my husband has low iron levels. I remember seeing different articles about the safety of taking iron supplements for someone who has Parkinson’s. I can’t seem to find the threads. Can anyone tell me about the safety of taking iron supplements? I would like to be prepared for a conversation with the doctor who ordered the bloodwork (hematologist ).
Thsnk you so much!
My husband has borderline anemia according to his last blood test but the doctor isn't prescribing any iron, just keeping an eye on it. My husband is on Madapar for his Parkinsons and the side effects leaflet mentions this so I wondered if your husband is also on it?
My wife has a iron infusion because iron tablets are not recommended to be taken orally if taking Parkinson drugs, in her case Madapar and Sinemet+ The last infusion lasted approx 2 years. The information is on the Iron Supplement information sheet
Systemic inflammation can be cause low iron and modern diest can be highly inflamatory containing many processed foods containing refined carbohydrates and seed oils. youtu.be/eqCensiK8Ac?si=kH7...
yes, my husband has low iron and his doctor prescribed some over-the-counter supplement. I researched this and I chose to give him Thorne ferrasorb which need not be taken with food, in conjunction with lactoferrin. I usually buy Double Woods lactoferrin.
Also, did they figure out why? Men shouldn’t have low iron. Hubby had colon polyps which caused anemia several years ago. And he successfully supplemented with iron as well during that time. Make sure you get a diagnosis.
I just read an article that suggested that there can be a problem with iron metabolism and it said that sometimes a person can have a good blood test for iron but their system is not able to utilize it.
"A plethora of studies indicate that iron metabolism is dysregulated in Parkinson's disease (PD). "
sciencedirect.com/science/a...
"3.1. Iron is a double-edged sword
Iron is a critical trace element for multiple biological mechanisms with its deficiency leading to cell death, but it is also cytotoxic when in excess [102]. Thus, organisms have developed multiple intricate mechanisms for the maintenance of iron levels within optimal levels by controlling cellular iron uptake, transport, storage and release [103]. Iron in the brain accounts for less than 2% of whole-body iron content, and interestingly, is distributed heterogeneously in different brain regions. Iron accumulates in the brain with normal aging [104], but larger increases by two-fold, occur in specific brain regions in PD [105,106] and Alzheimer's disease [107]."
"Unbound excess cellular iron, particularly that which is not bound to the iron storage protein, ferritin, can be cytotoxic, as it can be involved in the generation of reactive oxygen species (ROS) via Fenton and Haber-Weiss chemistry [108]. In fact, the accumulation of intracellular iron can lead to the relatively recently discovered process of ferroptosis [109], which is a unique non-apoptotic mechanism defined by iron-induced lipid ROS and depletion of plasma membrane unsaturated fatty acids [110]. For ferroptosis to occur there is a need for coincident glutathione (GSH) depletion with inactivation of the GSH-dependent enzyme, glutathione peroxidase 4 (GPx4), with the incorporation of oxidizable polyunsaturated fatty acids into phospholipids [111,112]."
"Why does increased dopamine biosynthesis, which is likely potentiated by the accumulated iron in the SNpc, lead to neurodegeneration? This might be explained by the cytotoxic potential of dopamine, as it can readily auto-oxidize in the presence of iron and can also be metabolically deaminated to generate toxic dopamine metabolites (quinones) and ROS. The generation of hydrogen peroxide has been suggested to result in mitochondrial damage with this oxidant leading to the oxidation of GSH to glutathione disulfide (GSSG), which may participate in thiol-disulfide interchange to result in protein mixed disulfides. These latter species could reversibly inhibit thiol-dependent enzymes that affect their function [14,320]. Therefore, excessively synthesized dopamine and a failure to properly store dopamine into synaptic vesicles may lead to oxidative stress, terminal degeneration, and eventually cell death [14]."
I am wondering why treatment with l dopa does not cause more rapid disease progress if “This might be explained by the cytotoxic potential of dopamine as it can readily auto-oxidize in the presence of iron and can also be metabolically deaminated to generate toxic dopamine metabolites (quinones) and ROS“.
it is all so complicated and this seems like a good question
It is important to remember I have no more than a high school degree.
I have posted a number of times about some researcher's theories on too much iron causing or making PD worse.
From an article: "Many of these neurological disorders, including Alzheimer’s and Parkinson’s diseases, appear to be related to focal accumulation of iron in specific regions of the brain".
Does this mean the PwP had too much iron in their system? Or does it just mean the iron is accumulating? I don't know.
This post has links to a lot of what I was posting about: "Berberine Is a Promising Alkaloid to Attenuate Iron Toxicity Efficiently in Iron-Overloaded Mice" healthunlocked.com/cure-par...
And this post has good info also: Curcumin Update 2023/03/06 healthunlocked.com/cure-par...
Anybody that has not read that Curcumin post, really should. My advanced high school degree tells me something good is in Curcumin.
I'm going to make sure you don't need your Curcumin pills anymore!
Bolt_Upright and yet you know much more than those who have Masters degrees and Doctorates 🙇😬🤣✌️
Parkinson’s and Radon
autophagy and Parkinson’s
Metformin for Parkinson’s? 
The stages of Parkinson’s 
Parkinson’s and Cat’ Claw
