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post #1 of 26 (permalink) Old 09-03-2010, 06:58 PM Thread Starter
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Iron??


I went to the doctor and found out I am deficient in iron. Lately I have been very fatigued, feeling more depressed and my heart has been pounding. He ran a bunch of tests and it showed I'm low in iron. I did some reading when I got home and found some very interesting findings dealing with iron and serotonin/dopamine that I didn't expect. My SA seems to be getting worse and it appears iron has a big role in "neurotransmitters production and function, mainly in the dopamine-opiate systems". Here's one of the pages I read. Any thoughts??

http://moodfoods.com/iron.html



I also found some other stuff too...."Parkinson's disease (PD) is characterized by the selective loss of dopaminergic neurons in the substantia nigra (SN), and it has been suggested that dopamine is one of the main endogenous toxins in the genesis of PD. We demonstrated that thiol antioxidants (the reduced form of glutathione, N-acetyl-L-cysteine, and L-cysteine), which conjugate with one dopamine oxidation intermediate, o-quinone, provided almost complete protection from dopamine-mediated toxicity in SH-SY5Y, a human neuroblastoma cell line. In contrast, catalase partially provided protection against cell death caused by dopamine. These data suggest that the generation of dopamine oxidation intermediates, rather than hydrogen peroxide, plays a pivotal role in dopamine-induced toxicity. Iron accumulated in the SN of patients with PD can cause dopaminergic neuronal degeneration by enhancing oxidative stress. However, we found that iron reduced the total amounts of dopamine oxidation intermediates and enhanced the formation of melanin, a final product of dopamine oxidation. Also, addition of iron inhibited dopamine-induced cytotoxicity. These results suggest that iron can provide protection when it accelerates the conversion of dopamine oxidation intermediates."


Iron and Dopamine Abnormalities

The brains of patients with RLS exhibit abnormalities in the relationship between iron and dopamine. An enzyme involved in dopamine synthesis—tyrosine hydroxylase—requires iron for proper function. In animal studies, iron insufficiency appears to cause abnormal dopamine function (Allen RP et al 2001a). It is believed that patients with RLS may have impaired iron absorption in the brain (Connor JR et al 2003). The iron deficiencies are pronounced in certain parts of the brain that help control body movement. In autopsies of people with RLS, iron levels have been particularly low in a region of the brain called the substantia nigra (Connor JR et al 2003).
Further evidence of the relationship between iron deficiency and RLS is found in the three major secondary causes of RLS—end-stage renal disease, pregnancy, and iron deficiency, which all involve low levels of iron (Allen RP et al 2001b).

Iron deficiency decreases dopamine D1 and D2 receptors in rat brain.

Erikson KM, Jones BC, Hess EJ, Zhang Q, Beard JL.
Department of Nutrition, Graduate Program in Nutrition, The Pennsylvania State University, S-126 Henderson Building, University Park, PA 16802, USA.
Abstract

Iron deficiency (ID) in early life is known to alter neurological development and functioning, but data regarding specific effects on dopamine biology are lacking. The objective of this study was to determine the extent of functional alterations in dopamine receptors in two dopaminergic tracts in young, growing, iron-deficient rats. Forty male and 40 female weanling Sprague-Dawley rats were fed either an iron-deficient (ID) diet or control (CN) diet for 6 weeks. ID decreased densities of D(1) and D(2) receptors in the caudate-putamen and decreased D(2) receptor densities in the nucleus accumbens. There were no apparent effects of ID on the affinities for the ligands in either receptor in several brain regions. In situ hybridization studies for both dopamine receptors revealed no significant effect of ID on mRNA expression for either receptor. Iron-deficient rats had a significantly higher ED(50) for raclopride-induced hypolocomotion in male and female rats compared to control rats of each sex. The loss of iron in the striatum due to dietary ID was significantly correlated with the decrease in D(2) receptor density; however, this relationship was not apparent in other brain regions. These experiments thus demonstrate abnormal dopamine receptor density and functioning in several brain regions that are related to brain regional iron loss. Importantly, the impact of ID on dopamine was more pronounced in males than females, demonstrating sex-related different sensitivities to nutrient deprivation.

Last edited by saosin80; 09-03-2010 at 07:13 PM. Reason: Forgot Link
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post #2 of 26 (permalink) Old 09-04-2010, 03:52 AM
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All I have to say is, people should be very careful supplementing iron if they haven't been diagnosed with a deficiency!
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post #3 of 26 (permalink) Old 09-04-2010, 05:15 AM Thread Starter
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Quote:
Originally Posted by Duke of Prunes View Post
All I have to say is, people should be very careful supplementing iron if they haven't been diagnosed with a deficiency!

yeah, I'm not telling anyone to go out and start taking Iron. I was diagnosed with having low iron so I'll be taking a supplement. I just thought that stuff I read was very interesting but I guess I'm the only one lol
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post #4 of 26 (permalink) Old 09-04-2010, 07:54 AM Thread Starter
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Quote:
Originally Posted by LaRibbon View Post
This is fascinating because I seem to have chronic low iron (diagnosed by a dr).

*edit*
And come to think of it, I had a major bout of anemia when I was 15 which was right before I developed bad SA. However I also went to a new school which stressed me out at that time..so idk what happened really.

I too have probably had chronic low iron for awhile too. I've had Ulcerative Colitis for years now which can cause iron to be low because of bleeding. My SA did start to really surface after my first flair of Ulcerative colitis and blood loss. I didn't realize Iron is so important when it comes to neurotransmitters like dopamine
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post #5 of 26 (permalink) Old 09-04-2010, 07:59 AM Thread Starter
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Here is someone talking about anxiety and low iron...

Does low Iron/Ferritin cause heart palpitations and anxiety? Gosh, does it EVER cause anxiety. At least for me. I was/am only mildly anemic and had to see an acupuncturist for the anxiety/panic attacks. In fact, I was also so anxious, I developed bruxism to the point where I had to get a night guard because I had developed terrible tooth pain. (When I went to the dentist and he asked if I was under stress, I decided then and there that anemia DOES cause all this anxiety - it's just too freakin' weird how it all hit at once like that.)

I've always had occasional benign heart palps (verified by recent tests), but when the anemia got bad enough, I had a scare where I had to call 911 because my heart was racing so badly after walking up a flight of stairs. Until I started the iron supplement, I was having major heart flutters which my doctor wanted to chalk up to peri-menopause. I haven't had a single incident since starting the iron, so it's the anemia, I am certain of it.

I acknowledge that part of my anxiety *might* be due to simply reckoning with the diagnosis of anemia and how it scared me. (That was a baaaaad week.) But the tachycardia on the stairs happened independent of the diagnosis and it all made sense once the blood work was done and the diagnosis was confirmed. If I look back on it, I was also very fatigued leading up to the stairs incident.

I think if you were to take a poll here, many would agree that these symptoms can be caused by anemia. Can it also be due to other causes such as those you mentioned? I would think so too. Have you had your thyroid checked?
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Iron, Neurotransmitters and the Brain

Sachin Gupta MD




T2* MRI distribution of Brain Tissue Iron Stores




Decreased Neurotransmitter Levels in IDA

  • Iron deficient anemic women and rats had elevated plasma NE levels
    • rapid loss of NE from peripheral sympathetic nervous system pools

  • Iron deficiency decreases monoamine uptake mechanisms

  • In-vivo microdialysis in rats provided evidence for decreased rates of uptake of NE




DA / NE transporters and Iron

Dose response relationship between iron chelation and expression of the DA and the NE transporter

* Weisinger, J., Connor, J. R. & Beard, J. L. (2002) Iron chelation alters dopamine transporter expression in cell culture models. FASEB abstract from EB2002

Desferal

Desferal

PC12 – pheochromocytoma cells

N2a – neuroblastoma cells




DOPAMINE RECEPTORS




Dietary Iron deficiency and Neurotransmitters in the brain

DOPAMINE TRANSPORTERS and RECEPTORS

  • Regional brain iron deficiency leading to heterogeneous effect on DA neurobiology

  • Extracellular DA and NE elevated in brains of iron-deficient rats

  • Decrease in density of D2 and D1 receptors and DA transporters in striatum




Iron deficiency and Neurotransmitters in the brain

SEROTONIN TRANSPORTERS

  • Serotonin transporter density significantly lower in brains (striatum) of iron deficient mice




Iron in Neurotransmitter Metabolism

  • Essential for enzymes involved in neurotransmitter synthesis
    • tryptophan hydroxylase (serotonin)
    • tyrosine hydroxylase (NE and DA)

  • Cofactor for ribonucleotide reductase
    • electron transfer reactions related to lipid metabolism and brain-energy metabolism




Iron in Neurotransmitter Metabolism

  • Activity of monoamine oxidase
    • an enzyme critical for proper rates of degradation of neurotransmitters
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Info on ADHD and low iron


ADHD Causes - Iron Deficiency

By Dr. Yannick Pauli
Dr. Yannick Pauli
Level: Platinum

Dr. Yannick Pauli is the Director of Centre Wellness NeuroFit in Lausanne Switzerland. He is the founder of Brain Potential, a rehabilitation program that combines ...

Article Word Count: 559 [View Summary] Comments (0)


Although a deficiency in neurotransmitters may be the most "obvious" biological cause of attention deficit hyperactivity disorder, doctors do not bother investigating what could be causing this deficiency. Instead, they treat the symptom with stimulant medications that give short-term improvements in behavior at a long-term cost. Before any treatment for ADHD is put into place, there must be an effort to identify all the possible causes of the disorder, instead of being simply satisfied with suppressing the symptoms.
A growing number of research points to a link between iron deficiency and ADHD in children. In fact, iron deficiency is one of the most common nutrient deficiencies among American children. This discovery makes sense - iron is an important mineral needed to produce neurotransmitters. It is also responsible for regulating the activity of dopamine, the neurotransmitter that handles attention and movement. Too much or too little dopamine causes chronic inattention and hyperactivity, and with too little iron to regulate its release, it's no wonder so many schoolchildren experience behavior and attention problems.
Did you know that iron deficiency can occur as early as pregnancy? If a pregnant woman has too little iron in her body, the developing fetus in the uterus may suffer from intrauterine growth retardation as well as increased risks of complicated childbirth. What kind of milk you give to your child will also determine the iron content in his or her body. Cow's milk not only contains very little iron, it is difficult for a baby's body to absorb what little iron there is in cow's milk. Assuming that the mother carries a healthy amount of iron in her body, breast milk is the best source of iron for a growing infant. Finally, the poor eating habits of children and teenagers also put them at risk for iron deficiency.
Researchers believe that there is a relationship between iron deficiency in infanthood and poor school performance and delayed brain development in childhood. A study done in France in 2004 concluded that children with low iron levels were the most inattentive, impulsive, and hyperactive among the participants. Their conclusions show that iron deficiency can account for as many as 30% of ADHD cases.
Besides behavioral and developmental problems, a child with an iron deficiency is also at great risk for absorbing toxins. Children with low iron levels have been found to easily absorb heavy metals like cadmium, lead, and mercury. In fact, toxicologists have observed a correlation between low iron stores and high blood levels of lead in children.
Although the link between iron deficiency and ADHD symptoms seems to have been determined, very few researchers have explored using iron to treat the disorder. One study performed in Israel has shown promising results: after giving iron supplements to 14 boys with ADHD for 30 days, their parents found remarkable improvements in their children's behavior. This study suggests that hyperactive and inattentive behavior can be treated if the child's iron deficiency is corrected.
As promising as this finding might seem, don't go around treating an iron deficiency yourself! If you suspect that your child might have an iron deficiency, have him or her tested for blood mineral content and consult a physician for the appropriate dosage. Excess iron in the body is toxic and remains in the system for a very long time, aggravating neurological problems and causing other disorders.
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post #8 of 26 (permalink) Old 09-04-2010, 08:12 AM Thread Starter
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Iron Deficiency’s Long - Term Effects

Abstract: Betsy Lozoff is among the world’s leading experts on iron deficiency and its effects on infant brain development and behavior. Iron deficiency is the most common single nutrient disorder in the world, affecting more than half of the world’s infants and young children. Research by Lozoff and others has shown that there are long-lasting developmental disadvantages among children who experienced severe, chronic iron deficiency as infants—disadvantages that are not corrected by giving iron later.
Council Member Betsy Lozoff a developmental-behavioral pediatrician, is a professor of pediatrics in the Department of Pediatrics and Communicable Diseases at the University of Michigan Medical School and former director of the University’s Center for Human Growth and Development. Her research focuses on iron deficiency anemia and infant behavior, primarily in developing countries, and the health and development of children who grow up in poverty in the U.S. Her recent research seeks to relate behavioral changes to the effects of iron deficiency on the developing brain. She has served on several review panels for the National Institutes of Health and the National Institute of Child Health and Human Development, as well as on the Executive Council of the Society for Developmental and Behavioral Pediatrics. She was a member of the Committee on Integrating the Science of Early Childhood Development for the Institute of Medicine and the National Research Council of the National Academy of Sciences.
For many years, you have studied the link between iron deficiency in children and their long-term health and development. What can you tell us about that connection and how it affects the growing brain’s architecture?
We know that the human body needs iron to perform some of the most basic and essential functions. It needs iron to manufacture hemoglobin—the protein in red blood cells that carries oxygen throughout the body. It needs iron for proper muscle function, too. And—most relevant to this discussion—the body needs iron to carry out many critical processes in our brain and central nervous system.
When it comes to the growing brain, we’re learning pretty definitively that the right level of iron is required for healthy neurotransmission, or the way the brain sends and receives “signals” from one area to another. Iron is essential for myelination—the process by which the brain produces a fatty insulation around the nerves. The insulation helps speed transmission of electrical signals. Based on studies of lab animals, we know iron has clear effects on the function of dopamine and probably serotonin, two brain chemicals that help send and receive signals (neurotransmitters) and have many roles in the brain. When iron deficiency anemia occurs in the young animal, important changes in both myelin and neurotransmitters persist to adulthood, despite iron therapy in infancy. We have to make a bit of a leap, but we can say that the behavioral changes we see in children who had iron deficiency in infancy are consistent with the brain effects we’re finding in animals. Children who suffered iron-deficiency anemia as infants have evidence of brain differences 10 years later.
Iron-deficiency anemia is considered the most common nutritional disorder in the world today, but we’ve managed to dramatically reduce its incidence among infants in the United States. What are some proven solutions?
In the U.S. and most economically developed countries, we have dramatically reduced anemia and iron deficiency through a few widespread interventions. From a clinical standpoint, this is a problem that can be solved if the community makes it a priority.
As late as the 1970s, we in the U.S. had levels of iron deficiency in infants on a par with much of the developing world. Federal government programs like Food Stamps and WIC (supplemental nutrition for Women, Infants and Children) started to make a big difference. In addition, baby formula companies started producing and marketing iron-fortified formula, prompted largely by calls from the American Academy of Pediatrics. Major cereal companies began adding iron to baby cereals. More vitamin C (also known as ascorbic acid, which enhances the body’s ability to absorb iron from the intestines) was added to infant foods. There was a big effort to encourage breast feeding; the iron in breast milk is easily absorbed. Another solution for infants and children at greater risk of iron deficiency is the use of iron-fortified drops, also readily available. Together, these interventions have worked well for U.S. children.
Your work with children in Costa Rica and Chile has yielded very important findings.
We’ve now been following our research group of children in Costa Rica for more than 20 years. All those who had iron deficiency in infancy were treated with a closely supervised full course of iron therapy, which corrected all cases of iron-deficiency anemia.
And here’s what we’ve been learning. When it comes to their motor development, children who had chronic, severe iron deficiency in infancy started with lower motor functioning and stayed lower over time; there’s no evidence they catch up with their peers. In terms of social-emotional functioning, in early adolescence their parents and teachers rated them as showing significant symptoms of anxiety, depression, and *inattention. At ages 11 to 14, the proportion repeating a grade in school was twice that of children who had good iron status in infancy. In terms of cognitive skills, the evidence is especially troubling: the gap in test scores actually increased over time. By late adolescence, the gap was bigger, regardless of whether they started with low or high scores as babies. The cognitive gap was also worse for those children from the most disadvantaged families who also had chronic, severe iron deficiency in infancy.
By failing to solve this problem for millions of youngsters around the globe, aren’t we risking that they won’t meet their full potential?
In Chile, we’re finding that even after treatment for a year with iron drops, children who suffered iron-deficiency anemia as infants have evidence of brain differences 10 years later. Using electrophysiologic tests, we’ve been able to “look” into their brains and find that electrical signals move more slowly through their auditory and visual systems. Both the Costa Rican adolescents at 19 years and the Chilean children at 10 years who were treated for severe, chronic iron deficiency in infancy do worse on higher-level cognitive tests shown by functional magnetic resonance imaging (fMRI) to involve specific neural circuits where dopamine is the major neurotransmitter.
These long-term effects make us even more worried about how they’ll do in adulthood. So we are looking at how the consequences of early iron deficiency might impact the kinds of jobs the Costa Rican subjects get as young adults, how much money they earn, and what kinds of relationships they establish. We hope to do the same for the Chile sample.
So clearly the implications are quite serious.
The evidence is certainly accumulating: There are effects of iron deficiency that are not reversed with iron therapy. It’s very important to prevent the brain from being iron deficient in the first place—during its most sensitive time of development, in early childhood.
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post #9 of 26 (permalink) Old 09-04-2010, 08:15 AM Thread Starter
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Effects of iron deficiency on iron distribution and gamma-aminobutyric acid (GABA) metabolism in young rat brain tissues.

Li D.
Department of Hygiene and Preventive Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
Abstract

Effects of iron deficiency on the distribution of iron and glutamate decarboxylase (GAD), gamma-aminobutyric acid transaminase (GABA-T) activities and GABA concentrations in different brain regions in young rats were investigated. Iron deficiency was induced by feeding an iron-depleted diet (0.32mg/100g) in weanling rats for 3 weeks or 6 weeks. The values of hemoglobin (Hb), hematocrit (Ht) and red blood cells (RBC) decreased with the progress of anemia. The concentrations of serum iron in the rats fed iron-depleted diets were lower than those of corresponding controls. On the other hand, the concentrations of total iron-binding capacity (TIBC) and unsaturated iron-binding capacity (UIBC) in serum were higher than those of corresponding controls. These results showed that hypochromic and typical iron-deficiency anemia had occurred in these rats. At the same time, iron deficiency also resulted in significantly low iron concentrations in the brain, especially in the hypothalamus, midbrain and thalamus, and striatum and hippocampus. Although the changes in GABA concentrations in corresponding brain regions were not observed, the activities of the GABA-synthesizing enzyme GAD and GABA-degrading enzyme GABA-T of the rats fed iron-depleted diets for 6 weeks decreased significantly. This study provides evidence that iron deficiency in the brain could change the utilization and metabolism of GABA.
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post #10 of 26 (permalink) Old 09-04-2010, 08:19 AM Thread Starter
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Restless Legs: The Iron Connection

Before you rush out to buy the latest expensive prescription drug for “restless legs,” you might consider that one cause of this condition is iron deficiency.1 The prescription drugs used to treat restless legs stimulate the function of dopaminergic neurons. Iron deficiency is known to cause a reduction in dopaminergic activity (as well as a rise in serum prolactin).2
Many people these days have reduced their intake of red meat, the best dietary source of iron. White meat (such as poultry) contains much less. Moreover, those who eat a diet rich in polyphenols—as are found in fruits, in vegetables, and in green, black, and oolong tea, etc.—may be absorbing much less than the quantity of iron they ingest because of the potent iron-chelating properties of many polyphenols (such as quercetin). If you are eating a diet like this and have developed restless legs, it is quite possibly due to iron deficiency.
In a recent study,1 rats were fed diets that were either iron-deficient (ID) or iron-adequate (CN). Another group of ID rats was given iron supplements (IR). Studies were done on the dopamine, serotonin, and noradrenaline transporter binding in various brain areas. The results showed that ID male rats (but not ID females) had a decrease of 20–40% in dopamine transporter binding in the nucleus accumbens, caudate putamen, and substantia nigra. ID males also had a 20–30% reduction in serotonin transporter binding in the nucleus accumbens, olfactory tubercle, and colliculus, while ID females had 15–25% increased serotonin transporter binding in the olfactory tubercle, zona incerta, anteroventral thalamic nucleus, and vestibular nucleus. [It is possible that this increased serotonin transporter binding is linked to increased sensitivity to depression in females, at least in those who are iron-deficient, since the serotonin reuptake inhibitors, such as fluoxetine (Prozac®), inhibit the serotonin transporter.] Iron deficiency reduced binding to the noradrenaline transporter in the locus ceruleus and anteroventral thalamic nucleus in ID and IR males but not females. Some, but not all, of the changes induced by iron deficiency were reversed by iron supplementation.
The authors state, “This experiment extends our knowledge to include the olfactory tubercle as a tissue sensitive to iron deficiency. This might implicate iron deficiency in endocrinological difficulties such as hyperprolactinemia.” Prolactin is regulated by dopamine. High levels of prolactin stimulate the growth of breast and prostate tissue; they may thus be a risk factor for developing breast and prostate cancers and would certainly stimulate the growth of such cancers.
We became interested in the connection between iron deficiency and restless legs when Sandy developed the latter condition. It has been completely eradicated with daily RDA-level iron supplementation. Iron supplements should be taken at separate times from other supplements because of the possibility of chemical interactions with vitamin C, resulting in free radical generation, or with irreversible binding to polyphenols, especially quercetin. We suggest using ferrous gluconate; iron-EDTA chelates produce hydroxyl radicals very efficiently in the presence of vitamin C, and ferrous sulfate can be quite irritating.
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post #11 of 26 (permalink) Old 09-04-2010, 08:37 AM Thread Starter
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Iron and Dopamine Abnormalities

The brains of patients with RLS exhibit abnormalities in the relationship between iron and dopamine. An enzyme involved in dopamine synthesis—tyrosine hydroxylase—requires iron for proper function. In animal studies, iron insufficiency appears to cause abnormal dopamine function (Allen RP et al 2001a). It is believed that patients with RLS may have impaired iron absorption in the brain (Connor JR et al 2003). The iron deficiencies are pronounced in certain parts of the brain that help control body movement. In autopsies of people with RLS, iron levels have been particularly low in a region of the brain called the substantia nigra (Connor JR et al 2003).
Further evidence of the relationship between iron deficiency and RLS is found in the three major secondary causes of RLS—end-stage renal disease, pregnancy, and iron deficiency, which all involve low levels of iron (Allen RP et al 2001b).
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post #12 of 26 (permalink) Old 09-04-2010, 08:50 AM Thread Starter
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IRON
Iron is one of the metals that the body needs in order to maintain good health. In fact,
an imbalance of iron in the body, meaning too little or too much of it, can lead to Alzheimer’s disease.
Although it is vitally important in creating hemoglobin, which transports oxygen from the lungs to the body’s cells and returns carbon dioxide back to the lungs, most iron is used by the brain. 80% of the iron found in the brain was deposited there in the first years of life. When iron deficiency in childhood prevents this from happening, Alzheimer’s disease later on in life may be the result.
Iron deficiency or overload is a heavy metal nutrient disorder. Deficiency can be caused in three specific ways: inadequate dietary intake, poor absorption caused by digestive distress, or by chronic bleeding. Women tend to need more iron than men because they lose iron every month in their menstrual blood. Undiagnosed bleeding can also cause blood loss. Examples are blood loss from intestinal lesions that result from the chronic use of pain medications like NSAIDS (asprin), or from certain parasites that feed off their host causing blood loss, or bleeding hemorrhoids. The elderly, or others who take a lot of asparin for pain have the greatest risk of a developing an iron deficiency disease later on in life.
The best source of dietary iron is found in meat, fish, and poultry. However, many vegetables have iron in them, as well. Listed in order from highest to lowest content, they are:
Kelp, sunflower seeds, Jerusalem artichokes, brewers yeast, millet, Brazil nuts, wheat bran, almonds, beet greens, pumpkin seeds, dried prunes, dandelion greens, squash seeds, cashews, english walnuts, wheat germ, raisins, dates, cooked dry beans, green peas, broccoli, sesame seeds, hulled brown rice, whole wheat bread, pecans, ripe olives, cauliflower, peanuts, artichokes, tofu, and mung bean sprouts.
The absorption of iron is increased by vitamin C and reduced by calcium, which competes with it for uptake by receptor sites. Calcium may decrease iron absorption by up to 50% for the remainder of the day. Iron also competes with zinc for uptake. These two metals are often found together in the same foods, which is one of the ways the body regulates absorption.
Children who are deficient in iron do not have enough of it in their brains. All of the body’s cells require adequate iron for normal functioning. It is involved in the creation of dopamine, seratonin and GABA, which are neurotransmitters that regulate mood, attention, and create feelings of peace and calm.
The most prominent feature of deficiency is to slow down the neurotransmission of nerve signals in the dopamine neurons in various parts of the brain.
The consequence of diminished dopamine is an alteration in behavior. In children, it reflects as hyperactivity, inattention and behavior problems. Lack of dopamine in adults, which can be caused by numerous things, creates a craving for methamphetamines, caffeine, and sugar, for both of these chemicals temporarily increase dopamine levels in the brain, giving one that customary feeling of being turned on, alert, and ready for action, and like one has turned on all the “lights“ and can finally see.
In middle age, iron deficiency can also cause lethargy, fatigue, irritability, listlessness, apathy, shortened attention span, and inability to concentrate. This results from lack of oxygen in the body, as well as reduced dopamine. In children, iron deficiency can produce a permanent decrease in IQ, which reduces their ability to learn. Iron deficiency disease is the most prevalent nutritional disorder in the world.
Because too much iron can also be a problem, Iron absorption is tightly regulated by the body according to need. Excess iron is stored in the liver, pancreas, pituitary, adrenals, heart, and skeletal muscles. When the body gets too much iron, which can only happen through over supplementation, or through a genetically caused disease process called hemochromatosis, it leaches out of its storage sites and moves into the blood stream where it is taken to the brain. Too much iron in the brain destroys neurons, leading to neurodegenerative diseases and neurological dysfunction, with Alzheimer‘s like symptoms. So here is a case where either too much or too little of a substance cause the same symptoms.
Because too much iron causes Alzheimer’s symptoms, one should never supplement with iron unless they know, via blood test or hair analysis, if they have a deficiency.
If they do decide to supplement, only small amounts should be taken at once. Iron fumerate and/or iron sulfate are better sources than iron sulfate, which is not well absorbed. Ferrous lactate also absorbs well. Or better yet, buy ionic forms of iron that are instantly absorbed through the stomach lining. Whichever you choose, don’t over do it. Iron levels will restore themselves only slowly over time, so be patient as you take your supplements, and monitor the results with blood tests or hair analysis.

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post #13 of 26 (permalink) Old 09-06-2010, 07:33 AM Thread Starter
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Iron, serotonin and anxiety and depression

posted Thursday, 29 January 2009


Vanderbilt University Medical Center investigators have found a surprising link between brain iron levels and serotonin, a neurotransmitter involved in neuropsychiatric conditions ranging from autism to major depression.
Appearing in the Proceedings of the National Academy of Sciences this week, the study by Randy Blakely, PhD, and colleagues also demonstrates the utility of a powerful in silico (performed on computer or via computer simulation) approach for discovering novel traits linked to subtle genetic variation.
The serotonin transporter protein (SERT) regulates serotonin availability in the brain and periphery, and variations in human SERT have been linked to many neurobehavioral disorders - including alcoholism, depression, autism and obsessive-compulsive disorder. SERT is also a major target for medications like the selective serotonin reuptake inhibitors (SSRI) used for treating depression.
Thanks to a serendipitous mix-up in an animal order, Blakely and first author Ana Carnerio, PhD, discovered that a mouse strain they had been using to studying SERT function - called C57BL/6 - actually carries a mutation that reduces the function of the transporter.
"Importantly, low-functioning variants of human SERT have been associated with anxiety, depression, and reduced efficacy of SSRI medications," notes Blakely, senior author and director of the Vanderbilt Center for Molecular Neuroscience.
By querying an online resource called the Mouse Phenome Database, they found that most mouse strains possess a SERT version called "ER" - which is identical to the sequence found in human SERT. A small number of strains, however, including the commonly studied C57BL/6 strain, carry a different version (called "GK").
Carneiro realized that she could utilize her identification of SERT GK to elucidate new aspects of brain chemistry and behavior. Vanderbilt collaborator David Airey, PhD, helped Carneiro and Blakely exploit a separate panel of mice where the SERT GK variant is presented on many different genetic backgrounds - a so-called "recombinant inbred" population termed BXD mice.
Using lines from this population, the team found that SERT GK mice performed differently than SERT ER mice on tests of anxiety and depression, consistent with reduced function of SERT GK. Importantly, a public database of anatomical, biochemical and behavioral features exists for all mice in the BXD population, allowing Blakely and colleagues to identify novel traits linked with the low functioning SERT. From this in silico approach, Blakely and colleagues identified multiple trait differences affected by the SERT GK/ER variation, including traits associated with alcohol consumption and brain dopamine signaling.
Additionally, they found that iron levels in the brains of mice with the GK variant were significantly higher than in the ER variant mice. Iron is required to synthesize both serotonin and dopamine, and serotonin receptors are known to regulate iron-carrying proteins. But SERT had not been previously shown to control brain iron levels. Follow-up studies with mice where the SERT gene was eliminated (SERT "knock-out" mice) verified a critical role for the transporter in controlling brain iron levels.
"Because SERT is such an important drug target in treating anxiety, depression and OCD, we need to stop and think about how iron might be influencing these disorders," Blakely said. The study also demonstrates the power of an in silico approach - combined with traditional experimentation - in understanding how genes affect complex traits.
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post #14 of 26 (permalink) Old 09-06-2010, 11:49 AM
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I never supplement iron
the best way is leeched iron from cast iron pans when cooking
also by the way my cast iron pan is more "Non stick" then a teflon pan



maybe it's becoming a big issue after the switch to Teflon pans
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post #15 of 26 (permalink) Old 09-06-2010, 01:30 PM
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I never noticed any difference when I was taking iron from when I was not
...
but that's just me
*shrugs*

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post #16 of 26 (permalink) Old 09-06-2010, 01:35 PM
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yeah, I'm not telling anyone to go out and start taking Iron. I was diagnosed with having low iron so I'll be taking a supplement. I just thought that stuff I read was very interesting but I guess I'm the only one lol

dude, really nice article finds, Im glad i saw this thread. Ive been having the same symptoms that you described, however I never supplemented with Iron because my Iron capsules were colored with Red coloring, ( which Im scared of, my OCD makes me avoid red food coloring).

I knew Iron was important for Dopamine , but I didnt know how important it actuallly was in relation to RLS and depression and other stuff Ect.

Because I know that here today, the Black Knights,..... will emerge victorious, once again.
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post #17 of 26 (permalink) Old 09-06-2010, 01:38 PM
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i Actually thought it would be Bad to take Iron with my Amphetamine, because Iron supposedly contributes to the theoretical neurotoxicity of Amphetamine .

I never really thought much about it though,

Because I know that here today, the Black Knights,..... will emerge victorious, once again.
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post #18 of 26 (permalink) Old 09-06-2010, 01:41 PM
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wow this is insane............. I am referring to the impact Iron has on Tyrosine Hydroxylase and GABA-T or whatever that enzyme is, and the Dopamine receptor expression

-----------


Do you know anything about Vitamin C and the relationship to Dopamine ?

Because I know that here today, the Black Knights,..... will emerge victorious, once again.
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post #19 of 26 (permalink) Old 09-06-2010, 02:37 PM Thread Starter
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Originally Posted by Vini Vidi Vici View Post
dude, really nice article finds, Im glad i saw this thread. Ive been having the same symptoms that you described, however I never supplemented with Iron because my Iron capsules were colored with Red coloring, ( which Im scared of, my OCD makes me avoid red food coloring).

I knew Iron was important for Dopamine , but I didnt know how important it actuallly was in relation to RLS and depression and other stuff Ect.

There's a ton of interesting info out there dealing with iron and brain health. I had no idea it was so vital to our brains. I ordered NOW's Ferrochel Chelated Iron Bisglycinate which is supposed to be highly absorbed. My doctor agreed that was the best form of iron currently available. I'll keep you updated if you're interested in how I feel and if it affects my SA in a positive way!
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post #20 of 26 (permalink) Old 04-18-2012, 01:12 PM
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Restless Legs: The Iron Connection

Before you rush out to buy the latest expensive prescription drug for “restless legs,” you might consider that one cause of this condition is iron deficiency.1 The prescription drugs used to treat restless legs stimulate the function of dopaminergic neurons. Iron deficiency is known to cause a reduction in dopaminergic activity (as well as a rise in serum prolactin).2
Many people these days have reduced their intake of red meat, the best dietary source of iron. White meat (such as poultry) contains much less. Moreover, those who eat a diet rich in polyphenols—as are found in fruits, in vegetables, and in green, black, and oolong tea, etc.—may be absorbing much less than the quantity of iron they ingest because of the potent iron-chelating properties of many polyphenols (such as quercetin). If you are eating a diet like this and have developed restless legs, it is quite possibly due to iron deficiency.
In a recent study,1 rats were fed diets that were either iron-deficient (ID) or iron-adequate (CN). Another group of ID rats was given iron supplements (IR). Studies were done on the dopamine, serotonin, and noradrenaline transporter binding in various brain areas. The results showed that ID male rats (but not ID females) had a decrease of 20–40% in dopamine transporter binding in the nucleus accumbens, caudate putamen, and substantia nigra. ID males also had a 20–30% reduction in serotonin transporter binding in the nucleus accumbens, olfactory tubercle, and colliculus, while ID females had 15–25% increased serotonin transporter binding in the olfactory tubercle, zona incerta, anteroventral thalamic nucleus, and vestibular nucleus. [It is possible that this increased serotonin transporter binding is linked to increased sensitivity to depression in females, at least in those who are iron-deficient, since the serotonin reuptake inhibitors, such as fluoxetine (Prozac®), inhibit the serotonin transporter.] Iron deficiency reduced binding to the noradrenaline transporter in the locus ceruleus and anteroventral thalamic nucleus in ID and IR males but not females. Some, but not all, of the changes induced by iron deficiency were reversed by iron supplementation.
The authors state, “This experiment extends our knowledge to include the olfactory tubercle as a tissue sensitive to iron deficiency. This might implicate iron deficiency in endocrinological difficulties such as hyperprolactinemia.” Prolactin is regulated by dopamine. High levels of prolactin stimulate the growth of breast and prostate tissue; they may thus be a risk factor for developing breast and prostate cancers and would certainly stimulate the growth of such cancers.
We became interested in the connection between iron deficiency and restless legs when Sandy developed the latter condition. It has been completely eradicated with daily RDA-level iron supplementation. Iron supplements should be taken at separate times from other supplements because of the possibility of chemical interactions with vitamin C, resulting in free radical generation, or with irreversible binding to polyphenols, especially quercetin. We suggest using ferrous gluconate; iron-EDTA chelates produce hydroxyl radicals very efficiently in the presence of vitamin C, and ferrous sulfate can be quite irritating.
I have restless leg and all I have to do is take 3 or 4 children's multivitamin and it goes away within 30 minutes and I sleep like a baby. I was taking Active Kids the ones you get at Walmart. It comes back if I don't keep taking them but once it comes on I run to the kids vitamins and it has never failed me.
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