Iron and autism

Iron is a mineral necessary for most forms of life. In humans it is a constituent of the heme protein found in red blood cells. Heme proteins are used in the transport of oxygen to all tissues of the body as well as for the removal of carbon dioxide, the latter a waste product of cellular metabolism. Iron also catalyzes the formation of so-called reactive oxygen species. These reactive chemical intermediaries engender a cascade of interactions that ultimately end up modifying or destroying the function of biological macromolecules, i.e., proteins, carbohydrates, lipids, and nucleic acids. Whenever there is an imbalance between reactive oxygen species and the body’s ability to neutralize them, cells in the body experience oxidative stress. This deleterious cascade of events may lead to premature cell death, including those found in the brain. Recent research suggests the involvement of oxidative stress and iron metabolism dysregulation in several neurodegenerative disorders including Alzheimer’s, Parkinson’s, amyotrophic lateral sclerosis (ALS) and Huntington’s disease, as well as in a syndromic type of autism.

In the brain, iron is needed for the synthesis of neurotransmitters and for myelin (the insulation of axons) formation. Normal brain development requires the availability of iron in a tightly controlled age- and brain-region-dependent manner. Iron-deficient infants manifest behavioral and cognitive developmental delays. Despite iron supplements, some iron-deficient babies may never recover as manifested in tests of learning, memory and thinking. Even more striking, many of these iron deficient infants may actually get worse as they get older. These cognitive deficits appear to be directly associated to the iron deficiency and not the comorbid anemia.

Recent studies suggest that children with attention-deficit/hyperactivity disorder have low levels of iron in their brains. In animals, iron deficiency has been linked to deficits in spontaneous exploratory activity and anxiety-like behaviors. In both ADHD and animal models, the behaviors appear to be associated to abnormalities of a neurotransmitter known as dopamine. Deficits in the bioavailability of iron often result in alterations in the production and function of dopamine and opiates neurotransmitters.

Iron-Deficiency-Prevalence-Children
Click on the graphic to enlarge

Some studies claim that iron deficiency and anemia are common in children with autistic spectrum disorder. Low iron levels when combined with advanced maternal age, is associated with a 5-fold increase for autism. In these cases the level of iron deficiency is not related to the severity of autistic symptoms

You should consider iron deficiency if you are feeling tired and weak, your work or school performance diminishes, experience difficulties in maintaining body temperature, have mood changes, suffer from multiple infections, and/or have an inflamed tongue. Your threshold for investigating this possibility should be lower if you are dealing with a baby that was born prematurely (more than three weeks before term) or has a low birth weight.

Many autistic individuals receive iron supplement as a preventive measure. If not followed carefully these supplements may cause nausea, vomiting, constipation and ulcerations of the gastrointestinal tract. Because of this danger you should keep iron supplements well outside the reach of younger children. Although the body absorbs only 10% of the iron consumed in the diet, it may be best to try and supplement iron, when necessary, through dietary means. Some suggestions to supplement your iron by dietary means include the following: Be aware that iron in meat sources is more easily absorbed than that available in grains and plant foods. Iron absorption may be reduced by antacids, calcium, zinc, magnesium, phytates, soy, nonsteroidal anti-inflammatory agents (may produce bleeds in the GI tract), coffee and tea. Iron rich foods include red meat, dark poultry, tuna, salmon, eggs, tofu, dried fruits and leafy green vegetables.

Anemia-Rich-food-in-Iron
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References

Herguner S, et al. Ferritin and iron levels in children with autistic disorder. Eur J Pediatr 171(1):143-6, 2012.
Latif A, et al. Iron deficiencyin autism and Asperger syndrome. Autism 6(1):103-114, 2002.

Schmidt RJ, et al. Maternal intake of supplemental iron and risk of autism spectrum disorder. Am J Epidemiol 180(9):890-900, 2014.

Veeravigrom M, et al. Neurodegeneration with brain iron accumulation disorder mimics autism. Pediatr Neurol 51(6):862-3, 2014.

4 responses to “Iron and autism

  1. This is very interesting,but like so many autism studies,it only looks at one aspect of metabolism,that does not make any sense until you look at the overall big picture and connect some dots.I am five and a half years into going from doctor to doctor,in severe states,collecting test results,Including Arkansas Children’s Hospital.Almost all these tests being metabolic and mitochondrial.

    Along the way,I have been found to have cerebral folate deficiency,a couple of inborn errors of metabolism,and probable mitochondrial disease of Complex I and IV.I still need more tests to confirm the mito diagnosis.

    My picture largely mirrors the one discussed here,with the addition of another IEM of folate metabolism not mentioned on this page,but not unknown in autism.
    http://www.mitoaction.org/autism/january-2014-teleconference

    As stated on this page,Dr. Frye has mentioned in his articles that many of the children he has studied have both elevated porphyrins,and signs of abnornal heme metabolism.One of the initial tests done on me was a urinary porphyrin test.My levels were very high,and they still are.

    The reason I believe I was tested was because the first doctor who was willing to do any tests on me was a DAN doctor,with all of the belief about vaccines and toxins.High porphyrins are one of the markers that those who believe vaccines cause autism of cite as proof.Parents will often use the porphyrin tests as evidence their child has heavy metal poisoning.

    I could not make any sense of the porphyrin tests,until I started getting abnormal mitochondrial tests,and did a lot of digging on the web.I came up with a few articles like this,that connect abnormal heme transport,with mitochondrial disease or dysfunction.

    http://www.jci.org/articles/view/66607
    http://www.hematology.org/Thehematologist/Diffusion/1082.aspx

    These articles suggest a possible link to a combined mutation of the FLVCR1 virus and abnormal heme transport in humans,with mitochondrial disease or dysfunction.The first article is especially interesting,because it connects heme abnormalities with mutations of the Hcp1 folate transporter.This article also offers a possible explanation why people like me have abnormalities of porphyrins and heme,but not iron deficiency anemia.The second article offers a better explanation of how FLVCR1 effects the mitochondria.

    Clearly more research needs to be done about the role of FLVCR1a and FLVCR1b in human mitochondrial disease and dysfunction,and by extension,autism.

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  2. I am tired and weak a lot but on the other hand, if that was true for me I probably would have known a long time ago. I still think the main problem is my nose breathing.

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  3. Hi Maneul Casanova –

    I’m interested in your thoughts on how findings such as this, or as another example, the vitamin d studies in the autism population, with several studies recently, interact with your thoughts on the dysplasia(s) as a cause of (some?) autism?

    I’m struggling to see a mechanism by which the altered structures described by you and others at a brain pathology level could *cause* altered iron levels, but I am only a simple drone. I can maybe think of a way that problems with iron metabolism could result in disturbed neuronal migration patterns, but again, only at a very conceptual level.

    Thanks.
    pD

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    • One of the problems in autism research is trying to distinguish between core causes and pathology vs. secondary findings. Iron levels may be abnormal in a fraction of autistic individuals; however, this does not indicate it is causally implicated in the condition. The same may be secondary to disturbances in dietary intake due to low meat consumption. You can propose any other similar explanation. I am also a simple drone 🙂

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