Copper Deficiency In Humans

[Waynish]

Too much sulfur causes copper deficiency:
Studies of a naturally occurring sulfur-induced copper deficiency in Przewalski’s gazelles

Garlic, onions and eggs are the worst. Sulfites contribute too. You will know you have way too much sulfur (or improperly metabolized sulfur) when your pee smells like sulfur and people say you smell like eggs.
To process sulfur molybdenum and vitamin b6 come up. Salt apparently increases sulfur, with copper, calcium and potassium antagonizing it along with "vitamin b15". ( Selenium Sulfur DRI/RDA, benefits, side effects, overdose, toxicity, requirements )

So those with copper deficiency may be having too much sulfur in their diet. Wines, dried fruits have sulfites added and so on.

Salicylates can hinder the pst pathway and thus interfere with metabolism of sulfur. Coconut oil and aspirin are high sources of salicylates. ( a list of foods Salicylate Foods - sensitivity, intolerances and food list. - ATP Science Pty Ltd )

Thus consuming too many salicylates with your sulfur may interfere with proper metabolism of sulfur, thereby causing elevated levels that hinder copper absorption.

Excessive sulfur also can induce a selenium deficiency, which is necessary for thyroid function.
High caffeine is touted to interfere with the body utilizing vitamin b6, which is needed for sulfur metabolism.

Thus say a high coffee diet with coconut oil and too many eggs with too many dried fruits could induce excessive sulfur leading to these mineral deficiencies.

I am researching this for myself, as I noted extraordinarily negative effects from consuming raw garlic (2 cloves a day) Mind you large quantities of eggs are a staple in my diet, as is coconut oil.

So much to research.

Roger that Jack - I'm always trying to think of more robust systems for diagnosis and qualification. We need better ways to catch the many edge cases out there when we open the Pandora's box of supplementation. Things are much simpler when all inputs are whole foods, but for those of us who want to do better or heal faster: either we're delusional, impatient, or just in need of better systems for real time determination of cause & effect.

 

[yerrag]

Interesting, could be an explaination. I havn't had garlic in a long while since the bad reactions and same as you I've always had better results with onions. Never-ending variables.

I also remembered that Ray cautions not to have flowers of sulphur for extended periods because it depletes copper.

I've wodered why my electroic Omron blood pressure monitor occasionally flashes the arrythmia symbol. Maybe it's the garlic. I have to lower the dosage then. Thanks for the heads up guys!

 

[yerrag]

Do you have an idea when serum ceruloplasmin levels are considered low other than being below range? Would you consider ceruloplasmin levels above middle of range to be ideal, given that being on the high side of range might indicate that other metals such as iron and zinc aren't sufficiently absorbed in the cells? I just got my results back and I got 0.21 g/L, with a range of 0.15 - 0.30 g/L.

 

[Frankdee20]

Interesting, could be an explaination. I havn't had garlic in a long while since the bad reactions and same as you I've always had better results with onions. Never-ending variables.

I also remembered that Ray cautions not to have flowers of sulphur for extended periods because it depletes copper.

I swear if I eat Garlic, I'm brain dead for hours. Many people report lethargy, but maybe don't make the connection to garlic effecting brain hemispheres negatively. The stuff kills vampires, and brain cells too.

 

[yerrag]

High dietary intake of ascorbic acid has also been shown to lower serum ceruloplasmin and Cu levels (27).

This is one gotcha to be aware of when taking plenty of Vitamin C.

I understand that it's not advisable to drink OJ after a meal with meat, because it will increase assimilation of iron. Would it make sense to drink OJ with or right after a meal that is high in copper? As in shrimps, oyesters, liver? Or should I not include liver because liver is high in iron as well?

 

[Waynish]

I swear if I eat Garlic, I'm brain dead for hours. Many people report lethargy, but maybe don't make the connection to garlic effecting brain hemispheres negatively. The stuff kills vampires, and brain cells too.

Could be die off effect. It's an antibiotic. If you drink a bunch of activated charcoal and that decreases the effect, then wouldn't that count as confirmation of this theory?

 

[Amazoniac]

Some random links that seem interesting, but not sure if I will read them:
- Copper and Alzheimer's
- Evidence for widespread, severe brain copper deficiency in Alzheimer's dementia - Metallomics (RSC Publishing)
- Error encountered - PubMed - NCBI

- Alzheimer’s disease as copper deficiency - ScienceDirect
- Metabolic interactions among dietary cholesterol, copper, and fructose
- Extra dietary copper inhibits LDL oxidation​

- Intake of copper has no effect on cognition in patients with mild Alzheimer’s disease: a pilot phase 2 clinical trial
- https://www.researchgate.net/public...etabolism_in_rats_fed_a_copper-deficient_diet
- Impact of antioxidants, zinc, and copper on cognition in the elderly: A randomized, controlled trial*
- Interactions in indices of vitamin A, zinc and copper status when these nutrients are fed to rats at adequate and increased levels | British Journal of Nutrition | Cambridge Core
- Alzheimer’s disease causation by copper toxicity and treatment with zinc
- Role of copper in human neurological disorders
- EmeraldInsight
- EmeraldInsight
- http://www.jbc.org/content/106/1/343.full.pdf
- Сopper and the regulation of lipid and carbohydrate metabolism, cardiovascular system function and physical performance - Научные статьи - Библиотека международной спортивной информации
- https://www.intechopen.com/books/li...e-of-copper-as-a-modifier-of-lipid-metabolism
- Effect of copper on carbohydrate metabolism in rats. - PubMed - NCBI
- [The effect of copper on the metabolism of iodine, carbohydrates and proteins in rats]. - PubMed - NCBI [Article in Russian]

 

[Luann]

I thought I read that milk-heavy diets can cause copper to be poorly absorbed. Can't find the study now except for this one: http://www.journalofdairyscience.org/article/S0022-0302(71)86078-2/pdf

Can anyone interpret this and give an idea of how much milk would be too much for someone who is trying to raise copper levels?

 

[What-a-Riot]

Copper Absorption as Affected by Supplemental Calcium, Magnesium, Manganese, Selenium and Potassium
via Amazoniac here
"Results indicated that the calcium supplements depressed fecal copper losses and improved body copper retention as did potassium supplements."

 

[paymanz]

Good to know!

 

[Amazoniac]

Interesting book:
Inflammatory Diseases and Copper -- (Editor: John R. J. Sorenson)

Hepatic Adaptation Process during Inflammatory Conditions: Role of Trace Elements, Lipid Peroxidation and Ceruloplasmin​

"One of the features at the molecular level of inflammatory disorders is the enhanced peroxidative conversion of polyunsaturated fatty acids, both enzymatically, to prostaglandins, thromboxane and (poly)hydroxy-fatty acids, and also nonenzymatically. Lipid peroxidation may be induced by altered levels of copper and iron in and around cells. Both metals have more than one valence state, which render them to redox-active ions. Paradoxically, hydrated copper ions and copper chelated by amino acids or bound to superoxide dismutase and ceruloplasmin, have the ability to catalyze the dismutation of superoxide radicals. Another trace element, zinc, has a univalent cationic form and is an inhibitor of lipid peroxidation. Interactions of copper and zinc will speculatively be discussed in relation to inflammation and inherent hepatic changes."

"Trace elements, free radicals and lipid peroxidation

While contemplating peroxidative processes one inevitably comes across interactions of copper with iron and zinc. Free radical generation is an interesting aspect of copper. Cupric ions added to fatty acid emulsions, lysosome or erythrocyte suspensions, cause lipid peroxidation and inherent malonaldehyde formation. In erythrocytes, Heinz bodies consisting of crosslinked hemoglobin readily appear. It is likely that not cupric ions as such are involved in these reactions, but that reducing substances, for instance ascorbic acid, cysteine and glutathione, convert cupric to cuprous ions (Janelle, 2018). When associated with chloride, as CuCl2 the latter can reduce dissolved oxygen to free radicals. Increased lysosomal lipid peroxidation occurs in the liver of rats fed high levels of copper, whereas in animals with chronic copper poisoning lipofuscin accumulates in the liver. The sequence of reactions occurring during lipid peroxidation, ultimately leading to the formation of malonaldehyde and products of biological substances cross-linked by malonaldehyde , is shown in Figure 1 as a simplified scheme (see: Bonta et al., 1980). Free radicals may be generated by radiation, enzymatic reactions or the interactions of copper and iron with reducing substances in the presence of oxygen. Prevention of lipid peroxidation can be pursued by decreasing the accessibility of free radicals to lipids, or by the application of free radical scavengers, which react with radicals and render them less harmful. The radical which is undoubtedly the most prominent one in biological systems, is the superoxide anion, 02. It is formed enzymatically during the actions of, for instance, xanthine oxidase and a specific NADPH-linked oxidase of granulocytes and monocytes. With regard to free radicals, copper has an ambivalent role, a term which has previously been used in the same context, as for which the present point of view is thought to be relevant (Whitehouse, 1976). Besides the capacity of generating free radicals, copper is effectively involved in the scavenging of superoxide radicals in biological systems. Cytosolic superoxide dismutase, containing 2 atoms copper and 2 zinc per mole, catalyzes the dismutation of superoxide to hydrogen peroxide and molecular oxygen. Hydrated cupric ions and copper-amino acid chelates have almost the same scavenging efficacy (Brigelius et al., 1974). Interestingly, ceruloplasmin, the serum copper storage and transport protein containing 6-7 Cu per mole, is a superoxide scavenger (Goldstein et al., 1979). Ceruloplasmin accounts for more than 90 percent of total serum copper and copper bound cannot be removed by the copper chelator, diethyldithiocarbamate. Albumin and transferrin contain less than 10 percent of serum copper, which is loosely bound, whereas dialysable copper chelates, for instance with histidine and glycine, account for the rest. Zinc is a nutritional copper antagonist, which can alleviate copper toxicity, whereas copper deficiency seems to be an underlying phenomenon of zinc toxicity (Underwood, 1971). While copper is a potential inducer of lipid peroxidation, zinc inhibits. Zinc deficiency, like chronic copper overdosage, leads to enhanced liver microsomal lipid peroxidation in rats (Sullivan et al., 1980). Copper binds to sulfhydryl moieties and may oxidize them, whereas zinc binds and protects against oxidation. Both copper and zinc are active centre atoms of cytoplasmic superoxide dismutase. Low zinc levels occur in the serum of carbon tetrachloride treated rats, whereas administered zinc protects against cirrhosis induced by this compound (Kahn & Ozeran, 1967)."

"Speculations on matching the role of trace elements with hepatic changes during inflammation

Speculation is within the scope of symposia devoted to subjects which are still in the beginning of being well understood. Therefore, with a rather subjective interpretation of existing data, we will make an attempt to combine some observations into a speculative concept. Inflammation characterized by its typical symptoms, is a complex entirety of reactions to combat noxious stimuli. Activated polymorphonuclear leukocytes invade the inflamed area to phagocytose the invader. During phagocytosis, superoxide and hydroxyl radicals are released into the extraphagocytic space. Superoxide is not adequately scavenged as the levels of superoxide dismutase in the extracellular fluid are very low. Because of inadequate scavenging mechanisms, free radicals will react with biologically important molecules, for instance, hyaluronate polymers and membrane fatty acids, the latter reaction resulting in lipid peroxidation (Bragt et al., 1979). Peroxidized fatty acids are chemotactic and will attract more granulocytes and monocytes from the circulation. Many substances are formed at the inflamed site and some of them with a relatively long half-life will reach the liver and "trigger" the acute phase response. Fatty acids and products of their oxidative metabolism, prostaglandins, have already been shown to be potential trigger substances (Carlson et al., 1978). The acute phase proteins are subsequently synthesized at an enhanced rate and released into the blood. The hepatocyte is so occupied by the synthesis of acute phase reactants, that it apparently fails in other functions. This leads to decreased production of catalase (Canonico et al., 1977), glutathioneS-transferases (Fujihara et al., 1979), b-galactosidase and S-N-acetylglucosaminidase (Kaplan & Jamieson, 1977) and possibly glutathione synthetase and reductase. The resulting decrease of hepatic glutathione is as such sufficient to account for the occurrence of lipid peroxidation (Younes & Siegers, 1980). Lipid peroxides are metabolized by the cytochrome P-450 system, which is subsequently inactivated (Svingen et al., 1979) and decreased metabolism of drugs will be a consequence (Adolfs et al., 1980). Decreased hepatic drug metabolism may lead to liver damage due to the lack of conjugation of reactive drug metabolites, whereas the longer half-life of drugs during inflammation enables such high levels to occur, that untoward effects readily manifest themselves.
Enhanced lipid peroxidation may be one of the underlying mechanisms in the development of liver abnormalities, which have been reported to occur during rheumatoid arthritis (Lefkovits & Farrow, 1955). Lipid peroxidation is counteracted by increased serum levels of the protein antioxidant ceruloplasmin. Inhibition of superoxide mediated lipid peroxidation at the inflamed site leads to a decrease in the amount of chemotactic substances and of proteolytic enzymes from granulocytes and macrophages. This may explain the anti-inflammatory effects of copper chelates, which are effective superoxide scavengers. Administration of zinc may lead to an amelioration of inflammatory conditions by displacing copper from low-affinity binding sites or directly, by virtue of being an antioxidant. In this respect, it is important to consider that many anti-rheumatic drugs are antioxidants and that selected antioxidants have antiinflammatory properties (see Bonta et al., 1980). Prevention of hydroxyl radical formation at the inflamed site seems to be a target of anti-inflammatory drugs, as these radicals cause synovial fluid degradation (McCord, 1974).

We were able to demonstrate that scavenging of preformed radicals did not inhibit granuloma formation (Bragt et al., 1980b). Thus, it is likely that the inhibition of hydroxyl radical formation is much more effective than scavenging the radicals after their formation. Copper chelates of low molecular weight are anti-inflammatory drugs (Sorenson, 1978). As drugs they are more advantageous than administered superoxide dismutase, which is a large molecule with a molecular weight of about 34,000 daltons. The large size will prevent the enzyme from crossing membranes, whereas copper chelates of amino acids are rather lipophilic and will rapidly enter cells. This may be an important factor in the lack of superoxide dismutase as an anti-inflammatory drug and this may be amplified by the fact that superoxide dismutase is inactivated by its own product, namely hydrogen-peroxide (Bragt et al., 1980b). Zinc may directly act as an antioxidant, stabilizing lysosomal membranes. Another possibility is that the administration of zinc causes displacement of copper from low-affinity ligands. This kind of displacement is less likely than the displacement of endogenous zinc by administered copper, as the affinity of copper for amino acids is far greater than of zinc. For instance, the stability constants (log Ks) of copper and zinc complexes with histidine are 18.3 and 12.9, respectively. It has also turned out that many anti-rheumatic drugs are free radical scavengers or inhibitors of free radical generation, whereas some antioxidants are anti-rheumatic drugs (see Bonta et al., 1980). With regard to hepatic changes during rheumatoid arthritis and the occurrence of liver damage in arthritic patients, it seems to be rational to consider trials for hepatoprotective agents. Stabilization of the hepatic thiol content may protect the liver from oxidative damage, as it prevents lipid peroxidation and covalent binding of reactive drug (e.g. paracetamol) metabolites to subcellular structures. Finally, it is worth considering a new pharmacological approach, namely the development of drugs, which selectively stimulate the hepatic synthesis of anti-inflammatory acute phase proteins."

 

[Yggr]

Copper Absorption as Affected by Supplemental Calcium, Magnesium, Manganese, Selenium and Potassium
via Amazoniac here
"Results indicated that the calcium supplements depressed fecal copper losses and improved body copper retention as did potassium supplements."

So this would suggest supplementing with calcium when one eats liver would
1. Decrease iron absorption
2. Improve copper absorption

Leading to better ratios of these minerals.

 

[Amazoniac]

I suspect that red light increases the need for copper and the sunny might increase it further when you factor in its involvement in melatonin synthesis. If you feel off after a session of either, consider it.

Another point is that if yousupplement zinc, it might be better not to take it early in the day because it can interfere with the absorption of copper from the current and perhaps next meals, it's possible to induce a copper deficiency this way without realizing. If the dose is low, it's just something to be watchful, perhaps it's still worth supplementing it away from the richest sources of copper in your diet.

Effect of zinc intake on copper excretion and retention in men

"Dietary zinc above the requirement but within a physiological range may have an antagonistic effect on copper balance by reducing copper absorption and increasing fecal copper excretion. To complicate the problem, the estimated intake of dietary copper in US diets may be well below the suggested adequate level of 2 to 3 mg/ day (1-7), creating a possible negative balance situation in man. Our study shows that feeding 18.5 mg of zinc/day, an amount only 3.5 mg above the RDA for adults (8), in diets containing 2.63 mg of copper/day resulted in elevated fecal copper excretion and reduced copper retention during two-week periods. Zinc intakes of this magnitude are quite possible in segments of the population consuming large amounts of protein and with high energy intakes, such as military personnel (44) and adolescent males (45), as well as in those individuals who consume zinc supplements. Whether the negative copper balance would persist in our subjects if they were maintained on the high zinc diet beyond two weeks is unknown."​

But this can also be used to avoid the absorption of excess copper from meals, liver for example.

 

[Steven Bussinger]

This is an excellent thread. I hope I remember to check it the next time I'm researching copper.

 

[Amazoniac]

- Advanced Nutrition and Human Metabolism (978-1-133-10405-6)

Spoiler: Overview of copper digestion, absorption, enterocyte use, and transport

- Speciation of copper in a range of food types by X-ray absorption spectroscopy

"Like many other metals, the chemical form of Cu affects its toxicity. It is known that highly soluble species, such as the sulfate or nitrate, are readily absorbed, while others, such as copper carbonate, are absorbed only after dissolving in the acid secretions of the stomach (WHO, 1996). Less soluble forms, such as copper oxide, are less bioavailable, while insoluble Cu compounds, such as copper sulfide, are not taken up by the body at all. Most copper in foods of plant or animal origin is tightly bound to specific proteins, with a small proportion chelated by amino acids like histidine (Linder & HazeghAzam, 1996)."

"In mammals, Cu is absorbed in the stomach and small intestine, although there appear to be differences among species with respect to the site of maximal absorption (Stern et al., 2007). The liver is central to Cu homeostasis, and most of the newly absorbed Cu first enters this organ. Here it is supplied to endogenous enzymes, incorporated into ceruloplasmin (Cp), and secreted into the blood; if in excess, it is secreted in the bile (Collins, Prohaska, & Knutson, 2010; Gaggelli, Kozlowski, Valensin, & Valensin, 2006). A portion of endogenous Cu is reabsorbed from digestive juices. The Cu in the blood can be viewed as in two pools, one covalently bound to Cp, which accounts for 85–95% of blood Cu in normal humans, and the other more loosely bound to albumin and small molecules, which accounts for the remainder. The term 'free Cu' has been applied to this second pool (Brewer, 2010a). Free or incorrectly bound Cu(II) may act as a catalyst for the generation of the most damaging radicals (Gaggelli et al., 2006). Inappropriate compartmentalization or elevation of Cu(II) in the cell, and inappropriate binding of Cu(II) to cellular proteins are currently being explored as sources of pathological oxidative stress in several neurodegenerative disorders (Gaggelli et al., 2006)."

"[..]dietary Cu, like iron, must be reduced from Cu(II) to Cu(I) for transport across the apical membrane into enterocytes. Amino acids, particularly histidine, methionine, and cysteine, bind to Cu to allow absorption through an amino acid transport system (Gaetke & Chow, 2003). These copper-binding peptides and proteins have little affinity for Cu(II), but their thiol functions may also act as effective reductants (Xiao, Donnelly, Zimmermann, & Wedd, 2008). Once reduced, the metal is likely transported into the enterocyte by copper transporter 1 (CTR1) (Nose, Kim, & Thiele, 2006)."

"Information on the chemical speciation of copper from vegetable and animal foodstuffs is limited (Wapnir, 1998), however it has been shown that the amount of Cu absorbed increases as the amount in the diet increases, but absorption is much more efficient and a higher percentage is absorbed when intake is low (Turnlund, 1998). The mode of absorption in the intestine and subsequent movement within the body is dependent upon the chemical form of the element, therefore, the information on speciation can be used to predict and interpret how the element will be metabolized (Dendougui & Schwedt, 2002)."

"(Brewer, 2010b) presents evidence that ingested soluble inorganic Cu is handled differently to the organically bound Cu found in food. In particular, when giving doses of radioactive 64Cu as an inorganic salt to human subjects as a drink, much of the radioactivity appeared in the blood very quickly and too soon to be processed by the liver (Hill, Brewer, Juni, Prasad, & ****, 1986). When considered in conjunction with the XAS findings, it is not surprising that the bioavailability of Cu species within tap water would be distinct from that of other foods, as this was the only spectrum to consist entirely of Cu(II) species. It is possible that such a large and rapid ingestion of Cu(II), in the form of drinking water, provides the digestive tract with little opportunity to reduce all the ions to Cu(I) prior to uptake. As a result the Cu(II) species may pass directly into the bloodstream by diffusion, as opposed to being transported by CTR1 by enterocytes and then processed via the liver, which is central to this metal's regulation within the body."

"The Cu K-edge XANES spectra of all food samples provided evidence for both Cu(I) and Cu(II) speciation, with Cu(I) dominating in all samples excluding cocoa (identified by the low rising edge inflection energy around 8984 eV) and tap water. PCA [Principal Component Analysis] indicated that the samples had up to five primary Cu species present and, as such, the five model compounds with the lowest target transformation residuals were fitted to the sample spectra: Cu(I) acetate, Cu(II) acetate, Cu(I)-glutathione (GSH), Cu(I)-cysteine and Cu(II)-histidine."

Spoiler: Table 2: Percentage of Cu species in Cu-rich foods

Spoiler: As graph

"Given the differences in bioavailability of Cu species, this research suggests that absorption of dietary Cu could vary markedly, dependent on the types of Cu rich foods consumed. Further research is needed to determine how these species might be altered during the digestion process."​

 

[Amazoniac]

Just in case there are rats with a functional deficiency around:

- Copper Deficiency Decreases Complex IV but Not Complex I, II, III, or V in the Mitochondrial Respiratory Chain in Rat Heart

Spoiler: Table 2 - Cu deficiency and subunit expression levels of mitochondrial respiratory complexes

 

[Sulcuscentralis]

I suspect that red light increases the need for copper and the sunny might increase it further when you factor in its involvement in melatonin synthesis. If you feel off after a session of either, consider it.

Another point is that if yousupplement zinc, it might be better not to take it early in the day because it can interfere with the absorption of copper from the current and perhaps next meals, it's possible to induce a copper deficiency this way without realizing. If the dose is low, it's just something to be watchful, perhaps it's still worth supplementing it away from the richest sources of copper in your diet.

Effect of zinc intake on copper excretion and retention in men

"Dietary zinc above the requirement but within a physiological range may have an antagonistic effect on copper balance by reducing copper absorption and increasing fecal copper excretion. To complicate the problem, the estimated intake of dietary copper in US diets may be well below the suggested adequate level of 2 to 3 mg/ day (1-7), creating a possible negative balance situation in man. Our study shows that feeding 18.5 mg of zinc/day, an amount only 3.5 mg above the RDA for adults (8), in diets containing 2.63 mg of copper/day resulted in elevated fecal copper excretion and reduced copper retention during two-week periods. Zinc intakes of this magnitude are quite possible in segments of the population consuming large amounts of protein and with high energy intakes, such as military personnel (44) and adolescent males (45), as well as in those individuals who consume zinc supplements. Whether the negative copper balance would persist in our subjects if they were maintained on the high zinc diet beyond two weeks is unknown."​

But this can also be used to avoid the absorption of excess copper from meals, liver for example.

I frequently feel fatigued after sun exposure, red light seems to be fine.

 

[sunraiser]

Another point is that if yousupplement zinc, it might be better not to take it early in the day because it can interfere with the absorption of copper from the current and perhaps next meals, it's possible to induce a copper deficiency this way without realizing. If the dose is low, it's just something to be watchful, perhaps it's still worth supplementing it away from the richest sources of copper in your diet.

But at the same time it's important to put across that a long term zinc deficiency also implies a very likely copper deficiency. Not just because of their agonist/antagonist relationship but because zinc is necessary in the uptake of vitamin A and creation of retinol binding protein. Without properly metabolised retinol then the body can't make ceruloplasmin to bind and use copper.

Often a person will be recovering from both zinc and copper deficiency at the same time, and I wonder if liver is too intense a source of copper to sustain at first.

Anti peat but I personally enjoy and crave cashews and 70 percent dark chocolate with berries and yogurt as a copper rich meal.

 

[Amazoniac]

- An Interview With Dr. Raymond Peat | Mary Shomon

"The absorption and retention of magnesium, sodium, and copper, and the synthesis of proteins, are usually poor in hypothyroidism."​

 

[LeeLemonoil]

I'm always reading about an eye/corneal disease called Keratocons because I know some people plagued by it.

There is currently testing underway for eyedrops that might cure or help with that condition, and those drops are based on copper. The reasoning behind has to to do with LOX:

VMED-80 is a copper-based topical treatment for keratoconus that is currently under investigation by iVeena Delivery Systems, Inc, (founded by Bala Ambati, Professor of Ophthalmology, University of Utah, Salt Lake City, UT, USA). IVMED-80’s mechanism of action is believed to center on enhancing the activity of lysyl oxidase (LOX) – the enzyme responsible for corneal collagen crosslinking, and also known to be associated with keratoconus (1).

The essential cofactor for the enzyme? Copper. “And that led us to our hypothesis that if we supplement with copper, we could enhance LOX activity and corneal stiffening,” says Sarah Molokhia, Vice President of Research and Development at iVeena.

Variation in the lysyl oxidase (LOX) gene is associated with keratoconus in family-based and case-control studies. - PubMed - NCBI


Now having spent a lot of time researching KC I'm sure they will not suceed.

I'm stating this here because I chatted with Ella about it who is extremely knowledgebale about corneal healt and disease and she had the following to say about KC/LOX:


Yes, copper dysregulation. In KC corneas you find copper deposits Kayser Fleischer ring
Kayser–Fleischer ring - Wikipedia
This is due to liver not handling copper appropriately. We see this in Wilson's Disease and is treated with zinc supplementation.

This is why Peat's comment on copper dysregulation due to low thyroid function is important. We have a situation of being copper toxic yet deficient in bio-available copper.

KCers have a high need for zinc to compete, preventing the accumulation of bio-unavailable copper. However, the root cause is really the hypothyroidism which must be addressed for the proper regulation of copper.

I am certainly interested in those LOX SNPs.

The following Greek researchers ruled out VSX1, long time thought to be associated with KC. Interesting though, the variant for the SOD1 was associated with KC. SOD1 is a copper/zinc dependent enzyme. Copper dysregulation will greatly affect this enzyme. So when it comes to supplementation, its going to be tricky, tricky. However, if we address the hypothyroidism + a pro-thyroid diet, the copper dysregulation should resolve itself.