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Wednesday, February 8, 2017 1:12 AM | Venöse Multiple Sklerose, CVI & SVI, CCSVI shared their photo. Volg link
The Copper - Ceruloplasmin Connection & its influence on Iron metabolism

Copper - (Cu) is an essential trace element for humans and animals. This trace element plays an important role as essential Co-factor in oxidation-reduction reactions and in scavenging free radicals. Its enzymes regulate various physiologic pathways like energy production, connective tissue maturation, neurotransmission and iron metabolism.
Copper imbalance has been linked to impaired immune function, bone demineralization, and increased risk of cardiovascular and neurodegenerative diseases. Further copper deficiency can also lead to secondary Ceruloplasmin deficiency and hepatic iron overload and/or cirrhosis.
Copper deficiency includes symptoms like central nervous system demyelination, polyneuropathy, myelopathy, and inflammation of the optic nerve. Dysfunctional copper metabolism is suggested as a risk factor for AD, it could also be symptomatic of the disease and it may play a role in Parkinson Disease too. Copper deficiency of bound Cu can further result in heart abnormalities because outside the body, free (unbound/ not bound to Ceruloplasmin) Copper is known to be a pro-oxidant.

Iron - (Fe) is an essential trace element too and Fe-deficiency (anaemia) is a clinical sign of Cu-imbalance/deficiency. It’s indicating that more bio-available Copper (Cu bound to Ceruloplasmin) is required for Iron transport to the bone marrow for red blood cell formation. For adequate Iron metabolism, four copper-containing enzymes (MCO) are required and the MCO family comprises the circulating Ceruloplasmin.

Ceruloplasmin – (Cp) is a ferroxidase enzyme (produced in the liver, which depends on Magnesium, real Vitamin C and Vitamin A (retinol animal source) that has the capacity to oxidize ferrous iron (Fe2+) to ferric iron (Fe3+), which can be loaded onto the iron transport protein, transferrin. A lack in Ceruloplasmin displays iron overload in selected tissues, including liver, brain, and retina. The cuproenzymes, superoxide dismutase and Ceruloplasmin, are known to have antioxidant properties.
p.s. High supplemental Zinc intakes of 50mg/day or more for extended periods of time may result in a copper deficiency because such intakes increase the synthesis of an intestinal cell protein called metallothionein, which binds certain metals and prevents their absorption by trapping them in intestinal cells causing a decrease in copper absorption.

Summary:

LOW Magnesium & LOW REAL Vitamin C & A (Retinol/animal source) => LOW Ceruloplasmin (Cp) production => LOW amounts of bound/bio-available Copper => HIGH amounts of unbound/bio-unavailable Copper & Iron => toxic Copper & Iron storage in the liver or brain tissue => HIGH pro-oxidant status of the body.
LOW Magnesium caused by HIGH Calcium (e.g. dramatically increased with synthetic Hormone D intake [”Calcium on steroids”!]) => BLOCKS Iron absorption in the gut even further!
Multi-Copper Oxidase (MCO) requires 4 Copper ions to work => essential for Iron absorption and therefore it HAS TO HAVE enough REAL “C” because therefrom (wholefood “C”) it will get ALL of its SO MUCH NEEDED Ions.
And to make it work, at the end ALL HAS TO BE IN BALANCE = The Minerals/Trace elements: Magnesium - Calcium, Copper – Zinc – Iron and the Vitamins: Real “C”, animal based A and all the Bs!

Reference: Linus Pauling Institute http://lpi.oregonstate.edu/
https://www.facebook.com/117471578700/photos/a.393204943700.170906.117471578700/10154781903093701/?type=3&theater
Venöse Multiple Sklerose, CVI & SVI, CCSVI
The Copper - Ceruloplasmin Connection & its influence on Iron metabolism

Copper - (Cu) is an essential trace element for humans and animals. This trace element plays an important role as essential Co-factor in oxidation-reduction reactions and in scavenging free radicals. Its enzymes regulate various physiologic pathways like energy production, connective tissue maturation, neurotransmission and iron metabolism.
Copper imbalance has been linked to impaired immune function, bone demineralization, and increased risk of cardiovascular and neurodegenerative diseases. Further copper deficiency can also lead to secondary Ceruloplasmin deficiency and hepatic iron overload and/or cirrhosis.
Copper deficiency includes symptoms like central nervous system demyelination, polyneuropathy, myelopathy, and inflammation of the optic nerve. Dysfunctional copper metabolism is suggested as a risk factor for AD, it could also be symptomatic of the disease and it may play a role in Parkinson Disease too. Copper deficiency of bound Cu can further result in heart abnormalities because outside the body, free (unbound/ not bound to Ceruloplasmin) Copper is known to be a pro-oxidant.

Iron - (Fe) is an essential trace element too and Fe-deficiency (anaemia) is a clinical sign of Cu-imbalance/deficiency. It’s indicating that more bio-available Copper (Cu bound to Ceruloplasmin) is required for Iron transport to the bone marrow for red blood cell formation. For adequate Iron metabolism, four copper-containing enzymes (MCO) are required and the MCO family comprises the circulating Ceruloplasmin.

Ceruloplasmin – (Cp) is a ferroxidase enzyme (produced in the liver, which depends on Magnesium, real Vitamin C and Vitamin A (retinol animal source) that has the capacity to oxidize ferrous iron (Fe2+) to ferric iron (Fe3+), which can be loaded onto the iron transport protein, transferrin. A lack in Ceruloplasmin displays iron overload in selected tissues, including liver, brain, and retina. The cuproenzymes, superoxide dismutase and Ceruloplasmin, are known to have antioxidant properties.
p.s. High supplemental Zinc intakes of 50mg/day or more for extended periods of time may result in a copper deficiency because such intakes increase the synthesis of an intestinal cell protein called metallothionein, which binds certain metals and prevents their absorption by trapping them in intestinal cells causing a decrease in copper absorption.

Summary:

LOW Magnesium & LOW REAL Vitamin C & A (Retinol/animal source) => LOW Ceruloplasmin (Cp) production => LOW amounts of bound/bio-available Copper => HIGH amounts of unbound/bio-unavailable Copper & Iron => toxic Copper & Iron storage in the liver or brain tissue => HIGH pro-oxidant status of the body.
LOW Magnesium caused by HIGH Calcium (e.g. dramatically increased with synthetic Hormone D intake [”Calcium on steroids”!]) => BLOCKS Iron absorption in the gut even further!
Multi-Copper Oxidase (MCO) requires 4 Copper ions to work => essential for Iron absorption and therefore it HAS TO HAVE enough REAL “C” because therefrom (wholefood “C”) it will get ALL of its SO MUCH NEEDED Ions.
And to make it work, at the end ALL HAS TO BE IN BALANCE = The Minerals/Trace elements: Magnesium - Calcium, Copper – Zinc – Iron and the Vitamins: Real “C”, animal based A and all the Bs!

Reference: Linus Pauling Institute http://lpi.oregonstate.edu