Types of copper
Solid Copper, such as a penny, pipe or nugget.
Half oxidized, and properly chelated, this copper is bioavailable to your body and essential for cellular health.
This is the copper in MitoSynergy products.
Fully oxidized, this copper is non-bioavailable. Because Copper 2 is not absorbed when it enters the body, it accumulates in the extracellular matrix. This is the copper in ALL other supplement brands.
IMPORTANCE OF COPPER 1 TO OUR BODIES: ATP CYCLING
For every cell in your body, the source of energy that keeps everything working is called Adenosine triphosphate (ATP). ATP is your body’s way to store and use energy.
ATP is required for the active transport of nutrients into cells and waste out of cells.
Copper (I) is essential in completing the Electron Transport Chain, resulting in 34 ATP. That’s almost 90% of the energy that your body makes.
MitoSynergy is the only BioCopper1 supplement.
Other benefits of copper
Copper (Cu) is an essential transition metal serving as a catalytic cofactor for more than 20 enzymes, particularly those involved in cellular respiration and energy metabolism, neurotransmitter biosynthesis, iron metabolism, gene transcription, and antioxidant defense.1,2
A study using murine monocyte BV2 cells reported that Cu+ can polarize cells from a proinflammatory M1phenotype to a protective antiinflammatory M2 phenotype via inhibition of ni‐tric oxide production.1,3
Deficiency of copper could also be detrimental as it leads to aggravated glial responses and impaired antioxidative defense in the brain.4-6
Copper deficiency also resulted in aberrant microglial activation that contributed to neurodegenerative diseases, implicating that Cu+ plays a critical role in maintaining microglia homeostasis.4,6
VALENCY DETERMINES OUTCOMES
Valency of copper in food
Testing has shown that Cu(I) dominates food in all samples excluding cocoa and tap water.7 Essential Cu is primarily supplied from foodsources as Cu+, the same type found in MitoSynergy BioCopper1.
Cu++, on the other hand, may have limited nutritional value and exhibit negative health effects in the body.1 Cu++ from environmental sources (such as tap water or other dietary supplements) could elicit rather detrimental effects while Cu+ from dietary sources or MitoSynergy BioCopper1 fulfills biologically essential demand.1
Alzheimer’s disease and copper valency
George J Brewer, Emeritus Professor of Human Genetics and Internal Medicine at the University of Michigan, has written extensively on the connection between Cu++ and Alzheimer's Disease. In his paper Avoiding Alzheimer’s disease: The important causative role of divalent copper ingestion,8 he finds:
- It is clear that copper-2 is very toxic to cognition and can cause AD in animals.8
- Mammals, including humans, evolved ingesting copper-1 and not copper-2. As a result, we have an intestinal receptor, Ctr1 for copper, which will bind copper-1 but not copper-2. Binding to this receptor causes the copper-1 ingested with food to be transported to the liver, where it is put in safe channels.8,9
- Copper-2 does not get processed by the liver with much of it appearing in the blood immediately. Food copper, copper-1, is processed by the liver, put into safe channels, and takes days to appear in the blood.8
- A study giving rabbits water with copper in it found that the addition of 0.12 parts per million (ppm) of copper to the distilled drinking water greatly enhanced the amyloid plaques of AD in the brain, and caused memory loss in the animals. Copper in drinking water is copper-2. For reference, the Environmental Protection Agency (EPA) allows 1.3 ppm of copper in human drinking water, 10 times the amount found toxic in the animal studies. These same results were found in other animal models of AD, and the findings were also confirmed in another laboratory.8,10-13
- It was shown two decades ago that copper-2 induced amyloid beta (Aβ) aggregation.
This was elaborated on in further work where it was shown that copper-2 potentiates Aβ neurotoxicity.
Aβ reduces copper-2 to copper-1 and in the process generates hydrogen peroxide (HO), which is a potent source of damaging oxidant radicals.8,14,15
Aβ plaques are typically found in the brain tissue of Alzheimer patients.
Chronic exposure to copper (II) vs ingestion of copper (I)
The preponderance of Cu found in solid food is present in organic molecules as the cuprous Cu+ form, which is efficiently absorbed by the intestinal microvilli and has essential nutritional value. Cu found in drinking water, environment, or most dietary supplements (not MitoSynergy) is in the inorganic, cupric Cu++ form, whose uptake process in the intestine is less understood. Rapid elevation of Cu in the blood following ingestion of Cu-containing water (Cu++) indicates a possibility of bypassing the proper metabolic process to enter the circulation.4,7,16,17
Studies have shown that differential activation of microglial phenotypes and toxicity in the brain depend on the valency of Cu. For instance, the cuprous Cu+ ion shifts microglial cells from a pro-inflammatory phenotype to an anti-inflammatory state by inhibiting nitric oxide production. In contrast, the cupric Cu++ form of copper impairs phagocytosis and elevates the release of pro-inflammatory cytokines, thus substantiating that the Cu++ form perturbs inflammatory responses.1,3,4,18
Negative effects of Cu++ exposure
Excess dysregulated Cu may promote oxidative stress in vivo, contributing to pathology in a range of diseases, such as atherosclerosis and neurodegeneration.7,19
Copper (II) effects on microglia
Chronic copper exposure directs microglia towards degenerative expression signatures in wild-type and J20 mouse model of Alzheimer’s disease, Lim et al.4
"In the present study, we extended our investigation to evaluate whether chronic Cu exposure to wild-type (WT) and J20 mouse model of AD perturbs homeostatic dynamics of microglia and contributes to accelerated transformation of microglia towards degenerative phenotypes that are closely associated with neurodegeneration. We further looked for evidence of alterations in the microglial morphology and spatial memory of the Cu-exposed mice to assess the extent of the Cu toxicity."
- Excess Cu++ intake through drinking water shifts the microglial expression profile towards degenerative phenotypes, which may in part contribute to accelerated cognitive impairment observed in these mice.4
- Excess Cu++ exposure alone could lead to perturbed microglial homeostatic phenotypes and contribute to accelerated cognitive decline.4
- Results indicate that Cu++ exposure substantially drives microglia towards degenerative phenotypes at translational levels. Such phenotypes could contribute to accelerated degenerative processes including excessive synapse pruning and neuronal loss,20,21 secretion of pro-inflammatory cytokines and oxidative damage,22-24 impairment of effective containment of Aβ,25,26 and subsequent cognitive decline.4