Iron Not Only Bad In Excess, But Also Bad In Deficiency?

Discussion in 'Minerals' started by Gabriel, Jul 13, 2013.

  1. michael94

    michael94 Member

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    upload_2016-3-13_0-50-39.png

    dose was 100mg/kg in rats so a few fold less than that in humans, easily achievable
     
  2. paymanz

    paymanz Member

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    @marcar72 by what mechanism you think iron deficiency or anemia can cause easy bruising?

    I had that problem few years ago and I had prety high iron intake in that period.

    Was you successful resolving it?
     
  3. DaveFoster

    DaveFoster Member

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    I think you're misunderstanding the quote. He's saying that at menopause, women stop bleeding and have higher (functional) estrogen levels. Both of those factors contribute to rapid iron accumulation so they "catch-up" to men.
     
  4. DemiDee

    DemiDee Member

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    I'm sorry to be a latecomer to this incredibly important and interesting discussion. Like Isabella, I have very low ferritin (ranges between 4-7 throughout the year) though my haemoglobin levels are normal. For as long as I can remember, I've been waking up utterly exhausted, and throughout the day I am more tired than I should be whereby sometimes just walking up the stairs or getting out of my chair to go to another room feels like an effort. Like Isabella, I've had an early traumatic experience - in fact, a few - which makes me wonder if this alone can knock our bodies out of sync. Hands and feet always cold, palpitations and - most recently, hair loss in clumps during certain months of the year, and hangnails/broken jagged nails. I've recently been given a prescription for iron sulphate 200mg per day, but haven't yet redeemed it.

    FERRITIN: 7 (normal 10-420)
    Haemoglobin: 125 (normal 115-165)
     
  5. Amazoniac

    Amazoniac Member

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    It's interesting that it's possible to develop a true iron deficiency when inflammation persists:

    - Anemia and inflammatory bowel diseases

    "Compared with the average awareness of other extraintestinal disease complications such as arthritis or osteopathy, the topic of anemia in IBD has received little attention: perhaps it is so common that sometimes it is considered an unavoidable manifestation of the disease[2,3]. Although efficient therapeutic options have been developed for the treatment of IBD-associated anemia, treating anemia often has had a low priority for gastroenterologists[4]."

    "Anemia is a disease and should be approached as such. Anemia in IBD is not just a laboratory marker, it is a condition which needs a specific diagnostic and therapeutic approach. Moreover, it is a complex condition, because there are many factors which can cause anemia in IBD patients."

    "It is also common to consider that iron deficiency is an exceptional finding in IBD[2]. On the contrary, this condition is even more common than anemia, but to demonstrate it requires active investigation. In fact, iron deficiency is the main cause of anemia in IBD patients, as a consequence of dietary restrictions, malabsorption (in part as a result of inflammation), intestinal bleeding, and/or undertreatment of anemia (achieving normal hemoglobin values does not mean normal iron stores). In a recent systematic review[1], the prevalence of iron deficiency ranged from 36% to 90% (depending on the definition of iron deficiency and on the type of cohort included)[16,21,26,31-33]. In the most recent systematic review[2], mean prevalence of iron deficiency in IBD was 45%, which underlines the fact that this condition may be considered the rule rather than the exception in these patients, especially in severe cases."

    "Anemia in patients with IBD results primarily from iron deficiency because of chronic intestinal blood loss from inflamed mucosa, although in active disease more complex mechanisms involving absorption are also important[34]. However, the anemia in IBD is likely to be multifactorial in origin, frequently being the result of a combination of iron deficiency (the first cause) and anemia of chronic disease (the second major cause)[35]."

    "[..]in some patients with Crohn’s disease, impaired absorption of vitamin B12 and/or folate because of small intestinal inflammation and/or extensive bowel resection, may contribute to anemia[35], and all these conditions frequently overlap. Therefore, anemia in IBD is often complex and commonly represents a particular example of the combination of, at least, iron deficiency anemia and anemia of chronic disease, and may be a challenge even to the most astute clinician[4,24]."

    "[..]diagnosing iron deficiency in the setting of IBD may be difficult, particularly when both iron deficiency and the anemia of chronic disease are present (as previously mentioned, both conditions frequently coexist). In these circumstances, many of the laboratory measures of iron status may be unreliable, as inflammation influences parameters of iron metabolism[24,37]. For example, in the presence of chronic inflammation, the elevation in transferrin levels typical of iron deficiency may not be found, as patients with low albumin tend also to have low transferrin concentrations[38]. Similarly, iron and total iron binding capacity levels are often difficult to interpret in the presence of inflammation[35]. Finally, serum ferritin, the most accessible and well known measure of stored iron and the most powerful tests for iron deficiency[39], can be normal or even increased - in response to inflammation, as it is an acute phase reactant - even in the presence of severe iron deficiency[24]. Therefore, although at present ferritin is generally considered as the most efficient indicator of iron deficiency, this parameter may not provide adequate information about the storage compartment in the setting of inflammatory conditions such as IBD[24]. Testing for increased soluble transferrin receptor concentration distinguishes reliably between iron deficiency and anemia of chronic disease, but it is not yet widely available[40,41]."

    "Accordingly, it has been suggested that diagnostic criteria for iron deficiency need to be adapted to the level of inflammation. Thus, in patients without biochemical (C-reactive protein, etc) or clinical (diarrhea, endoscopic findings, etc) evidence of inflammation, the cut-off point for defining a low level of serum ferritin is < 30 µg/L; however, in the presence of inflammation, the lower limit of this parameter consistent with normal iron stores should be increased up to 100 µg/L[37,42]. Some authors do suggest considering the presence of ferropenia if there are low iron values and < 16% transferrin saturation[43]."​

    - Iron deficiency anemia in inflammatory bowel disease

    "Most cases of anemia in patients with IBD result from functional or absolute iron deficiency. Functional iron deficiency is a state in which there is insufficient availability of iron for incorporation into erythroid precursors despite normal or increased body iron stores[5,6]. In patients with absolute iron deficiency, iron is stored in the bone marrow. Other parts of the monocyte-macrophage system in the liver and spleen become depleted, making iron unavailable for normal or increased rates of erythropoiesis. This may occur as the result of poor dietary intake of iron, reduced iron absorption, and/or increased blood loss."

    "Signs and symptoms of iron deficiency depend on the severity and chronicity of the anemia, in addition to the usual signs of anemia, including fatigue, pallor, and reduced exercise capacity. Cheilosis and koilonychia are signs of advanced tissue iron deficiency which are not frequently seen in the modern world, due to early diagnosis and timely correction."

    "Key symptoms of anemia, such as dyspnea and tachycardia, are caused by decreased blood oxygen levels and peripheral hypoxia. Compensatory blood shifting from the mesenteric arteries may worsen perfusion of the intestinal mucosa[7]. Motility disorder, nausea, anorexia, and even malabsorption have been attributed to anemia. Reduced metabolic and energy efficiency during physical activity also contribute to weight loss in anemia[8]."

    "Central hypoxia may lead to symptoms such as headache, dizziness, vertigo, or tinnitus. Several studies have confirmed that treatment of anemia improves cognitive function[9]. Iron is a component of hemoglobin myoglobin, cytochromes, and many other enzymes. Thus, anemia negatively impacts almost every aspect of daily life in patients with IBD. Men with iron deficiency anemia (IDA) may suffer from impotence. Loss of libido contributes to impaired quality of life in both sexes[10]. In addition, latent iron deficiency may be responsible for “non-hematological” symptoms such as hair loss, paresthesias of the hands and feet, and reduced cognitive function, and may also be significantly associated with restless leg syndrome."

    "Anemia in IBD patients involves multiple pathogenic mechanisms resulting in low hemoglobin levels and compromised quality of life. Although ongoing blood loss from chronically inflamed intestinal mucosa and micronutrient deficiency (iron and B12) are the main mechanisms underlying the development of anemia in patients with IBD, chronic inflammation, hemolysis, and medication-induced myelosuppression may also play important roles in both the development of anemia and the management of this condition[12,13]. Anemia of chronic disease (ACD) and IDA are the two most common causes of anemia in patients with IBD[14,15]. Patients with IDA and concomitant ACD tend to have more severe anemia compared with patients with ACD alone[14]."

    "Up to 3-4 g of iron is stored in the human body. Around 1-2 mg of iron is lost every day through desquamation of epithelial cells of the skin, gastrointestinal tract, bile ducts, and urinary tract, and through blood loss in menstruating women[16]."​

    - Diagnosis and treatment of anemia in patients with inflammatory bowel disease

    "In IBD patients, anemia represents a systemic complication or extra-intestinal manifestation that can be multifactorial in origin (Fig. 1), but is typically caused by a combination of ID and anemia of chronic disease (ACD) [21]. It is well known that a significant number of IBD patients develop ID. A combination of chronic intestinal blood loss, dietary restrictions and/or iron malabsorption caused by mucosal inflammation or surgical bowel resections (especially in CD patients) leads to a disequilibrium of iron demand and absorption [4,11,22]."

    "In the circulation, elemental iron is almost entirely bound by transferrin and distributed throughout the body [11,23]. Iron absorption is crucially regulated by the peptide hepcidin which is principally produced in the liver [24]. It reduces iron absorption in cases of iron overload or upon induction by proinflammatory cytokines, including interleukin (IL) -6 and bone morphogenetic protein [25,26]. Notably, these proinflammatory cytokines are elevated in active IBD, while hepcidin levels can be further increased by malignancies, autoimmune diseases (e.g. rheumatoid arthritis) or chronic kidney diseases [27-29]. Elevated levels of hepcidin then result in internalization and degradation of ferroportin, leading to impaired iron absorption [30] as well as to iron retention in macrophages and monocytes [31]. Recently, several studies confirmed increased serum levels of hepcidin in IBD patients. For example, Basseri et al observed a strong correlation between hepcidin expression and proinflammatory IL-6 levels in patients with CD [32]. In line with this observation, Semrin et al demonstrated that intestinal iron absorption was decreased in CD patients with active disease compared to CD patients in remission [33]."

    "ACD represents the second major cause of anemia in IBD. Although its pathophysiology remains complex, three core mechanisms have been identified which jointly culminate in ACD: 1) iron redistribution out of the serum due to increased hepcidin levels, including retention in macrophages and monocytes (blurring the differentiation between ID and ACD, see above); 2) deficient maturation and proliferation of erythroid progenitor cells; and 3) a reduced erythrocyte lifespan [34]. Additionally, several cytokines that are overexpressed in chronic diseases, such as tumor necrosis factor (TNF)-a, IL-1 or interferon (IFN)-γ, further contribute to this process. In 1987, Roodmann et al were the first to report that TNF-a inhibits erythropoiesis [red blood cell production] [35]. It is now known that TNF-a not only directly inhibits erythropoiesis [36], but also indirectly impairs this process by downregulation of erythropoietin [37,38]. Likewise, hepcidin and IL-1 are also capable of reducing the concentration of erythropoietin [38,39]. Additionally, IFN-γ further drives the development of anemia by inhibiting erythroid colony growth [40], shortening the lifespan of erythrocytes via increased turnover in the spleen [41], and increasing apoptosis mediated by TNF-related apoptosis-inducing ligand or TNF-like weak inducer of apoptosis in erythroid progenitor cells [42,43]."

    "Aside from ID and ACD, anemia in IBD patients can result from impaired vitamin B12 and folic acid absorption. Vitamin B12 and folic acid deficiency is found in up to 33% and 29%, respectively, of patients with CD [44-47]. Reasons include dietary restrictions, as well as impairment of ileal absorption (typically through a combination of ileal inflammation, bacterial overgrowth and/or surgical resection, leading to reduced vitamin B12 and folic acid absorption) [45,46]. In UC, vitamin B12 and folic acid deficiency is less common but can occur in up to 16% and 8.6%, respectively [44-47]. Possible causes include ileal dysfunction following proctocolectomy and ileal pouch-anal anastomosis, bacterial overgrowth and reduced intestinal transit time [44,48]."

    "Normal diets usually provide sufficient iron supplies in the form of elemental and heme iron. As already discussed, in patients with active IBD, the inflammation of the mucosa leads to maldigestion, malabsorption and changing nutrition habits [33,70,71], which may aggravate ID and make exclusive nutritional supplementation impossible."

    "However, in the light of several reports of adverse events [74] and additional mucosal harm [72] in IBD patients during oral iron replacement therapy, oral supplementation must be evaluated in terms of effectiveness and tolerability [75-77]. Animal trials indicate that oral and rectal iron intake can lead to an aggravation of disease activity through the increased production of proinflammatory cytokines, such as IL-1, IL-6, TNF-a and IFN-γ [78]. This may be linked to increased flux in the classic [Fe2+]-catalyzed Fenton reaction that triggers the production of reactive oxygen species by neutrophils in the mucosa [79]."​

    - Iron - Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc - NCBI Bookshelf

    "Decreased stomach acidity, due to overconsumption of antacids, ingestion of alkaline clay, or pathologic conditions such as achlorhydria or partial gastrectomy, may lead to impaired iron absorption (Conrad, 1968; Kelly et al., 1967)."

    "Meat, fish, and poultry improve iron nutrition both by providing highly bioavailable heme iron and by enhancing nonheme iron absorption. The mechanism of this enhancing effect on nonheme iron absorption is poorly described though it is likely to involve low molecular weight peptides that are released during digestion (Taylor et al., 1986)."​

    - Temporary Strict Iron Avoidance And Its Potential Advantages


    --
    Does the presence of vit C in leaves help herbivores to absorb nonheme iron?
     
  6. Amazoniac

    Amazoniac Member

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    - Iron in red meat–friend or foe

    "The diverse mechanisms of absorption of heme iron and non-heme make these two forms of Fe definitely different in bioavailability. According to literature data, heme iron absorption from the intestinal lumen is 15-35% and it is not dependent on other food components (Turhan, Altunkaynak, & Yazici, 2004), while the non-heme iron absorption is in the range of 2-20%, and the increase or decrease of this process is influenced by a substance present in the diet, i.e. vitamin C, glutathione, meat protein, free amino acids (cysteine, serine, tyrosine), polyphenols, or other minerals (Hallberg, & Hulthén, 2000; Kongkachuichai, Napatthalung, & Charoensiri, 2002; Lombardi-Boccia, Lanzi, & Aguzzi, 2005). The level of absorption of both forms of iron, heme and non-heme, also depends on the current status of this nutrient in the body (Geissler, & Singh, 2011; Tapiero, Gaté, & Tew, 2001)."

    "[..]mechanisms of systemic iron homeostasis, to a limited extent, affect the absorption of this element in the form of heme, whereby a high intake, especially of red meat and its products, can contribute to an increase in systemic iron level (Gkouvatsos, Papanikolaou, & Pantopoulos, 2012; Schümann, 2001). In addition, there are a number of diseases causing impairment of the mechanisms regulating the iron level, which leads to an excessive absorption of this element, and its accumulation in internal organs: heart, liver, pancreas and others, and a substantial increase of ferritin levels in blood (typically from 1,000 to 10,000 ng/mL) (Bao, Rong, Rong, & Liu, 2012)."

    "On average, during the day from the body is excreted 1-2 mg of iron (Geissler, & Singh, 2011; Papanikolaou, & Pantopoulos, 2005). These losses must be supplemented by the diet. Because the bioavailability of iron from meals is on average 5-15%, Recommended Nutrient Intake (RNI) for this component is proportionally higher. The demand for iron depends on many factors. Nutrition standards for individual countries/regions of the world usually take into account variables such as age and sex. Recommended Nutrient Intake by the WHO/FAO (2004) also takes into account the iron bioavailability resulting from the traditionally consumed diet (Table 2). For the traditional European/North American diets, which includes meat (also red meat), the bioavailability is on average 15%. The bioavailability of iron from the semi-vegetarian, vegetarian, and vegan diets are correspondingly lower, and thus RNI higher."

    "[..]it should be remembered that the level of demand for various nutrients, including iron, is very individual; enterocyte absorption capacity depends on the composition of meals, as well as the current needs of the body (EFSA, 2015; Geissler, & Singh, 2011; Papanikolaou, & Pantopoulos, 2005; WHO/FAO, 2004)."

    "The first signs of an inadequate supply of iron is a general feeling of fatigue, difficulty concentrating, and increased susceptibility to infection (Geissler, & Singh, 2011; Lynch, 2011; Umbreit, 2005). Prolonged deficiency is associated with dysfunction of all proteins described in Table 1. Iron deficiency effects all systems of the body. In recent years, special attention was paid to the neurological consequences of anemia. Iron is involved, inter alia, in the synthesis of serotonin, dopamine, or norepinephrine. Insufficient levels of this nutrient in the body translates into lower neurotransmitter synthesis (Geissler, & Singh, 2011)."

    "For several years, more often, draws attention to the adverse effects of large doses of iron in the diet, which can directly cause damage to the intestinal mucosa and systemic toxicity. Because the role of this element in the body is extremely versatile, its homeostasis disorders affect nearly every system. High intake of iron, and body burden of this component, is associated with increased risk of many diseases (Zacharski, Ornstein, Woloshin, & Schwartz, 2000)."

    "Raw meat is rarely consumed. In order to obtain unique flavour attributes, improved protein digestibility, and microbiological safety, the meat is subjected to a heat treatment process. However, cooking of meat can lead to significant modifications of iron level, which depend on the type of thermal process and its parameters. Iron in meat is mainly bounded to protein structures and, thus, cooking treatment such as roasting, frying, and grilling cause the element condensation in the final product, as a result of thermal leakage. The iron content in 100 g of ready-to-eat product is 10-40% higher than in 100 g of raw material (Czerwonka & Szterk, 2015; Kongkachuichai, Napatthalung, & Charoensiri, 2002; Lombardi-Boccia, Lanzi, & Aguzzi, 2005; USDA, 2015). Simultaneously, the share of heme iron during thermal process is reduced by about 4-25% (Czerwonka & Szterk, 2015; Lombardi-Boccia, Lanzi, & Aguzzi, 2005; Lombardi-Boccia, Martinez-Dominguez, & Aguzzi, 2002; Purchas, & Busboom, 2005)."

    "According to the Schönfeldta and Hall (2011), the average bioavailability of heme iron of the meat is 23%, and non-heme is 3%. Assuming an average content form of heme in the overall iron concentration is 70% (Czerwonka & Szterk, 2015; Lombardi-Boccia, Martinez-Dominguez, & Aguzzi, 2002), and total iron content of the ready-to-eat portions of red meat (120g) is about 1.8 mg, the level of absorption of iron from red meat portions will be approximately 0.3 mg."

    Average daily loss: 1.5 mg
    How much it takes to replenish that (being conservative): i * 15% = 1.5 mg → i = 10 mg/d

    The problem is if there's a true deficiency and something is getting in the way of enhancing the absorption.
    10 mg * 8% = 0.8 mg​

    "[..]have shown that a high intake of red meat and its products, the main sources of heme, is directly related with an increase in the iron level in the body, which promotes the development of diseases such as cancer, diabetes, and cardiovascular diseases (Bao, Rong, Rong, & Liu, 2012; Hurrell, & Egli, 2010; Tappel, 2007)."


    "Selected heme-iron containing proteins and non-heme-iron containing proteins and their biological functions in the human body (Geissler, & Singh, 2011; Murray et al., 2012; Solomon et al., 2000).":

    "HEME PROTEINS

    Hemoglobin
    Oxygen transport in the body

    Mioglobin
    Oxygen handling in the muscles

    Cytochromes a, b, c
    Electrons transport in the process of oxidative phosphorylation

    Cytochrome C oxidase
    Transfer of electrons from cytochrome c per oxygen molecule (the last protein in electron-transport chain)

    Cytochrome P450
    Catalysis of hydroxylation:
    - The metabolism of xenobiotics
    - Transformation of squalene to cholesterol and cholesterol to steroid hormones and bile acids

    Duodenal cytochrome B (Dcytb)
    Reduction of Fe3+ to Fe2+ in the duodenum of mammals

    Cyclooxygenase (COX)
    Formation of prostanoids: prostaglandins, prostacyclin, thromboxane

    Catalase
    Catalysis of hydrogen peroxide decomposition (without any additional substrate)

    Peroxidases:
    Catalysis oxidation with hydrogen peroxide (H2O2 decomposition with additional substrates)

    Glutathione peroxidase
    Protection the organism from oxidative damage caused by peroxides formed during the biochemical processes

    Thyroid peroxidase
    Oxidation of iodine, iodination of tyrosine residues

    Myeloperoxidase
    Production of hypochlorous acid in neutrophil granulocytes​

    Tryptophan 2,3-dioxygenase

    Catalysis the conversion of tryptophan to kynurenine

    NON-HEME PROTEIN

    Ribonucleotide reductase
    Catalysis the formation of deoxyribonucleotides from ribonucleotides

    Aconitase
    Citric acid cycle enzymes

    Isocitrate dehydrogenase
    Citric acid cycle enzymes

    Succinate dehydrogenase
    Citric acid cycle enzymes

    NADH dehydrogenase
    Catalysis the first reaction of the mitochondrial electron transport chain

    Lipoxygenase
    Dioxygenation of PUFA containing a cis,cis-1,4- pentadiene structure; participation in the synthesis of eicosanoids: leukotrienes, lipoxins

    Dioxygenases:
    Degradation of aromatic compounds; the metabolism of xenobiotics

    Catechol 2,3-dioxygenase
    Catalysis catechol ring cleavage​

    Aldehyde oxidase

    Catalysis the oxidation of aldehydes into carboxylic acid

    Xanthine oxidase
    Catalysis the reaction: hypoxanthine – xanthine - uric acid

    Amino acid hydroxylases:
    Introduction of hydroxyl group into amino acids

    Phenylalanine hydroxylase
    Hydroxylation of phenylalanine to generate tyrosine

    Tyrosine hydroxylase

    Catalysis the conversion of tyrosine to dihydroxyphenylalanine (a precursor for dopamine, noradrenaline, adrenaline)

    Tryptophan hydroxylase
    Hydroxylation of tryptophan; involve in the synthesis of serotonin

    Prolyl hydroxylase

    Hydroxylation of proline; Formation and stabilization of collagen

    Lysyl hydroxylase

    Hydroxylation of lysine; Formation and stabilization of collagen"​

    - Iron

    Vitamin A
    Vitamin A deficiency often coexists with iron deficiency and may exacerbate iron-deficiency anemia by altering iron metabolism (15). Vitamin A supplementation has been shown to have beneficial effects on iron-deficiency anemia and improve iron nutritional status among children and pregnant women (15, 16). The combination of vitamin A and iron seems to reduce anemia more effectively than either supplemental iron or vitamin A alone (17). Vitamin A may facilitate the mobilization of iron from storage sites to developing red blood cells for incorporation into hemoglobin (15, 16). Moreover, studies in rats have shown that iron deficiency alters plasma and liver levels of vitamin A (18, 19).

    Copper
    Adequate copper nutritional status is necessary for normal iron metabolism and red blood cell formation. Anemia is a clinical sign of copper deficiency, and iron has been found to accumulate in the livers of copper-deficient animals, indicating that copper (via copper-containing ceruloplasmin) is required for iron transport to the bone marrow for red blood cell formation (20). The connection between copper availability and iron metabolism has also been established in humans; copper deficiency can lead to secondary ceruloplasmin deficiency and hepatic iron overload and/or cirrhosis (21). Oral copper supplementation restored normal ceruloplasmin levels and plasma ferroxidase activity and corrected the iron metabolism disorder in a copper-deficient subject (22). Moreover, infants fed a high-iron formula absorbed less copper than infants fed a low-iron formula, suggesting that high iron intakes may interfere with copper absorption in infants (23).

    Zinc
    Zinc is essential to maintain adequate erythropoiesis. When zinc deficiency coexists with iron deficiency, it may exacerbate iron-deficiency anemia (24). On the other hand, high doses of iron supplements, taken together with zinc supplements on an empty stomach, may inhibit the absorption of zinc. When taken with food, supplemental iron does not appear to inhibit zinc absorption. Iron-fortified foods have not been found to impair zinc absorption (25, 26).

    Calcium
    The presence of calcium decreases iron absorption from both nonheme (i.e., most supplements and food sources other than meat, poultry, and seafood) and heme sources (27). However, calcium supplementation up to 12 weeks has not been found to change iron nutritional status, probably due to a compensatory increase in iron absorption (28). Individuals taking iron supplements should take them two hours apart from calcium-rich food or supplements to maximize iron absorption.

    Iodine

    Severe iron-deficiency anemia can impair thyroid metabolism in the following ways: (1) by altering the thyroid-stimulating hormone response of the pituitary gland; (2) by reducing the activity of thyroid peroxidase that catalyzes the iodination of thyroglobulin for the production of thyroid hormones; and (3) in the liver by limiting the conversion of T4 to T3, increasing T3 turnover, and decreasing T3 binding to nuclear receptors (29). It is estimated that goiter and iron-deficiency anemia coexist in up to 25% of school-age children in west and north Africa (30). A randomized controlled study in iron-deficient children with goiter showed a greater reduction in thyroid size following the consumption of iodized salt together with 60 mg/day of iron four times per week compared to placebo (31). Additional interventions have confirmed that correcting iron-deficiency anemia improved the efficacy of iodine supplementation to mitigate thyroid disorders (reviewed in 29, 30).​

    Compensanting a functional deficiency with extra iron is a bad idea. But I'm posting these because it's possible to take a restriction too far. Also, some conditions might deplete the person over time and perhaps having enough iron is needed for the resolution of the problem.
     
  7. Amazoniac

    Amazoniac Member

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    - Advanced Nutrition and Human Metabolism (978-1-133-10405-6)

    upload_2020-1-17_8-16-57.png

    - Amino Acid Supplementation For People With Poor Digestion

    upload_2020-1-17_8-17-16.png

    "The restriction of Cys availability, particularly through inhibition of system Xc- has revealed a potential anti-cancer strategy but has also highlighted some intriguing aspects of Cys metabolism, particularly in the mitochondria. Cys depletion activates glutamine metabolism and TCA cycle anaplerosis leading to ETC flux (Gao et al., 2019)."

    "It is intriguing to consider that Cys restriction increases mitochondrial respiration given the dependence of oxidative metabolism on Fe-S clusters (Fig. 6). As noted, Cys serves as the sulfur source in the biosynthesis of these redox cofactors, and deficiencies in Fe-S cluster biosynthesis are associated with defects in oxidative metabolism (Alvarez et al., 2017; Crooks et al., 2018). This suggests that despite the disruption of Cys-dependent processes in the cytosol under Cys restriction, mitochondrial processes persist (Lo et al., 2010)."

    upload_2020-1-17_8-17-31.png

    "This would require the compartmentalized maintenance of mitochondrial Cys independent of changes in cytosolic availability. Though transport of Cys across the plasma membrane has been characterized, mediators of mitochondrial Cys transport have yet to be defined. Given that Cys exists predominantly in the form of GSH and the oxidizing nature of the mitochondria, it is likely that a significant portion of mitochondrial Cys is also stored in the form of GSH. GSH synthesis is strictly cytosolic, thus GSH must be imported into the mitochondria."​
     
  8. Ableton

    Ableton Member

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    Just my 2 cents here:

    Past 3 months were the worst of my life, health wise. ZERO ******* drive and power, hair loss, pale skin, always cold, water retention etc.
    Finally had bloodwork done and results showed im iron deficient (i drink tons of coffee and rarely eat meat)...
    Biggest giveaway for me that i might be iron deficient were angular cheilitis.

    I am feeling so much better after only 2 weeks of supping iron it's insane. I have never had such clear and awesome results taking anything. I'm well rested and can concentrate after like 6h of sleep now, before I needed like 11 for this performance lol.

    Might be a bit hypo, got high TSH. Dunno if the iron tackles that, certainly feels like it. IF you have low iron levels but don't want to supp because of peaty advice, I would advise you to try it for at least a week or something, and see if symptoms (energy, body temp, paleness whatever) improve.

    For me the question will be: When do I stop the supplementation?
     
  9. Ableton

    Ableton Member

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    Just my 2 cents here:

    Past 3 months were the worst of my life, health wise. ZERO ******* drive and power, hair loss, pale skin, always cold, water retention etc.
    Finally had bloodwork done and results showed im iron deficient (i drink tons of coffee and rarely eat meat)...
    Biggest giveaway for me that i might be iron deficient were angular cheilitis.

    I am feeling so much better after only 2 weeks of supping iron it's insane. I have never had such clear and awesome results taking anything. I'm well rested and can concentrate after like 6h of sleep now, before I needed like 11 for this performance lol. My skin is ******* glowing I can hardly believe it

    Might be a bit hypo, got high TSH. Dunno if the iron tackles that, certainly feels like it. IF you have low iron levels but don't want to supp because of peaty advice, I would advise you to try it for at least a week or something, and see if symptoms (energy, body temp, paleness whatever) improve.

    For me the question will be: When do I stop the supplementation?
     
  10. Kingpinguin

    Kingpinguin Member

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    Yeah its very common. Iron deficiency is the most common nutrient deficiency in the world. Above vitamin D, B12, magnesium, potassium etc. Still people ignore it and its role in the body. Cellular respiration depends on it. Production of the most powerful endogenous antioxidants depend on it etc... dopamine, thyroid. There comes a point where food and other supplements doesnt help.
     
  11. Steven Bussinger

    Steven Bussinger Member

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    People are overlooking the role of copper here, specifically multi-copper ferroxidases (MCF). Morley Robbins has been researching this for several years now, check out his appearances on Matt Blackburn's podcast and Extreme Health Radio. I don't agree with some of the conclusions he has come to, though.

    It's important to note that many of the symptoms attributed to "iron deficiency" in this thread actually sound like thyroid deficiency. I usually attribute angular cheilitis to riboflavin deficiency, not iron deficiency. Riboflavin is also important for hemoglobin formation, which is the true clinical marker of anemia.

    In my nascent and evolving view of this particular arena, high levels of serum copper are usually not a positive finding. They are consistent with many chronic diseases. I think it's because the copper is not being properly managed. Copper is very similar to iron and this extends to an ability to create free radicals. Morley is afraid of Metallothionein because it's an incredibly strong binder of copper, and he thinks it prevents copper from being incorporated in MCFs. But I've read in one study that is not the case, MT does release copper in appropriate situations. I need to review that, though.

    In states of copper deficiency and copper dysregulation, fatty liver occurs. A fatty liver is less functional and won't be able to convert T4 to T3. Copper supplementation has been shown to correct hemoglobin deficiency.

    It would be a more appropriate course of action to correct your copper status instead of supplementing iron. Liver has many of the nutrients involved in hemoglobin production.
     
  12. Kingpinguin

    Kingpinguin Member

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    Yeah copper certainly helps. I got my ceruloplasmin from 15 to 30 in a year just eating copper and vitamin A. Reference range was like 15-40. Improved some of mu symptoms but mosy of the fatigue it didnt touch. Only once I started Iron did my hands become warm, slept better. Slept only 6–7 hours, woke up felt rested. Didnt Even need coffee anymore. Before I slept 11 hours and still felt awfull. Couldnt get out of bed. 0 motivation. Once I started iron supplement my energy was sky high and mood was always good. Now I’m getting so much stuff done. Yeah people tend to dismiss copper or nutrient deficiencies in general. You need copper, retinol, B12, folate, magnesium, vitamin C etc but dont overlook iron either. Just because you read excess causes oxidative damage. So does almost all other minerals aswell in excess. Too little iron also causes oxidative stress.
     
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