Temporary Strict Iron Avoidance And Its Potential Advantages

Amazoniac

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Everyone is familiar with Ray's writings on the dangers of iron, and we're all accustomed to the idea of its moderate restriction. However, in some situations such as infections, a strict avoidance can also be beneficial, especially if there are antibiotics involved. In fact, if the forum had a thread named "Towards a safer antibiotic course" part of "Becoming an unwanted host", temporary* iron avoidance should be one of the priorities when it comes to getting rid of infections successfully (whoa, many repeated letters).
I suspect that starch during iron deprivation would not be as problematic for some people as it's when combined with iron, such as rice with leafy greens, potatoes, fortified wheat with dark fruit jello, bananas and molasses/unrefined cane sugar, etc.

https://www.researchgate.net/publication/47791544_Depletion_of_luminal_iron_alters_the_gut_microbiota_and_prevents_Crohn's_disease-like_ileitis

oral iron replacement therapy is poorly tolerated and may even contribute to the inflammatory processes and tissue pathology in patients with IBD
mice fed an iron sulfate containing diet or iron sulfate free diet revealed significant differences in the regulation of proteins participating in energy metabolism and stress responses when comparing inflamed with non-inflamed conditions.
[..]results suggested that the iron sulfate free diet almost completely depleted hepatic iron stores without shifting the mice to an anaemic state.
We clearly demonstrated that a diet free of iron sulfate prevents the onset of severe ileitis. Most importantly, iron repletion by weekly injections maintained the protective effect of the iron sulfate free diet, suggesting a critical role for luminal but not systemic iron in the pathogenesis of chronic ileitis in the genetically susceptible host.
[..]luminal iron depletion led to a significant reduction of ER stress in primary ileal epithelial cells. Consistently, iron exposure to cultured epithelial cells triggered ER stress responses, and as a consequence, co-culture experiments revealed a higher susceptibility of ER-stressed IEC towards cytotoxic Tcell-mediated apoptosis. These results clearly suggest that reduction of ER stress could be one of the main mechanisms by which a decrease in luminal iron exposure reduces inflammation. Recent studies indicate that ER stress responses at the epithelial cell level play an important role in the pathogenesis of IBD.(reviewed by Kaser and Blumberg15)
We speculate that an oral iron supplementation strategy may lead to an exacerbation of intestinal inflammation. There is accumulating evidence in patients with chronic inflammation that oral iron supplementation may contribute to inflammatory processes and tissue pathology because of the pro-oxidative capacity of iron.
Erichsen et al showed that oral supplementation with ferrous fumarate for patients with Crohn’s disease led to an increasing trend of the disease activity index accompanied by diarrhoea, abdominal pain and nausea. Additionally, patients had significantly decreased plasma-reduced cysteine as well as plasmareduced glutathione as possible markers of oxidative stress
Bacteria might drive oxidative and ER stress as well as apoptosis in the epithelium, and iron deprivation might induce both compositional and functional changes within the gut microbiota. Accordingly, our study revealed major alterations in microbial composition by the iron sulfate free diet, while host genotype, inflammatory response, and systemic iron application [injection] had a smaller effect. Interestingly, Desulfovibrio spp., which decreased through the iron sulfate free diet, produce toxic sulfides, which have been suggested to contribute to pathogenesis in IBD, and which have been shown to be increased in patients with ulcerative colitis.
An iron sulfate free diet induced a significant increase in the abundance of bifidobacteria, which are often used as probiotics and have been shown to prevent inflammation in murine models of IBD.
We clearly demonstrated that deprivation of luminal iron sulfate led to a significant change in microbial composition independently of systemic iron repletion.
most importantly, these data imply that systemic iron repletion in contrast to oral iron supplementation with iron sulfate should be preferred in the treatment of patients with anaemia and Crohn’s disease.

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Low dietary iron intake restrains the intestinal inflammatory response and pathology of enteric infection by food-borne bacterial pathogens

There is evidence suggesting that untargeted oral iron supplementation in regions with high prevalence of malaria transmission and infectious diseases can cause an increase in infections, hospital admission and mortality in young children [4–6]. This might be at least partly ascribed to iron also being an essential requirement for the growth of most bacterial species [7].
Importantly, iron uptake by the upper intestine is generally limited [8], which results in a large fraction of unabsorbed iron entering the colon, being potentially available for the gut microbiota. It is therefore not surprising that iron has been shown to influence the gut microbiota composition in a number of studies, among which were two studies among African children and infants which showed that iron fortification caused a potentially more pathogenic gut microbiota profile [9–11].
Importantly, also iron deficiency is associated with an impaired immune response, but may remarkably increase the resistance against intracellular pathogens, probably due to increased nutritional immunity [6, 16, 17].
Interestingly, mice on the iron-deficient diet seemed to recover most quickly as only this group had at day 28 an average body weight that was above that of day 14, while mice on a diet with normal iron content tended to suffer most from the colitis.
findings suggest that the intestinal inflammatory response was blunted in both the iron-deficient and high-iron diets.
[..]This analysis shows that during infection mice that were held on the iron-deficient diet were able to maintain part of their gut microbial diversity.
Together, these analyses show that dietary iron had a large impact on the mouse gut microbiome, especially during intestinal inflammation.
These data confirm a subtle, but reproducible, protective effect of low dietary iron intake on the pathology of enteric infection. Importantly, these data also confirm that iron can increase the virulence of an enteric pathogen as we previously showed in vitro [32].
*
Interestingly, previous studies showed that non-infected rats on an iron-deficient diet for 5 weeks gained less weight and ate less, while also mice on an iron-deficient diet had a lower body weight compared to control mice after 12 weeks of intervention [40, 41]. This suggests that an iron-deficient diet in a non-inflamed situation tends to decrease weight gain on the longer term, while it may prevent weight loss during intestinal inflammation.
In summary, our descriptive data suggest the existence of a maximum in the inflammatory response with regard to dietary iron content, with the peak lying around the normal daily intake of iron, something which has not previously been described in literature. Mainly the iron-deficient diet dampened the intestinal inflammatory response, and which also seemed to lower intestinal pathology. The latter was however more evident in our simple nematode gut model, in which iron-limitation restrained pathology as reflected by a prolonged survival of C. elegans that foraged on the intestinal pathogen S. Typhimurium under iron-limitation. Furthermore, it confirms that supplementary iron can enhance the virulence of S. Typhimurium as we previously have shown in vitro [32]. These findings underscore an undesired combination of a possible increase in the virulence of intestinal pathogens, and a decrease of host intestinal defenses at the same time. This undesired combination may provide intestinal pathogens with increased opportunities to evade the host immune response during oral iron therapy and strengthens the idea that oral iron administration programs in developing countries need to be set up with the highest amount of care, with close monitoring until the remaining questions about the actual effect of iron at the intestinal host-microbiota interface have been unraveled.

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Iron Availability Increases the Pathogenic Potential of Salmonella Typhimurium and Other Enteric Pathogens at the Intestinal Epithelial Interface
 
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Makrosky

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Thanks Amazoniac!

Beef liver has quite a decent ammount of iron .... :-|
 

Makrosky

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@Amazoniac might I suggest you to put on bold the parts you find most relevant when you publish this kind of posts? Just as your idol* haidut does. It would be greeeeeat!! :):

* Yes, I know you have teenage posters in your room like pop stars but with haidut's face.
 

Amazoniac

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@Amazoniac might I suggest you to put on bold the parts you find most relevant when you publish this kind of posts? Just as your idol* haidut does. It would be greeeeeat!! :)

* Yes, I know you have teenage posters in your room like pop stars but with haidut's face.
I usually avoid highlighting on purpose since those are already selected parts. In my opinion it's a bit distracting unless there's a detail that might pass unnoticed. But thank you for the suggestion as it can indeed appear monotonous..
I don't have a poster yet, only a tattoo that required me to think a lot on how to divide Idealabs for each butt cheek.
 
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Amazoniac

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I recently shared a link about a team of researchers activating dormant microbes with energy and iron but also magnesium. I suppose that this is relevant for those that are trying to eradicate some fungal (mitochondria) problems.

Magnesium in biology - Wikipedia
Magnesium is very important in cellular function. Deficiency of the nutrient causes disease of the affected organism. In single-cell organisms such as bacteria and yeast, low levels of magnesium manifests in greatly reduced growth rates. In magnesium transport knockout strains of bacteria, healthy rates are maintained only with exposure to very high external concentrations of the ion.[26][27] In yeast, mitochondrial magnesium deficiency also leads to disease.[28]

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Magnesium and control of yeast growth and metabolism - DORAS - DCU
Ray Peat Glossary - Ray Peat Forum Wiki
THE EFFECT OF MAGNESIUM AND CALCIUM ON YEAST GROWTH - Saltukoglu - 2013 - Journal of the Institute of Brewing - Wiley Online Library
 

Amazoniac

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Related to the previous post:

Treatment & prevention of side effects induced by oral, high-dose magnesium therapy of mental illnesses (by burtlan's mentor)

"Concentrated magnesium solutions without calcium exponentially worsen Candida albicans infections of the upper and lower gastrointestinal tract, increase rhinovirus release up to 310-fold at 30 mM concentration and greatly increase herpes-simplex viral count."​

Magnesium is required by various organisms, it's silly to think that it can't feed gut infections. The solution is not to starve yourself to clear them, but to spread a single massive dose in multiple doses to maximize absorption.

People who had a great part of their intestines resected benefited more from magnesium (bis)glycinate than oxide. I'm commenting this because even though various forms can provide similar amounts of magnesium, some might be absorbed earlier and this can be another point to consider.

Bioavailability Magnesium Diglycinate vs Magnesium Oxide in Patients with Ileal Resection
 
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