbators are bald))
2) If you live with an allergic irritant of some sort( a dog, or cat ) for a long time.
3) if you take antibiotics
etc.
This can lead to this dead end cycle.
And then you get a dead end situation. Where there is not enough histidine, this causes high CRH, and very sensitive histamine even after the allergic irritant is gone. SO this can happen
1) overmasturbation. over sex. ( that is why masturbators are bald))
2) If you live with an allergic irritant of some sort( a dog, or cat ) for a long time.
3) if you take antibiotics
etc.
This can lead to this dead end cycle.
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http://www.encognitive.com/files/Urinary Histidine Excretion in Patients with Classical Allergy_1.pdf
s Because dietary uptake is unlikely to increase. Histidine above body requirements is excreted in the urine. In deficit this loss can be recouped by an increase in proximal tubular renal reabsorption. In severe active allergic disease this alone may not be sufficient to meet the needs of the system. The seminal study by Bray [1], conducted and originally published in 1931, drew attention to the existence of hypochlorhydria in children with asthma and in some of their allergic parents. At the time the biochemical significance of these findings was not apparent because histamine had not yet been identified. When it was, this study was no longer at the forefront of researchers’ minds and no connection was made. Peptic hydrochloric acid secretion depends on gastric histamine production. In active allergy it seems likely that peptic histamine secretion is reduced as a second stage mechanism for histidine conservation, when urinary recovery of histidine in patients with active allergy is insufficient to meet metabolic needs. The resulting hypochlorhydria would depress gastric protein catabolism and diminish the availability of essential amino acids from diet. This would have the unwanted effect of exacerbating the diminished histidine status [27]. In routine clinical management we do not see hypochlorhydria in the milder cases, indicating that this is likely to be an effect caused by deficiency
@Nighteyes read this study, very interesting.
SO it is not regulatory the histidine, since urine excretion diminishes. it looks like a deficiency which leads to low stomach acid according to this study
s Because dietary uptake is unlikely to increase. Histidine above body requirements is excreted in the urine. In deficit this loss can be recouped by an increase in proximal tubular renal reabsorption. In severe active allergic disease this alone may not be sufficient to meet the needs of the system. The seminal study by Bray [1], conducted and originally published in 1931, drew attention to the existence of hypochlorhydria in children with asthma and in some of their allergic parents. At the time the biochemical significance of these findings was not apparent because histamine had not yet been identified. When it was, this study was no longer at the forefront of researchers’ minds and no connection was made. Peptic hydrochloric acid secretion depends on gastric histamine production. In active allergy it seems likely that peptic histamine secretion is reduced as a second stage mechanism for histidine conservation, when urinary recovery of histidine in patients with active allergy is insufficient to meet metabolic needs. The resulting hypochlorhydria would depress gastric protein catabolism and diminish the availability of essential amino acids from diet. This would have the unwanted effect of exacerbating the diminished histidine status [27]. In routine clinical management we do not see hypochlorhydria in the milder cases, indicating that this is likely to be an effect caused by deficiency
@Nighteyes read this study, very interesting.
SO it is not regulatory the histidine, since urine excretion diminishes. it looks like a deficiency which leads to low stomach acid according to this study
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Canari
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I liked this even more than having some sort of answer to my question just above! Southern Cyprus may smoothen the russian angles ? 
And a little fight makes remember that there is more important than disagreeing.
And a little fight makes remember that there is more important than disagreeing.
What is the relationship with glutamine?
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histidine converts to glutamic acid with active form of folate. And this makes sense to me, and may be this is the answer to the methylation problems that people have. If histidine is low, I would assume active folate will be low , which will stop the methylation. And taking active folate will lower histidine, and I see tons of people have insane histamine reactions from taking methylfolate plus methlyl b12 and they don't get how them increasing methylation increases their histamine reactions.
I guess the best thing to test here is histidine in serum and urine at the same time.
I guess the best thing to test here is histidine in serum and urine at the same time.
Orion
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I have histidine and alanine , with all the other aminos arriving today. Coming off a long fast but might experiment adding them slowly in a week.
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@Orion
I would not in your case. I would be very careful. We are trying things now. You have fasted for 50 days, dont screw up your progress , man
We are testing differnt angles now with 2-3 people taking this stuff. I will let you know how it all goes. be patient.
This is still in a discussion category. I think @mattyb will agree.
I would not in your case. I would be very careful. We are trying things now. You have fasted for 50 days, dont screw up your progress , man
We are testing differnt angles now with 2-3 people taking this stuff. I will let you know how it all goes. be patient.
This is still in a discussion category. I think @mattyb will agree.
Orion
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Will hold off, just get excited reading all the approaches and want to try everything!
mattyb
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Yes, I am much more interested in a sane discussion of these things.
Systemic histamine levels (blood, tissue, and urine) and mast cell activation are both typically high in bowel disorders (UC/IBD/Crohn's):
https://www.ncbi.nlm.nih.gov/pubmed/7549499?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/1690156?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4724914/
https://www.nature.com/articles/ajg2002779
I think it's too early to say histidine can fix everything. But if it does work in these populations, then it's likely as we hypothesized earlier that we can overload HDC because it's enzymatic rate constant isn't crazy high and histidine can act as a negative regulator of HDC when in higher amounts. I like the idea that it could be regulatory with CRH and cortisol, which is immunosuppressant, as well. The histidine could also help digest protein if the individuals are having problems with that. People with IBD/Crohn's/UC often have weird fungal infections that have integrated themselves seemlessly into the microbiome matrix, so I think depleting those infections of nutrients or killing them with anti-fungals is also very important, because intestinal fungi alkalize their environments for survival (to survive the low pH that comes from the stomach), so until those infections are dealt with you can't fully recover because you'll never be able to re-acidify and digest protein properly.
I am not surprised to see low histidine in many other conditions like hair loss that could be a direct driver of the condition. But in the rheumatic diseases I would expect histidine to be low due to increased HDC depleting histidine for histamine. This is why it's very important to separate discussion on diseases, because each has it's own particularities. I would expect many conditions, in the end stage, to present with low histidine because there could be upregulation of HDC when there's lots of necrosis and tissue death, and I would expect diminished protein digestion (and low histidine as a result) in many end-stage conditions due to systemic failure on many fronts (loss of K, Cl, H+, histidine, etc.). If I see a commonality between dozens of seemingly unrelated conditions that have completely different ages of onset, symptoms, and progression (hair loss, IBD, aging, MS, CFS) I am more likely to take the position that many of those conditions may have that commonality because it is related to the end conditions present when systemic biological function is failing. I think zinc finger is a lot like this. Yes, it is a ubiquitous necessity for DNA transcription and very important, and yes it could definitely be integral for treating some conditions, but for many others I simply see it as an end result of systemic biological failure. I think there are problems that are levels above that when fixed, and paired with a robust nutritional recovery plan to provide substrate for re-establishing these fundamental molecules, would result in full recovery. I think from that perspective, your plan for recovering zinc finger and digestion with proper nutrients is very important, but I am reluctant to say that it will fix every problem out-right, but rather I'm more ready to say that it could be part of the recovery plan after the treatment has addressed the underlying cause (if there is one).
I focus on the relationship between mitochondrial fission and irradiation for inflammatory disorders a lot, because we know from many many studies that fragmentation of mitochondria happens with minutes to hours of exposure, and that this sets off an inflammatory cascade because it mimics the initial conditions of early infection. We also know that radiological exams and exposure to solar radiation/geomagnetic disturbances (which we are all exposed to, some more than others though depending on geography), and that exposure during G2/S phase (like during stress or certain periods of growth in childhood), dramatically increases the risk of developing these problems. This is why I think it's integral in many inflammatory disorders to fix that underlying problem first, because the other issues will sort themselves out as long as you provide proper nutrition afterwards.
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@mattyb
I dont think you can resolve the underlining issue. that is the thing. it is a circle once CRH got activated that is it. that is why all those people chasing imaginary bugs, killing candida, viruses etc doing probiotics just fail. It never works for them.
Candida overgrowth goes to zero on histidine zinc, once copper is under control. I tried it many times with zinc carnosine. kills candida to zero.
Free copper feeds those bugs. . Copper wont be made bioavailable if potassium is not in the cell. You can put potassium in the cell only in 2 cases- sensitive cortisol. And ability to utilize CO2. Otherwise You will fail every single time. If you force it there with hyperventilation , your candida levels will grow. same if you force potassium in the cell with alklaline water, which was used by so many. This is why candida grows when people not in the know are trying to force potassium in the cell with the magnesium. Magnesium grows candida like you read about.
once CRH is activated you cant not lower cortisol and increase potassium and digestion. It is simply impossible. You can do whatever , but unless you feed what is needed to stop CRH which is zinc finger, it wont stop. and all PH balancing will be worthless. And the prolonged irritant that existed in the body cant be suppressed by anything but stopping not needed inflammation .
It is like cancer. There is an irritant. body inflames it , if this irritant stays there long enough, histidine is depleted , digestion is zero, histidine cant be repleted. CRH is up all the time. and may be the irritant is already dead 5 times, but it does not stop. This is cancer mechanism.
I posted a study with active allergies, they came up with the same conclusion that it is a dead end. Slowly and slowly body loses more and more protein.
This suppressed the immune system more and more.
This is why Kelly was so succesful at curing cancer. He was giving protein in the form of catalatic triad , trypsins etc
This and IDO inhibition stopped my cancers. And I had serious cancers.
That is why I think the most important thing is to stop CRH first. then refeed and your immune system will overcome all of those. Once copper is in the cell, those things bugs etc will cry uncle.
I dont think you can resolve the underlining issue. that is the thing. it is a circle once CRH got activated that is it. that is why all those people chasing imaginary bugs, killing candida, viruses etc doing probiotics just fail. It never works for them.
Candida overgrowth goes to zero on histidine zinc, once copper is under control. I tried it many times with zinc carnosine. kills candida to zero.
Free copper feeds those bugs. . Copper wont be made bioavailable if potassium is not in the cell. You can put potassium in the cell only in 2 cases- sensitive cortisol. And ability to utilize CO2. Otherwise You will fail every single time. If you force it there with hyperventilation , your candida levels will grow. same if you force potassium in the cell with alklaline water, which was used by so many. This is why candida grows when people not in the know are trying to force potassium in the cell with the magnesium. Magnesium grows candida like you read about.
once CRH is activated you cant not lower cortisol and increase potassium and digestion. It is simply impossible. You can do whatever , but unless you feed what is needed to stop CRH which is zinc finger, it wont stop. and all PH balancing will be worthless. And the prolonged irritant that existed in the body cant be suppressed by anything but stopping not needed inflammation .
It is like cancer. There is an irritant. body inflames it , if this irritant stays there long enough, histidine is depleted , digestion is zero, histidine cant be repleted. CRH is up all the time. and may be the irritant is already dead 5 times, but it does not stop. This is cancer mechanism.
I posted a study with active allergies, they came up with the same conclusion that it is a dead end. Slowly and slowly body loses more and more protein.
This suppressed the immune system more and more.
This is why Kelly was so succesful at curing cancer. He was giving protein in the form of catalatic triad , trypsins etc
This and IDO inhibition stopped my cancers. And I had serious cancers.
That is why I think the most important thing is to stop CRH first. then refeed and your immune system will overcome all of those. Once copper is in the cell, those things bugs etc will cry uncle.
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mattyb
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I am going to stick solely to inflammatory conditions for the time being for the sake of clarity. So I won't be discussing allergies/cancer/etc.
I agree that stopping CRH is important. But, you can fix the underlying problem in inflammatory conditions - you fast, and then mitochondria fuse, then the underlying problem is cleaned up. This will also lower CRH once you refeed since cortisol will be re-sensitized. Fasting will starve the fungi and bacteria. Then the healing happens during the refeed, where we create the right conditions for mitochondria not to fuse, for proper mineral regulation, stomach acid production, healthy gut bacteria to be established, and for fungi not to grow. It checks every box.
I agree that other conditions that are not autoimmune are likely different, in that we don't need to inhibit mitochondrial fission so that first phase (fasting) is different or non-existent. I didn't use a long fast on myself because I didn't have an autoimmune condition, instead I took cyproheptadine for a week before implementing my protocol because it suppresses CRH and sensitizes cortisol. Then I kept pressure on cortisol demand with intermittent fasting immediately after while introducing all the other strategies in stages.
I think we are on the same page here, ultimately. The difference is that I am focused on inflammatory conditions while your scope is wider.
I agree that stopping CRH is important. But, you can fix the underlying problem in inflammatory conditions - you fast, and then mitochondria fuse, then the underlying problem is cleaned up. This will also lower CRH once you refeed since cortisol will be re-sensitized. Fasting will starve the fungi and bacteria. Then the healing happens during the refeed, where we create the right conditions for mitochondria not to fuse, for proper mineral regulation, stomach acid production, healthy gut bacteria to be established, and for fungi not to grow. It checks every box.
I agree that other conditions that are not autoimmune are likely different, in that we don't need to inhibit mitochondrial fission so that first phase (fasting) is different or non-existent. I didn't use a long fast on myself because I didn't have an autoimmune condition, instead I took cyproheptadine for a week before implementing my protocol because it suppresses CRH and sensitizes cortisol. Then I kept pressure on cortisol demand with intermittent fasting immediately after while introducing all the other strategies in stages.
I think we are on the same page here, ultimately. The difference is that I am focused on inflammatory conditions while your scope is wider.
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Matty, one thing that I noticed while fasting though. I forgot to mention to you . When you fast your histamine reactions go crazy. since when you refeed especially after a long fast. you get some type of IBS especially if you don't become selective. and this can last for weeks.
I know you told me you fasted also. I think you noticed it , that histamines and histamine activation is much higher during the fasting. That is why it helps sexual problems. We need to think about using this method for UC lets say.
I love fasting. and everything, but the refeed period is very tricky after the long fast even for the person with a normal gut.
I know you told me you fasted also. I think you noticed it , that histamines and histamine activation is much higher during the fasting. That is why it helps sexual problems. We need to think about using this method for UC lets say.
I love fasting. and everything, but the refeed period is very tricky after the long fast even for the person with a normal gut.
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mattyb
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In UC/IBD/Crohn's the histamine is being driven primarily by inflammation due to excessive ROS, not CRH.
I did a few 10 day fasts about 4-6 years ago, I had no health issues then, so I never noticed any histamine reaction. I only fasted because I thought it was good for general health. I did notice at first when I was doing IF this time around that I would occasionally get hives while fasting, but they went away after a week or so. I don't think it will be of any major concern.
When a UC person fasts, ROS will go down, inflammation will go down, and pressure will be taken off HDC. CRH may put a bit of pressure back on HDC while fasting, but it won't be even close to the stimulation they were getting from ROS/inflammation. UC is much more an issue of localized tissue damage and inflammation upregulating HDC.
The refeed is of course super important, but that's why I've outlined a refeed that emphasizes rebalancing key vitamins/minerals first, establishing good gut bacteria, upregulating stomach acid production and gallbladder function prior to introducing any significant amount of protein. Do you think my refeeding protocol could use any adjustments or present any problems?
I did a few 10 day fasts about 4-6 years ago, I had no health issues then, so I never noticed any histamine reaction. I only fasted because I thought it was good for general health. I did notice at first when I was doing IF this time around that I would occasionally get hives while fasting, but they went away after a week or so. I don't think it will be of any major concern.
When a UC person fasts, ROS will go down, inflammation will go down, and pressure will be taken off HDC. CRH may put a bit of pressure back on HDC while fasting, but it won't be even close to the stimulation they were getting from ROS/inflammation. UC is much more an issue of localized tissue damage and inflammation upregulating HDC.
The refeed is of course super important, but that's why I've outlined a refeed that emphasizes rebalancing key vitamins/minerals first, establishing good gut bacteria, upregulating stomach acid production and gallbladder function prior to introducing any significant amount of protein. Do you think my refeeding protocol could use any adjustments or present any problems?
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In any case, we should experiment with this. I still think that upping histidine and promoting MT and getting rid of inflammation is the way to go. I am worried about fasting in inflammatory intestine conditions, since those people usually already are very low on iron and most are already anemic.. And to do what you are saying you need a long fast.
If the person can just promote MT and get rid of inflammation and ROS created by free copper, which will kill the bugs and diarrhea bacteria which feeds on free copper, I have no idea why concentrate on the bacteria which is a side effect,
to me inflammation is created by free metals, and the growth of bacteria is a side effect. I am actually 100% sure of it.
You can clearly see this if you take copper for 10 days, 10 mg. in slow oxidation. You will have IBS for once, and then you will have candida on your penis and in your mouth, basically exactly the same as you have in UC in the intestines. Your skin on your penis will be all broken inflamed and red. And it will start bleeding. it is similar mucosal tissue as your intestine. This is exactly what is going on in your intestines. There are no bugs there . No weird crocodiles. LOL
YOu just take zinc carnosine and boom - gone. LIke it never happened.
I experimented with this many times.
If there were some strange bug in there , then histidine would simply not work since that bug would not care if bind copper or not. But it does work in UC, and ARL clears IBS and UC in a month , I saw 100s of cases like that. UC , IBS are the easiest imbalances cleared very fast on ARL programs. I remember when I worked with hairtests we did not even consider those anything special, since they would go away so fast, and thus I would not even pay attention to those.
I think ARL missed one important issue in those conditions and that is iron deficiency, thus people with UC could react much slower to zinc and manganese regimen since manganese will put strain on iron reserves.
If the person can just promote MT and get rid of inflammation and ROS created by free copper, which will kill the bugs and diarrhea bacteria which feeds on free copper, I have no idea why concentrate on the bacteria which is a side effect,
to me inflammation is created by free metals, and the growth of bacteria is a side effect. I am actually 100% sure of it.
You can clearly see this if you take copper for 10 days, 10 mg. in slow oxidation. You will have IBS for once, and then you will have candida on your penis and in your mouth, basically exactly the same as you have in UC in the intestines. Your skin on your penis will be all broken inflamed and red. And it will start bleeding. it is similar mucosal tissue as your intestine. This is exactly what is going on in your intestines. There are no bugs there . No weird crocodiles. LOL
YOu just take zinc carnosine and boom - gone. LIke it never happened.
I experimented with this many times.
If there were some strange bug in there , then histidine would simply not work since that bug would not care if bind copper or not. But it does work in UC, and ARL clears IBS and UC in a month , I saw 100s of cases like that. UC , IBS are the easiest imbalances cleared very fast on ARL programs. I remember when I worked with hairtests we did not even consider those anything special, since they would go away so fast, and thus I would not even pay attention to those.
I think ARL missed one important issue in those conditions and that is iron deficiency, thus people with UC could react much slower to zinc and manganese regimen since manganese will put strain on iron reserves.
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mattyb
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I don't disagree that exposure from metals could be the central cause of some inflammatory diseases, but I don't think that is the majority of cases. Ultimately I think most inflammatory diseases happen because of an interaction between genetics, toxin exposure, diet, and natural and non-natural sources of radiation. I think irradiation is often the straw that breaks the camels back so-to-speak. That is where we differ, but regardless, we agree on treatment for the most part. That is good enough for me.
I do think you raise a good point about iron - if the person is super low in iron/ferritin + RBC + hemoglobin than they should get those numbers up before fasting. For many this will mean not being in a flare-up and having adequately recovered for a period of time. But any are not truly low in iron though, because part of the inflammatory response is to sequester iron into long term ferritin stores. So they will have low iron in serum, but intracellular ferritin will be high. Once you reduce the inflammation through fasting, the iron is freed and able to reintegrate into hemoglobin.
I do think you raise a good point about iron - if the person is super low in iron/ferritin + RBC + hemoglobin than they should get those numbers up before fasting. For many this will mean not being in a flare-up and having adequately recovered for a period of time. But any are not truly low in iron though, because part of the inflammatory response is to sequester iron into long term ferritin stores. So they will have low iron in serum, but intracellular ferritin will be high. Once you reduce the inflammation through fasting, the iron is freed and able to reintegrate into hemoglobin.
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Matty, high ferritin would be the case in regular inflammation , but when you bleed from the intestine, most of those people cant even get any iron into ferritin to promote extra progesterone to cortisol conversion. I looked it up, most of them have very low iron. Same as HerrFisch, same as Wuf.
Plus very high copper, so it is caused by the copper in their case. All UC cases we saw here all have the same high copper thing going. check it out.
Plus very high copper, so it is caused by the copper in their case. All UC cases we saw here all have the same high copper thing going. check it out.
