01-31-2019, 09:12 PM
I'm curious how your blood fatty acid profile looks like.
I did one and almost every fatty acid was low except for linoleic acid (18:2) which was high. If you have low fatty acids in your blood it's clear that you won't become fat.
That probably has to do with the role of copper in fatty acid metabolism.
https://www.intechopen.com/books/lipid-m...metabolism
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5510220/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5619695/
But it must be dependant on more factors, there are thin and overweight people with copper deficiency.
I also had muscles twitches from the high zinc intake, probably nerve damage, already thought if it could be multiple sclerosis.
On your symptoms list I could also check 9 symptoms. I think I found an explanation for the vertical ridges on the nails. There are thiol oxidase (sulfhydryl oxidase) enzymes which are resposible for disulfide-bond formation.
These enzymes are copper-dependent. So if you lack copper then the enzymes will create less disulfide-bonds which are for example a part of keratin (hair, nails). As a side effect I think it's possible that you could get an excess of sulphur (could this be the yellow/brown ring in the inner iris? Or green eyes when in fact you have blue eyes)
https://www.cabdirect.org/cabdirect/abst...9471402845
The copper I take is 3x3 mg (analysis says 4 mg, it always varies) Nature's Plus because this is chelated with soy amino acids, has the advantage of several different amino acids plus the additional isoflavones.
That resembles more of a natural food, although I asked the producer (Biotron Laboratories) and it's divalent copper.
Food is usually a mix of monovalent (Cu+) and divalent (Cu++) copper.
https://sci-hub.se/10.1016/j.foodchem.2014.05.018
The 3rd step is to find the actual cause of the copper deficiency.
My best bet is it's either a genetic disorder where we can't convert enough Cu++ (transport version) to Cu+ or it's a viral infection where the virus either modified DNA to protect it from the macrophages' copper bursts or the macrophages simply shot all their copper and are depleted.
"The macrophage copper burst
When macrophages encounter pathogens, they can engulf and contain the microbe within a compartment known as the phagolysosome. This extremely hostile environment contains high ROS and reactive nitrogen, low pH and proteases, which are all designed to kill the microbe. With certain infectious agents, the phagolysosome can also accumulate high copper which, together with phagolysosomal ROS, can attack microbes through Fenton chemistry or through other pathways as described above. The high copper of macrophage phagolysosomes was first described for infection with Mycobacterium species including the M. tuberculosis pathogen for tuberculosis [33]. Since then, macrophage copper has been shown to be important in killing E. coli [34] and inducing copper toxicity stress for Salmonella [35, 36]. Even fungi such as Candida albicans show symptoms of high copper exposure during encounters with macrophages [37]. The mechanism by which macrophages accumulate this high copper is believed to involve a combination of increasing copper uptake by the high affinity copper transporter CTR1 and by activating the copper ATPase ATP7A, which can directly pump copper into the phagolysosome [34, 36, 38]."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5535265/
It would be interesting to know if there are any couples that both have PET, would speak for a viral cause, or a very rare coincidence where both partners have the same gene defect.
I did one and almost every fatty acid was low except for linoleic acid (18:2) which was high. If you have low fatty acids in your blood it's clear that you won't become fat.
That probably has to do with the role of copper in fatty acid metabolism.
Quote:The Role of Copper as a Modifier of Lipid Metabolism
By Jason L. Burkhead and Svetlana Lutsenko
https://www.intechopen.com/books/lipid-m...metabolism
Quote:Food Nutr Res. 2017; 61(1): 1348866.
Effect of dietary copper addition on lipid metabolism in rabbits
Liu Lei, Sui Xiaoyi and Li Fuchanga
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5510220/
Quote:UBMB Life. 2017 Apr; 69(4): 263–270.
The role of insufficient copper in lipid synthesis and fatty-liver disease
Austin Morrell, Savannah Tallino, Lei Yu, and Jason L. Burkhead
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5619695/
But it must be dependant on more factors, there are thin and overweight people with copper deficiency.
I also had muscles twitches from the high zinc intake, probably nerve damage, already thought if it could be multiple sclerosis.
On your symptoms list I could also check 9 symptoms. I think I found an explanation for the vertical ridges on the nails. There are thiol oxidase (sulfhydryl oxidase) enzymes which are resposible for disulfide-bond formation.
These enzymes are copper-dependent. So if you lack copper then the enzymes will create less disulfide-bonds which are for example a part of keratin (hair, nails). As a side effect I think it's possible that you could get an excess of sulphur (could this be the yellow/brown ring in the inner iris? Or green eyes when in fact you have blue eyes)
Quote:"Steely" wool caused by copper deficiency.
Agricultural Gazette of New South Wales 1947 Vol.58 pp.99; 106
https://www.cabdirect.org/cabdirect/abst...9471402845
The copper I take is 3x3 mg (analysis says 4 mg, it always varies) Nature's Plus because this is chelated with soy amino acids, has the advantage of several different amino acids plus the additional isoflavones.
That resembles more of a natural food, although I asked the producer (Biotron Laboratories) and it's divalent copper.
Food is usually a mix of monovalent (Cu+) and divalent (Cu++) copper.
Quote:Ceko, M.J., Aitken, J.B., Harris, H.H.
Speciation of copper in a range of food types by X-ray absorption spectroscopy
Food Chemistry (2014)
https://sci-hub.se/10.1016/j.foodchem.2014.05.018
The 3rd step is to find the actual cause of the copper deficiency.
My best bet is it's either a genetic disorder where we can't convert enough Cu++ (transport version) to Cu+ or it's a viral infection where the virus either modified DNA to protect it from the macrophages' copper bursts or the macrophages simply shot all their copper and are depleted.
"The macrophage copper burst
When macrophages encounter pathogens, they can engulf and contain the microbe within a compartment known as the phagolysosome. This extremely hostile environment contains high ROS and reactive nitrogen, low pH and proteases, which are all designed to kill the microbe. With certain infectious agents, the phagolysosome can also accumulate high copper which, together with phagolysosomal ROS, can attack microbes through Fenton chemistry or through other pathways as described above. The high copper of macrophage phagolysosomes was first described for infection with Mycobacterium species including the M. tuberculosis pathogen for tuberculosis [33]. Since then, macrophage copper has been shown to be important in killing E. coli [34] and inducing copper toxicity stress for Salmonella [35, 36]. Even fungi such as Candida albicans show symptoms of high copper exposure during encounters with macrophages [37]. The mechanism by which macrophages accumulate this high copper is believed to involve a combination of increasing copper uptake by the high affinity copper transporter CTR1 and by activating the copper ATPase ATP7A, which can directly pump copper into the phagolysosome [34, 36, 38]."
Quote:J Biol Inorg Chem. 2016 Apr; 21(2): 137–144.
The Yin and Yang of Copper During Infection
Angelique N. Besold, Edward M. Culbertson, and Valeria C. Culotta
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5535265/
It would be interesting to know if there are any couples that both have PET, would speak for a viral cause, or a very rare coincidence where both partners have the same gene defect.
