Iron, neuro-bioavailability and depression 2021

[pattismith]

https://onlinelibrary.wiley.com/doi/epdf/10.1002/jha2.321

french article

Iron, neuro-bioavailability and depression​

Abstract​

Medical management of iron deficiency (ID) requires to consider its consequences in biochemical and physiological plural functions, beyond heme/hemoglobin disrupted synthesis.

Fatigue, muscle weakness, reduced exercise capacity, changes in thymia and modified emotional behaviors are the commonest symptoms integrated in the history of ID, dependent or not of the hemoglobin concentration.

The relationship between depression and absolute ID (AID) is a condition which is often unrecognized.

Neuro-bioavailability and brain capture of blood iron are necessary for an appropriate synthesis of neurotransmitters (serotonin, dopamine, noradrenaline).

These neurotransmitters, involved in emotional behaviors, depend on neuron aromatic hydoxylases functioning with iron as essential cofactor.

Noradrenaline also has impact on neuroplasticity via brain-derived neurotrophic factor (BDNF), which is key for prefrontal and hippocampus neurons playing a role in depression. Establishing the formal relationship between depression and AID remains difficult.

Intracerebral reduced iron is still hard to quantify by neuroimaging and single-photon emission computed tomography (SPECT) now tends to explore the neurotransmission pathways.

AID has to be looked for and identified in the context of depression, major episode or resistant to conventional treatment such as serotonin reuptake inhibitor, and even in the absence of anemia, microcytosis or hypochromia (non-anemic ID). Confronted to brain imaging, blood iron status evaluation is indicated, especially in depressed, treatment-resistant, iron-deficient young women.

In patients suffering from depression, increase in the prevalence of AID should be considered, in order to deliver a suitable treatment, considering both anti-depressive program and iron supplementation if AID.

 

[pattismith]

Pr Berthou says that if your ferritin is low, then you don't have an inflammatory condition....Excepted if you have a gastrointestinal disease!

"Biologically, I-AID is defined by a normal Hb level and a serum ferritin <30 μg/L. Other studies support the definition of AID for a higher serum ferritin threshold (<50 μg/L) [9], inside which iron supplementation often corrects all or part of the symptoms found [10, 11].

AID with IDA or without anemia (I-AID if severe, ferritinemia <20 μg/L with recurrent or risk of gastrointestinal malignancy) both require a rigorous etiologic research:

1. By upper and lower gastrointestinal endoscopy, search of distilling (may be occult) digestive hemorrhage (gastric ulcers, polyps, cancer; duodenal ulcers; colon cancer, colonic polyps, angiodysplasia, diverticular bleeding, etc.), autoimmune gastritis, Helicobacter pylori gastric infection and duodenal malabsorption, such as coeliac disease and its appropriate serological tests (transglutaminase IgA, i.e., IgA-TTC antibodies, combined with IgA concentration, anti-endomysial antibodies). Endoscopy leads to the realization of regular biopsies in three sites (fundus, gastric antrum and duodenum), always performed, looking for H pylori and duodenal villous atrophy, together with appropriate localized biopsies if mucous lesion(s) is (are) identified, for anatomo-pathology analysis.
2. By a clinical (context of menorrhagia or meno-metrorrhagia), gynecological imaging and/or uterine endoscopy, search for a gynecological lesion, functional hormonal bleeding (premenopausal women and girls) or gynecological bleeding favored by a primary hemostasis defect (von Willebrand disease, platelet dysfunction, carrier for hemophilia A or B, etc.).
3. All these conditions could be amplified by deficient nutrition (iron-poor diet), inadequate stomach acidification (long-term use of proton pump inhibitors or antiacids, atrophic gastritis, H pylori, after gastric bypass), in patients with pica (addictive ingestion of non-nutritive foods, such as clay, soil, ice, etc.)."

An interesting test to detect some inflammatory disease even with low CRP is The Calprotectin test both in the blood and faecal.