Psyche said:This one is a very interesting article. He basically says that a poorly liganded iron is what makes taking vitamin C dangerous.
So from what I understand, unless there are chelators binding at each of the sites on iron, Vitamin C binds to it and turns it into OH, or a hydroxyl radical.
From Wikipedia:
_http://en.wikipedia.org/wiki/Hydroxyl_radical#Biological_significance
The hydroxyl radical can damage virtually all types of macromolecules: carbohydrates, nucleic acids (mutations), lipids (lipid peroxidation) and amino acids (e.g. conversion of Phe to m-Tyrosine and o-Tyrosine). PMID 7776173. The hydroxyl radical has a very short in vivo half-life of approximately 10−9 seconds and a high reactivity.[3] This makes it a very dangerous compound to the organism.[4][5]
Unlike superoxide, which can be detoxified by superoxide dismutase, the hydroxyl radical cannot be eliminated by an enzymatic reaction. Mechanisms for scavenging peroxyl radicals for the protection of cellular structures includes endogenous antioxidants such as melatonin and glutathione, and dietary antioxidants such as mannitol and vitamin E.[4]
If I'm following, it is the hydroxyl radical that we are concerned with with Vitamin C. But the problem is still that we have so much iron in our diets and in our tissues, especially our brain, wreaking havoc. And though we can detoxify the OH we're stuck with the iron unless we bleed it out.
Psyche said:The HFE gene
Simon et al. (26) first demonstrated in the late 1970s that the gene responsible for HH is closely linked to the human leukocyte antigen (HLA) locus on a short arm of chromosome 6. Twenty years later, this gene was identified and termed as HLA-H gene by Feder et al. (27). The HLA-H gene, now renamed as the HFE gene, is comprised of 7 exons and is expressed widely or at low level in most tissues, including brain.
I think this is a key concept. There is a genetic predisposition where HLA-DQ genes located on chromosome 6 makes you vulnerable to gluten intolerance. HLA stands for the human leukocyte antigen (HLA) system which is also known as the major histocompatibility complex (MHC). The important thing to know about this system is that it contains a large number of genes related to immune system function in humans.
So if I'm understanding you correctly, damage to this particular area of the genetic code associates gluten intolerance with hereditary hemochromatosis. Healing the gut helps heal the immune system, but all of the meat eaten in order to heal the gut results in an increase in iron. Looks like we found a bug in the program!
I found the following at _http://ghr.nlm.nih.gov/condition/hemochromatosis
What genes are related to hemochromatosis?
Mutations in the HAMP, HFE, HFE2, SLC40A1, and TFR2 genes cause hemochromatosis.
The HAMP, HFE, HFE2, SLC40A1, and TFR2 genes play an important role in regulating the absorption, transport, and storage of iron. Mutations in these genes impair the control of iron absorption during digestion and alter the distribution of iron to other parts of the body. As a result, iron accumulates in tissues and organs, which can disrupt their normal functions.
Each type of hemochromatosis is caused by mutations in a specific gene. Type 1 hemochromatosis is caused by mutations in the HFE gene, and type 2 hemochromatosis is caused by mutations in either the HFE2 or HAMP gene. Mutations in the TFR2 gene cause type 3 hemochromatosis, and mutations in the SLC40A1 gene cause type 4 hemochromatosis. The cause of neonatal hemochromatosis is unknown.
More info on the genes and their locations:
From: _http://www.mlpa.com/WebForms/WebFormProductDetails.aspx?Tag=tz2fAPIAupKyMjaDF\E\t9bmuxqlhe/Lgqfk8Hkjuss|&ProductOID=47XncHLCo0I|
The HFE gene comprises 6 exons, spanning about 8 kb of genomic DNA on 6p22.1.
The SLC40A1 gene contains 8 exons, spanning 20 kb and is located on chromosome 2q32.2.
The TFR2 gene consists of 18 exons and has a length of approximately 21 kb on chromosome 7q22.1.
The HFE2 gene comprises 4 exons, spanning about 4 kb of genomic DNA on 1q21.1.
The HAMP gene contains 3 exons, spanning 3 kb and is located on chromosome 19q13.12.
After doing a little more digging it looks like the C282Y mutation on the HFE gene is the most common. I found some research pointing out the positive contribution of this genetic anomaly for populations (I have starvation in mind at this point in time):
_http://www.clinchem.org/content/44/12/2429.full
The C282Y mutation is believed to have originated in a Celtic population. We suggest that the importance of its biological advantage decreased over time because iron deficiency is now less common because of reduced birth rates, the use of oral contraceptives, oxytocic drugs, medical iron supplementation, and improved nutrition. Notwithstanding a putative importance of the C282Y mutation in the past, its protective effect may still be relevant in present times for conditions of enhanced iron demand that may result from recurring pregnancies. Influences of the mutation on iron metabolism are supported by our study, which showed a difference in iron supplementation between the heterozygous and wild-type subjects. In addition, a history of metrorrhagia was reported by a greater percentage of heterozygous individuals, and this group also contained a higher proportion of multiparous women. These facts could have attenuated genotypic effects on some indicators reflecting iron metabolism. Interestingly, the prevalence of iron deficiency and iron deficiency anemia was considerably lower in our study population, which consisted exclusively of healthcare workers, than in other study cohorts of women with comparable age (2). Conceivably, such a sample bias could have attenuated the relevance of our results.
In conclusion, our data strongly suggest a role of the C282Y mutation in the HFE gene in preventing iron deficiency in young females. Protection against iron deficiency and its morbid consequences may have conferred a selection advantage for heterozygous carriers of the mutation in the past and may explain the high prevalence of this particular mutation, which accounts for the most frequent genetic disorder with an autosomal mode of inheritance.
So my logic might be off but I'm thinking is it possible that these genetic changes came about at a time when everyone was forced to eat plants and grains due to huge die-offs/plagues, and they benefited from this biological "hoarding" of iron while their immune systems were damaged by anti-nutrients and viruses. That could be just me using what's in my toolbox instead of looking for a new tool though. In the end I just hope this information is already helping those with adverse reactions to the Vitamin C protocols. You're in my thoughts everyone.