Muscular iron injections
 

Please keep this thread going.
I was Dx PD three ys ago, was anemic off and on forever.
Dr Paola Costa-Mallen, PhD at Bastyr Univ in Seattle, WA saw me because of her interest in how iron levels relate to PD. I'm forwarding this thread to her.

I did the oyster, beef, iron pill, leafy green regimen with little improvement.
THEN started muscle iron shots (my naturepath's idea:)) and now have improved rigidity and sleep through the night! Ten times more energy and iron levels almost normal.BUT tremors have increased slightly.

Possible reason--iron in food was having difficulty crossing from gut to blood?

Any thoughts?
Taking mucuna, neuroprotectors and rasagiline,

It may come back to the BBB
 

Everything that is good in the right place and time has the potential to be deadly in the wrong setting. The BBB plays a central role in this compartamentalization. An intact BBB allows a high level of iron or anything else to exist in blood and muscle while maintaining a different level in the CNS. Trouble comes with the failure of this system.


1. J Neurochem. 2010 Dec 7. doi: 10.1111/j.1471-4159.2010.07132.x. [Epub ahead of
print]

The relevance of iron in the pathogenesis of Parkinson's disease.

Sian-Hülsmann J, Mandel S, Youdim MB, Riederer P.

Clinical Neurochemistry, National Parkinson Foundation Centre of Excellence
Laboratories, Clinic and Polyclinic for Psychiatry, Psychosomatic and
Psychotherapy, Medical School, University of Würzburg, Würzburg, Germany Eve Topf
Centre of Excellence for Neurodegenerative diseases, Technion-Rappaport Faculty
of Medicine, Haifa, Israel Department of Biology, World Central Yonsei
University, Seoul, South Korea.

J. Neurochem. (2011) 10.1111/j.1471-4159.2010.07132.x ABSTRACT: Alterations of
iron levels in the brain has been observed and documented in a number of
neurodegenerative disorders including Parkinson's disease (PD). The elevated
nigral iron levels observed in PD may reflect a dysfunction of brain iron
homeostasis. Under normal physiological conditions excess iron can be
sequestrated in ferritin and neuromelanin. Alternatively, the excess iron may
represent a component of brain iron deposition associated with ageing. The
aetiology of idiopathic PD largely remains an enigma. However, intensive
investigations have provided a host of putative mechanisms that might contribute
to the pathogenesis underlying the characteristic degeneration of the
dopaminergic neurons in the substantia nigra (SN). The mechanisms proposed
include oxidative (and nitrative) stress, inflammation, excitotoxicity,
mitochondrial dysfunction, altered proteolysis and finally apoptotic induced cell
death. Iron-mediated cellular destruction is mediated primarily via reactive
oxygen or/and nitrogen species induced oxidative stress. Furthermore, these
pathogenic mechanisms appear to be closely interlinked to the cascade of events
leading to cellular death. There are conflicting reports about the stage during
disease progression at which nigral iron change occurs in PD. Some have found
that there are no changes in iron content SN in asymptomatic incidental Lewy body
disease, suggesting it may represent a secondary event in the cascade of neuronal
degeneration. In contrast, others have found an elevation of iron in SN in
pre-clinical stages. These discrepancies may be attributed to the occurrence of
different sub-groups of the disease. This concurs with the notion that PD
represents a group of related diseases with a number of potential pathogenic
pathways.


PMID: 21138437 [PubMed - as supplied by publisher]