15 Milligrams Of Copper In A Day Without Liver Or Supplements To Meet AI

[Amazoniac]

À la carte:

Spoiler: Poetry

Even though there are lists of food sources of copper everywhere (many are incomplete), what's missing is how they look like when integrated into practice.

Some of you may have been annoyed that I didn't include the specific content for each food in the potassium thread, but it was doned on the purpose: by ranking foods according to amount, the person is tempted to prioritize certain items over others based on a specific nutrient, which is as silly as this 'Absurd Intake' of copper.

I find it better to have a comprehensive list of decent sources (most here provide more than 0.1 mg of cupre/serving), and they can add up to at least 2 mg without difficulty even if your selection misses the best sources.

Sometimes it's difficult to decide what to leave and what to discard. As an example (for being one of the foods with lowest content/serving), 1 medium apple provides 0.05 mg of copper, and it would seem reasonable to exclude it, but if the person eats 4 of these a day, you have 0.2 mg, which is close to the amount that some avocados provide, being considered good sources; so the apple contribution doesn't end up being insignificant.

It's interesting that this could've been brutalized to something close to 30 mg (!) by the inclusion of liver. Hopefully this thread encourages people to reconsider their struggle in getting enough copper.

After thinking about how this information could be more valued, I arrived at this:
The fructose–copper connection: Added sugars induce fatty liver and insulin resistance via copper deficiency

<°)com)pli)ment)><​

Also relevant:
Copper Deficiency In Humans

Do red lights increase the need for copper or precipitate an insufficiency?

Spoiler: Notable copper food sources

Copper in health - Wikipedia

Spoiler: Comprehensive list of zinc food sources

- Oyster

Spoiler: >15 mg example

As a coincidence, it's providing more than 15 g of potassium.
The usual FDA serving is 85 g.

Before you leave an iron message, please remember how much copper it's providing.

 

[michael94]

iron message

 

[InChristAlone]

Why would you want 15 mg copper?

 

[Amazoniac]

Why would you want 15 mg copper?

Spoiler

1. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
2. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
3. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
4. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
5. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
6. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
7. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
8. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
9. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
10. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
11. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
12. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
13. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
14. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
15. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.

I still haven't deleted the list. If someone is having difficulty getting enough copper and wants me to post a personalized example, just leave a message with categories that you like and dislike from the list and I'll try to do it.

 

[Light]

Spoiler

1. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
2. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
3. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
4. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
5. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
6. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
7. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
8. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
9. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
10. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
11. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
12. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
13. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
14. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.
15. It's not a 15 fixation, it's not OCD. The current RDA is 0.9 mg/d, so it's an atttempt to be 15x healthier and some extra for apocalyptic reserves.

I still haven't deleted the list. If someone is having difficulty getting enough copper and wants me to post a personalized example, just leave a message with categories that you like and dislike from the list and I'll try to do it.

List of vegetarian, non-starchy foods, please.

BTW, how much copper is too much?
And do you happen to have Ray Peat's remarks on copper and aging (something about all the visible signs of aging being a result of copper deficiency??)

Thank you so much :)

 

[Aymen]

Hi @Amazoniac , is the copper in beef liver protective against excess iron or should i use caffeine with beef liver ?

 

[Amazoniac]

List of vegetarian, non-starchy foods, please.

BTW, how much copper is too much?
And do you happen to have Ray Peat's remarks on copper and aging (something about all the visible signs of aging being a result of copper deficiency??)

Thank you so much :)

Oh shiτ, I forgot to include shrimp/prawns on the list.

Is this what you's referring to?

Nothing bad observed from 10 mg of cupre gluconate a day for the given period:

Lack of effects of copper gluconate supplementation

Abstract
"A double-blind study was done giving 10 mg of copper/day as copper gluconate or placebo capsules for 12 wk. The seven subjects receiving copper gluconate had no change in the level of copper in the serum, urine, or hair. There was also no change in the levels of zinc or magnesium. There was also no significant change in levels of hematocrit, triglyceride, SGOT, GGT, LDH, cholesterol, or alkaline phosphatase. The side effects of nausea, diarrhea, and heartburn were the same in the subjects receiving copper gluconate and subjects receiving placebo capsules."​

But in a more detailed experiment they noticed differences with chronic great intakes:

Long-term high copper intake: effects on indexes of copper status, antioxidant status, and immune function in young men

"The men [of this experiment] lived in the Western Human Nutrition Research Center’s metabolic research unit for 18 d (MP-A) while consuming a diet containing 1.6mgCu/d, followed by a 129-d free-living period during which they consumed their usual diets along with copper supplements containing 7 mg Cu/d. They returned to the metabolic research unit for another 18 d (MP-B), and their diets were supplemented with 6.2 mg Cu/d for a total of 7.8 mg/d."

"[..]copper supplementation studies have shown that indexes of status do not tend to be influenced by additional dietary copper. For example, copper status did not change in healthy infants as a result of copper supplementation (35). Two different studies reported no change in indexes of copper status when adult men were supplemented with 2 or 3 mg Cu/d (5, 8). In 6- and 8-wk supplementation regimens with <6 mg Cu/d, consistent increases in traditional indexes of copper status were not observed (6, 9). Nor did indexes of copper status change after feeding diets containing 7.8 mg Cu/d for 24 d (4)."

"Although studies lasting up to 8 wk with < 6 mg Cu/d did not change indexes of copper status, if long-term copper supplementation results in the accretion of total body copper, then changes in indexes of copper status might be expected. The results of the current study show that increases in some indexes of copper status can occur after 5 mo of a high copper intake. The significant changes that were observed in SOD, ceruloplasmin activity, and BAO activity were found under the highly controlled conditions of our metabolic research unit. These were accompanied by increased urinary copper and hair copper concentration. Although urinary and hair copper represent routes of excretion, the amounts excreted by these routes were small and the increases would be expected to have little effect on copper retention. Taken together, these findings suggest that long-term high copper intake may alter copper status. [The body can regulate only up to a certain intake] The physiologic significance of these changes is unknown."

"Ceruloplasmin activity, benzylamine oxidase, and superoxide dismutase were significantly higher at the end of the second MRU [metabolic research unit] period than at the end of the first. Urinary copper excretion, hair copper concentrations, and urinary thiobarbituric acid–reactive substances were significantly higher during the second MRU period than during the first. Polymorphonuclear cell count, the percentage of white blood cells, lymphocyte count, and interleukin 2R were affected by copper supplementation. Antibody titer for the Beijing strain of influenza virus was significantly lower in supplemented subjects after immunization than in unsupplemented control subjects."

Added to juice​

"Under highly controlled conditions, long-term high copper intake results in increases in some indexes of copper status, alters an index of oxidant stress, and affects several indexes of immune function."​

A point against relying on this is that people were healthy and more apt to regulate and minimize issues with excesses; but on the hands of the others the majority of intake was from supplements, so it's likely safer when you're obtaining copper solely from diet.

The problem is that inorganic cupre is out there in the enwironment.

Dietary copper and human health: Current evidence and unresolved issues

"[..]the Cu concentration in drinking water may also vary depending on groundwater table composition and household plumbing systems. Soft acidic water causes corrosion in Cu pipes and increases tap water Cu concentration. For instance, tap water Cu concentration has been shown to vary largely in dwellings, with 0.02 mg/L to 3.5 mg/L in Berlin [36] and 0.1 to 5 mg/L in Uppsala and Malmö [37]. Altogether, these variations represent serious hindrances in the assessment of Cu intake both at individual and population levels, and Cu content in food composition databases must be considered with caution."

"Little information is available regarding Cu intake and adequacy in populations with specific diets such as vegetarians, vegans or those practicing macrobiotics. An analysis of duplicated meals has shown that the Cu density of a vegan diet was more than twice that of an omnivorous diet (0.7±0.29 vs 2.0±0.34 mg/1000 kcal for the vegan and omnivorous diet respectively) [44]. In the same way, daily Cu intake was 27% higher in vegetarians than in omnivorous adolescent females [45]. The higher Cu content of a plant-based diet has been consistently shown to compensate for the slightly reduced bioavailability of Cu resulting from the presence of phytates and fibers, suggesting that diets low in or devoid of animal products provide an adequate amount of Cu [17, 21, 46]."​

Ratos appear to be more vulnerable to high fructose intakes than humans, but many people are compromised and this hinders your ability to process everything properly. It's also worth mentioning that what they consider extremely high intakes of fructose in rat experiments (20% of energy in one of them for example) is still far what some members get: which can be 30% or more (60% sucrose).

Getting much more than enough (which is probably 3 mg or so for most) on a daily basis makes no sense if there are no benefits but risks to it. Not getting enough is likely more detrimental than the excess.

--
A light example:

Spoiler

I had a brilliant idea of adding 15 cups of table salt as a joke, only to realize later that everything was changed, having to shoot at the screen alll over the again.​

--

Hi @Amazoniac , is the copper in beef liver protective against excess iron or should i use caffeine with beef liver ?

What is concerning the most about liver is copper and vitamin A content, these will limit your consumption much earlier than the amount of iron.
Coffee is way more effective than caffeine in impairing iron absorption.

 

[Light]

Is this what you's referring to?

YES! Thank You:)

And thank you for this awsome information.
As a vegetarian (+gelatin) this is precious information.
I'm surprised to see you got 15mg of iron from an almost completely vegan diet, maybe the goat cheese made the difference.
There's no way I can eat so many fruits in a day, but 3-4 mg/day seems reasonable to achieve, plus whatever's in my water. (3mg/L sounds insane)

Ratos appear to be more vulnerable to high fructose intakes than humans, but many people are compromised and this hinders your ability to process everything properly. It's also worth mentioning that what they consider extremely high intakes of fructose in rat experiments (20% of energy in one of them for example) is still far what some members get: which can be 30% or more (60% sucrose).

Is there any indication that if you increase copper intake it can balance out increase of fructose intake, or should you just try to keep fructose relatively low? (- I have seen that increasing fructose leads to reduced copper and therefore increased iron and NAFLAD, but I don't know the mechanism)

 

[Amazoniac]

YES! Thank You:)

And thank you for this awsome information.
As a vegetarian (+gelatin) this is precious information.
I'm surprised to see you got 15mg of iron from an almost completely vegan diet, maybe the goat cheese made the difference.
There's no way I can eat so many fruits in a day, but 3-4 mg/day seems reasonable to achieve, plus whatever's in my water. (3mg/L sounds insane)


Is there any indication that if you increase copper intake it can balance out increase of fructose intake, or should you just try to keep fructose relatively low? (- I have seen that increasing fructose leads to reduced copper and therefore increased iron and NAFLAD, but I don't know the mechanism)

Major sources of iron in your example were: cheese, dates, figs, and kale. It's possible to reduce it to less than 10 mg without difficulty but the absorption of this kind of iron is already lower (5-12% on awerage) and you'll read below that for copper it's higher.


Advanced Nutrition and Human Metabolism (978-1-133-10405-6) - Sareen Gropper and Jack Smith

"Most copper in foods is found as Cu2+ and is bound to organic components, especially amino acids that make up food proteins. Thus, digestion is needed to free the bound copper before absorption can occur. Gastric hydrochloric acid and pepsin facilitate the release of bound copper in the stomach. Additional proteolytic enzymes in the small intestine hydrolyze proteins further to release copper."

"Typically, the gastrointestinal tract absorbs about 50% to 80% of ingested copper. Fractional absorption of copper increases as copper intake decreases, and vice versa. Absorption, for example, may average about 20% when copper intake is high, such as >5 mg/day, but increases to over 50% when intake is <1 mg/day [3–6]. Copper absorption was calculated at 75% with an intake of 350 μg of copper, an amount that is about one-half of an adult’s requirement for the mineral [1]."

"Examples of ligands or chelators that facilitate copper absorption include amino acids, especially histidine and cysteine. Whether copper bound to these amino acids can be absorbed through amino acid carrier systems is not clear. Copper also forms ligands with sulfhydryl groups in cysteine residues that are found within the tripeptide glutathione. Glutathione is found both within the lumen of the gastrointestinal tract and intracellularly.

The presence of organic acids in foods also improves copper absorption. Citric, gluconic, lactic, acetic, and malic acids act as binding ligands to improve solubilization and thus absorption of copper. Citric acid, for example, forms a stable complex with copper and improves its absorption. A more acidic environment, as found in the proximal intestine versus the distal intestine, also favors copper absorption."

"Just as an acidic environment facilitates copper absorption, the opposite is true of an alkaline environment. Excessive antacid ingestion or the use of medications such as H2 receptor blockers (such as Zantac [ranitidine], Tagamet [cimetidine], or Pepcid [famotidine]), and proton pump blockers (such as Prevacid [lansoprazole] or Prilosec [omeprazole]), which are commonly taken to treat heartburn, gastroesophageal reflux disease, and ulcers, results in a high-pH (more alkaline) environment and can diminish copper absorption. Copper atoms in an alkaline medium often bind to hydroxides (OH), forming insoluble compounds that are not readily absorbable."

"Zinc can also impede copper absorption. The use of zinc supplements, typically in amounts of about 40 mg or more, has been shown to impair copper absorption and diminish copper status. The detrimental effect of excessive zinc intake on copper absorption is thought to result from zinc’s stimulation of metallothionein synthesis in intestinal cells. Although its synthesis is stimulated by zinc, metallothionein more avidly binds copper than zinc, and thus reduces copper’s luminal-to-serosal flux (i.e., from the lumen of the gastrointestinal tract across the basolateral membrane) and entry into the blood. Copper deficiency induced by high zinc intake can be difficult to correct. For example, when zinc (110–165 mg) supplements were taken for 10 months, discontinuation of the zinc and 2 months of oral copper supplementation failed to correct the copper deficiency. Intravenous administration of cupric chloride for 5 days (total dose of 10 mg) was needed to bypass the intestinal cells and correct the deficiency, suggesting that the correction of a zinc-induced copper deficiency is a slow process [7]."

"Selected Functions of Copper

• Ceruloplasmin: iron oxidation and antioxidant
• Superoxide dismutase: antioxidant
• Cytochrome c oxidase: ATP production
• Amine oxidases: oxidation of biogenic amines
• Lysyl oxidase: collagen and elastin cross-linking
• Dopamine monooxygenase/hydroxylase: norepinephrine (catecholamine) synthesis
• Tyrosinase: melanin pigment production
• p-hydroxyphenylpyruvate hydroxylase: tyrosine degradation
• Peptidylglycine α-amidating monooxygenase: activation of selected hormones
• Factors V and VIII: blood clotting (!)
  
• Immune function
• Gene expression"

"With copper deficiency, the activity of ceruloplasmin and the expression of hephaestin are reduced, and iron remains mostly trapped within cells. Thus, copper deficiency results in a secondary iron-deficiency anemia, and treatment with copper (and not iron) is required to correct the problem."

"Another nutrient that interacts with copper is molybdenum, which can enhance copper excretion. Urinary copper excretion has been shown to rise as molybdenum intake increases. For example, urinary copper excretion rose from 24 to 77 μg/day as molybdenum intake increased from 160 to 1,540 μg/day [11]. No changes in fecal copper excretion were noted, suggesting that molybdenum may have increased copper mobilization from tissues and promoted excretion [11]."

"Copper is excreted primarily (>95%) through the bile into the feces. In fact, biliary copper excretion is regulated by the liver to maintain copper balance (homeostasis). Thus, with high dietary copper intake, biliary copper excretion via the feces increases, and with low dietary copper intake, fecal copper excretion decreases. At a copper intake of about 1.4 mg/day, fecal copper excretion is about 2.4 mg/day [12]."

"D-penicillamine therapy [for Wilson's disease is intended to] bind body copper and increase its urinary excretion."​

The fatty liver problem is related to mitochondrial dysfunction, inflammation, and excess iron.

Iron's Dangers

"Copper is the crucial element for producing the color in hair and skin, for maintaining the elasticity of skin and blood vessels, for protecting against certain types of free radical, and especially for allowing us to use oxygen properly for the production of biological energy. It is also necessary for the normal functioning of certain nerve cells (substantia nigra) whose degeneration is involved in Parkinson's disease. The shape and texture of hair, as well as its color, can change in a copper deficiency. Too much iron can block our absorption of copper, and too little copper makes us store too much iron. With aging, our tissues lose copper as they store excess iron. Because of those changes, we need more vitamin E as we age."​

With this in mind, getting plenty of copper (but not excess) should be protective.

Copper-Fructose Interactions: A Novel Mechanism in the Pathogenesis of NAFLD

"A growing body of evidence indicates that hepatic copper level is lower in NAFLD patients, and steatosis grades inversely correlate with hepatic copper content [52,53,54,55,56]. Moreover, dietary copper restriction induces hepatic steatosis and insulin resistance in rats, suggesting that copper availability may be involved in the development of NAFLD [52]. The mechanism leading to low copper levels in NAFLD patients is not clear. Multiple factors can lead to copper deficiency, including the amount of copper in the diet. The Western diet often is low in copper [57,58]. Other factors, including bariatric surgery, pancreatoduodenectomy, excessive use of denture cream high in zinc and excessive intake of soft drinks, with added fructose, can also induce copper deficiency by impairing copper absorption [59,60,61,62,63,64,65,66,67]."

"It appears that fructose-induced fatty liver is unlikely the direct effect of fructose metabolism. This leads to the hypothesis that the activation of lipogenesis and blockade of fatty acid oxidation signaling might account for the hepatic steatosis induced by fructose metabolism [27]."

"Analysis of 124 adult biopsy-proven NAFLD patients revealed that serum copper as well as liver copper levels are lower compared to healthy controls and patients with other types of liver diseases, including hepatitis C virus (HCV) infection, autoimmune hepatitis, and alcoholic liver disease. Among these NAFLD patients, NASH patients displayed even lower hepatic copper levels than those with simple steatosis. Hepatic copper level is lower in NAFLD patients with the metabolic syndrome and T2D compared to those without metabolic syndrome and T2D [52]. Moreover, NAFLD patients with lower serum copper and lower liver copper exhibited higher serum ferritin levels and hepatic iron levels, which were associated with decreased mRNA expression of liver ferroportin-1 (FP-1) [53]. Similar results were obtained from pediatric NAFLD patients [54,56]. More severe NAFLD (NAFLD activity score, NAS ≥5) patients, particularly in those with ballooning hepatocytes, displayed significantly lower serum copper and ceruloplasmin levels compared to the patients with less severe NAFLD (NAS ˂ 5) [56]."

"Of note, NAFLD patients displayed significantly lower hair copper concentrations [129]. Moreover, dietary copper restriction induces hepatic steatosis and insulin resistance in rats, further suggesting that copper availability may be involved in the development of NAFLD [52]."

"[..]both copper deficiency and excess may lead to hepatic steatosis and, in some cases, more severe distinct liver pathology. The relationship between copper and NAFLD has recently been reviewed [138,139]."

"Extensive studies in 1980’s demonstrated that dietary copper-fructose interactions worsened copper deficiency-induced metabolic syndrome. The severity of experimental copper deficiency was exacerbated by a diet containing high fructose compared to animals with diets containing high glucose or starch [50,51,69,70,71], and this was characterized by lower body weight and hematocrit, and increased liver weight, blood urea nitrogen, ammonia, cholesterol and triglycerides. Switching the type of dietary carbohydrate from fructose to either starch or glucose ameliorated the severity of copper deficiency [50]. In line with animal studies, a human study demonstrated that adult males displayed significantly reduced SOD1 activity in erythrocytes after consumption of a low copper (1.03 mg/day/2850 kcal) and high fructose (20% calorie) diet for 11 weeks compared to those who consumed diets with low copper and starch [60], suggesting dietary fructose intake can affect indices of copper status."

[60] I suppose that the amount of glucose in their diets balanced the purified fructose added to a group.​

"Iron overload is considered as a partial potential mechanism underlying copper deficiency and fructose induced metabolic syndrome [147,148,149,150]. We showed that marginal copper deficient and high fructose diet markedly increased liver iron level (Figure 4) [49] as well as plasma ferritin level in rats [48]. Similarly, NAFLD patients with low copper levels had hepatic iron overload [52,53]. Mechanism(s) by which copper deficiency induces iron overload have been partially elucidated. Cellular iron export requires members of a family of copper-containing ferroxidases, including ceruloplasmin and hephaestin which oxidize iron from the ferrous to ferric forms. The ferric form of iron binds to Apo-transferrin, thereby facilitating transferrin delivery to peripheral organs. Hephaestin functions to move iron across the basolateral membrane of intestinal epithelial cells into the circulation. Hephaestin-deficient mice display iron deficiency anemia with accumulation of iron in enterocytes [151]. Ceruloplasmin exerts its action on intestinal iron absorption, iron release from macrophages and hepatocytes [152,153]. A clinical phenotype of NAFLD that we regularly see is a young adult male with modestly decreased serum ceruloplasmin, increased serum ferritin, and high fructose intake via sugared pop."

"Copper deficiency induced hypercholesterolemia is likely due to increased cholesterol synthesis [172]. Hepatocytes isolated from rats fed with a copper deficient diet for 7-8 weeks exhibited 90% reduction of copper content compared to those from adequate copper fed rats. After three hours incubation, these cells displayed 2–3 fold increase in the intracellular glutathione (GSH) synthesis rate along with the increased intracellular and extracellular GSH [175]. Treatment with L-buthionine sulfoximine (BSO), a specific GSH synthesis inhibitor, abolished the hypercholesterolemia and increased HMG-CoA reductase (HMGCR) activity in rats fed with copper deficient diet [142]. These results suggest that copper deficiency induced hypercholesterolemia and increased HMG-CoA are the consequence of increased GSH synthesis. Moreover, the induction of FAS expression was also prevented by BSO in copper deficient rats [144]. One hypothesized mechanism for the increased synthesis of GSH is a compensatory mechanism to the decreased antioxidant defenses due to the decreased cuproenzymes [48,154]."

Fattening up the liver seems protective to prevent the iron reactions from continuing.​

"Several lines of evidence indicate that copper might be involved in the regulation of gut microbiota and gut barrier function. First, copper has been used as an antimicrobial agent throughout the ages [188], and the response to copper stress varies among different bacteria species [189,190]. Second, one of the copper containing enzymes, diamine oxidase, was found in high concentrations in intestinal mucosa and its circulating enzyme activity serves as a marker of mucosal maturation and integrity, as does the copper level [191,192,193]. Thus, decreased copper levels may exacerbate dietary fructose-induced gut microbiota dysbiosis and/or gut barrier dysfunction."​

 

[Amazoniac]

- Copper bioavailability and metabolism (978-1-4612-7855-9)

"Major mineral antagonists to copper utilization have been listed as being sulfur, silver, iron, molybdenum, potassium, cadmium, zinc, lead and selenium (Owen, 1982)."

"Other mineral interactions which might affect copper bioavailability have also been studied. Among these are the following:

• Bismuth (Szymanska and Zelazowski, 1979)
• Calcium (Hemmingway et al., 1962; Hoeferet et al., 1960; Schryver, 1974)
• Chromium (Owen, 1982)
• Cobalt (Veitrup, 1979; Autio and Sa ikonen , 1963)
• Fluoride (Imam, 1976)
• Magnesium (Mahler et al., 1971)
• Manganese (Burch et al., 1975; deRosa et al., 1980; Lehmann et al., 1971; Leu et al., 1971)
• Mercury (Li and Furst, 1977; Nielsen et al., 1980; Olsen and
• Jonsen, 1979; Schroeder and Nason, 1974; Schroeder et al., 1974; Spears et al., 1974; 1975)
• Phosphorus (Comar et al., 1949; Schryer et al., 1974; Spencer, 1966; Sultie and Field, 1970)
• Sodium (Schroeder and Nason, 1974; Harms and Eberst, 1974)
• Tin (deGrott, 1973; Schroeder and Nason, 1976)
• Germanium (Schroeder, 1976)
• Niobium (Schroeder, 1976)
• Zirconium (Schroeder, 1976)
• Rhodium (Schroeder, 1976)
• Yttrium (Schroeder, 1976)
• Vanadium (Schroeder, 1976)"

"Whether or not a mineral is an enhancer or inhibitor to copper utilization or whether no effect at all is demonstrated varies with the species, with the level of intake of the minerals, and with intakes of other dietary constituents. Because of the numerous possible primary and secondary interactions among minerals in the lumen of the gastrointestinal tract, predictions on whether or not one dietary element will have a positive or negative effect are impossible to ascertain. In addition, many other dietary constituents including vitamins (ascorbic acid, vitamin E, pantothenic acid, vitamin B6, and poison/"vitamin" A), amino acids, fiber, sugars and fat may have primary or secondary effects on copper absorption."​

 

[golder]

Tried to find ray's opinion on the best form of copper, as there's many different varieties. Can't seem to find anything on it...if anyone could help that would be amazing, thanks guys!

 

[southcesar]

Hi @Amazoniac , is the copper in beef liver protective against excess iron or should i use caffeine with beef liver ?

Wouldn't too much liver cause thyroid problems because of vitamin A? (I was thinking about eating a small piece of liver every day for copper) Has anyone ever looked at that Ayurvedic practice of drinking water in copper cups?