Root Cause Protocol & A Ray Peat Perspective

youngsinatra

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The statement mission of the Root Cause Protocol:

The RCP is designed to:

1. increase bioavailable COPPER (Ceruloplasmin) in order to...
2. decrease unbound IRON and...
3. decrease the MAGNESIUM burn rate in order to...
4. repair cellular mineral imbalance - the ROOT CAUSE of virtually ALL health challenges.

RCP Handbook (The Root Cause Protocol | Handbook Download)

I always found this concept quite fascinating as I have been struggling with low ceruloplasmin/copper mixed with iron dysregulation and magnesium deficiency symptoms for nearly 2 years, but for me, the RCP approach did not work out.

I think Ray‘s health philosophy could (theoretically) help us achieve the goals of the RCP, without following the protocol per-se.

This is just a hypothesis, that I have not yet tested out. But it might be interesting nonetheless.

In the following I want to present the peatarian perspective.

1. How to raise ceruloplasmin:

We know that thyroid hormone regulate ceruloplasmin and serum copper levels by controlling hepatic export and transport protein synthesis.

„In the present paper we show that serum copper levels are regulated by thyroid hormone, which stimulates the synthesis and the export of the hepatic copper-transport protein ceruloplasmin into the serum.“
(Serum copper as a novel biomarker for resistance to thyroid hormone)

In subclinical hypothyroid subjects, mean serum ceruloplasmin levels were found to be significantly lower in comparison to healthy subjects (p<0.0001).“
(Analysis and establish a correlation between serum ceruloplasmin, serum apelin level and thyroid profile in patients with hypothyroidism and healthy controls | International Journal of Research in Medical Sciences)

„Here we describe a 3-year-old Caucasian girl who was admitted to our Clinic due to pericardial effusion, muscle weakness and weight gain. At clinical examination, she presented with bradycardia, pale and round face, pseudohypertrophy of calf muscles and no pitting edema of the limbs. Routine blood investigations showed high serum aspartate and alanine aminotransferase levels, low serum ceruloplasmin without clinical signs of Wilson's disease, dyslipidemia. Thyroid function tests revealed a picture of severe hypothyroidism associated with HT. After the replacement treatment with L-T4, thyroid-stimulating hormone serum levels gradually decreased, with concomitant resolution of pericardial effusion and normalization of ceruloplasmin levels.“
(Hypoceruloplasminemia: an unusual biochemical finding in a girl with Hashimoto's thyroiditis and severe hypothyroidism - PubMed)

„Compared to euthyroid participants, patients with clinical hypothyroidism had statistically significant (P < 0.05) lower levels of serum copper and ceruloplasmin. The scenario was the opposite in the case of Grave's hyperthyroidism patients. Our study found statistically significant (P < 0.05) higher serum copper and ceruloplasmin levels in Grave's hyperthyroidism patients.
(Study of copper and ceruloplasmin in hypothyroidism and Grave's hyperthyroidism as compared to euthyroidism: Hospital-based case–control study Bhat VG, Patra R, K. Raju D S, Mohandas G V, Rao N L, - J Indian Prosthodont Soc)

Ray also recommended regular consumption of copper-rich foods like oysters, shellfish and liver.

A deficiency of copper causes our tissues to retain an excess of iron, so foods such as shrimp and oysters which contain abundant copper should be used regularly." - Ray Peat, PhD



The RCP recommends getting the serum copper to 100 mcg/dl and the serum ceruloplasmin to 30 mg/dl.
("Ideal" Values for Lab Tests - The Root Cause Protocol)

Ray said that the middle of the reference range for ceruloplasmin would be a good level. So roughly 30-40 mg/dl.

2. How to lower the iron footprint?

Ray recommended a low iron diet. He also recommended dairy (calcium) and coffee consumption with iron-rich meals to reduce iron absorption.

„Iron causes cell aging.

Drinking coffee with iron rich foods can reduce iron's toxic effects.

Use shrimp and oysters, etc., to prevent the copper deficiency which leads to excess storage of iron.

Avoid food supplements which contain iron.

Take about 100 units of vitamin E daily; your vitamin E requirement increases with your iron consumption.“
— Ray Peat PhD

He also wrote that a lower iron saturation is protective against cancer (I think he thought <25% was good, but I couldn’t find a quote, so I‘m not 100% sure)

This is in alignment with the RCP. The RCP also recommends a ferritin level between 20-50.

The RCP recommends lowering iron with blood donation.

Ray said:

„Blood transfusions damage immunity, and excess iron has been suspected to be one of the causes for this. People who regularly donate blood, on the other hand, have often been found to be healthier than non-donors, and healthier than they were before they began donating.“

3. How to restore magnesium levels?

Ray said that a hypothyroid person does not retain magnesium well and that a lot of benefits from thyroid supplementation come from increased magnesium retention.

„Magnesium is rapidly lost from cells in hypothyroidism.“ - Ray Peat PhD

„These data indicate that thyroid hormone has a direct stimulatory action on the cellular transport of magnesium. The ability of thyroid hormone, as well as altered extracellular concentrations of magnesium, to influence the cellular transport of magnesium is indicative of a regulated process involving either active transport or facilitated diffusion. A probable but not invariable result of the hormonal stimulation of magnesium transport appears to be a preservation of normal cellular concentrations of magnesium despite a tendency to depletion of extracellular magnesium in hyperthyroidism and to an excess of extracellular magnesium in hypothyroidism.“
(https://academic.oup.com/jcem/article-abstract/26/10/1081/2717825?redirectedFrom=fulltext)

„You can get enough magnesium from ordinary food if your thyroid let‘s you retain it“ (YouTube: „Ray Peat on magnesium from foods. Thyroid retaining magnesium.“)

4. How to restore mineral balance?

Ray said that thyroid/CO2 regulates mineral balance. So increasing thyroid activity or taking a thyroid supplement should restore mineral balance.

Ray also recommended the consumption of milk, eggs, oysters, shrimp, liver, orange juice and ripe fruits for adequate mineral intake.


View: https://m.youtube.com/watch?v=74oLBrVddFs

The RCP on other hand recommend HTMA testing for mineral balancing.

The big difference between the two remain:

• RCP avoids vitamin D. Ray thinks that vitamin D is helpful.
• RCP does not recommend a high calcium intake. Ray thinks it’s essential for keeping PTH in check.
• RCP avoids hormone therapy. Ray thinks it‘s sometimes necessary to overcome a problematic environment.
• RCP focuses on the adrenals. Ray focuses on the thyroid to ease off the adrenals from compensating for low thyroid function.
• RCP focuses on addressing liver function through diet and supplements. Ray thinks that a hypothyroid person has almost inherently a sluggish liver function.
 
Last edited:

Mad

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Thanks for the post. I’ve been listening to just a few Morley Robbins things lately and thinking…aren’t we sort of speaking the same language over here, kind of? Nice to see someone write up some connections
 

xeliex

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Thank you for this excellent post.

Putting it in writing like you did, helps a lot understand Ray's viewpoints that can be applied to anything.
Many other approaches overcomplicate things.
 

moa

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i stopped taking copper supplements with my zinc 4 weeks ago. i only take an average of about 10-15mg per day.

i wonder what's the truth about copper, how important is it really, and it's there anything like copper toxicity ?

i have a tendency to attention deficit, low zinc, IBS, and they always warry about copper toxicity, but it's it really such a thing as copper toxicity ? or is it only vitamin a toxicity, lack of antioxidants, lack of zinc, with copper being accused ?
 
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youngsinatra

youngsinatra

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i stopped taking copper supplements with my zinc 4 weeks ago. i only take an average of about 10-15mg per day.

i wonder what's the truth about copper, how important is it really, and it's there anything like copper toxicity ?

i have a tendency to attention deficit, low zinc, IBS, and they always warry about copper toxicity, but it's it really such a thing as copper toxicity ? or is it only vitamin a toxicity, lack of antioxidants, lack of zinc, with copper being accused ?
From my personal experience and all the people I‘ve texted with, who struggled with mysteriously low copper (and/or non-responsive low iron) blood levels (without genetic diseases) I think that copper-iron metabolism is one of the most complicated aspects of human physiology, which (to me) is still barely comprehensible.

From experience I can say that copper supplementation rarely raises ceruloplasmin. It does raise serum copper acutely, but the body rapidly removes copper from the blood and moves it into the liver, to store it relatively safely there. Free circulating copper is quite damaging in the blood stream. So we most likely have enough copper in our liver, but then we need adequate adrenal and thyroid function to fuel the enzymes that make ceruloplasmin.

And no, I don’t believe at all that vitamin A is a missing piece that is needed to „load copper into ceruloplasmin“ aka „make copper bioavailable“.

There is an animal study where the vitamin A deficient animals have the highest ceruloplasmin.

If anything, excess vitamin A lowers thyroid hormone function (by impairing iodine->thyroxine synthesis), which impairs adrenal function and liver function. All organ systems that are needed to regulate copper utilization and metabolism.

I think good copper/ceruloplasmin status is very important for proper iron metabolism (which is necessary for oxygenation and mitochondrial respiration)

Copper toxicity (excess) will likely impair the liver‘s detoxification (Copper quickly causes liver stagnation / impaired bile flow from my experience) and also place a burden on the adrenals by momentarily activating the sympathetic nervous system when freely circulating in the blood stream.
 
Last edited:

cs3000

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From my personal experience and all the people I‘ve texted with, who struggled with mysteriously low copper (and/or non-responsive low iron) blood levels (without genetic diseases) I think that copper-iron metabolism is one of the most complicated aspects of human physiology, which (to me) is still barely comprehensible.

From experience I can say that copper supplementation rarely raises ceruloplasmin. It does raise serum copper acutely, but the body rapidly removes copper from the blood and moves it into the liver, to store it relatively safely there. Free circulating copper is quite damaging in the blood stream. So we most likely have enough copper in our liver, but then we need adequate adrenal and thyroid function to fuel the enzymes that make ceruloplasmin.

I think good copper/ceruloplasmin status is very important for proper iron metabolism (which is necessary for oxygenation and mitochondrial respiration)

Copper toxicity (excess) will likely impair the liver‘s detoxification (Copper quickly causes liver stagnation / impaired bile flow from my experience) and also place a burden on the adrenals by momentarily activating the sympathetic nervous system when freely circulating in the blood stream.

you might find this interesting,
bodyfat plays a decent role in copper mobilization :

body has mechanisms for adjusting ceruloplasmin generation in other places than the liver when levels drop
SAT = subcutaneous fat
Previously, we have shown that the holo-Cp level in the blood serum of rats that received the Ag-fodder for 1 month dropped to practically zero. It was surprising that the blood holo-Cp level was approximately 50% of the normal value in rats that received the Ag-fodder for prolonged periods; thus, it was only decreased by a factor of two
the surgical isolation of the liver from the circulation with the subsequent [14C]amino acids pulse labeling of proteins in vivo indicated that there was a fraction of [14C]Cp that had a higher rate of secretion than hepatic Cp.

We hypothesized that the prolonged deficiency in holo-Cp in the circulation was compensated by the ectopic synthesis of holo-Cp in organ(s) in which the cells were not strongly affected by silver accumulation.
Two criteria were used to find the organ-candidate that can synthesize and secrete holo-Cp into the circulation: the ability to accumulate silver ions and express the Cp gene. Of the organs under study, only skeletal muscles, IAT, and SAT did not accumulate silver
It has previously been shown that sCp is synthesized in the SAT cells of obese patients and may enter the bloodstream [41].

Of all tested organs, the Cp gene was only overexpressed in the SAT of the Ag-rats. This allowed us to think that SAT is the first candidate compensating holo-Cp deficiency in the bloodstream.
The lungs, kidneys, spleen, IAT, and SAT were tested for the ability to activate Cp gene expression under conditions of holo-Cp deficiency.
The data presented in Fig 3A showed that the kidney, lungs, spleen, leukocytes, IAT, and SAT produced both Cp-mRNA forms. However, the Ag-fodder did not stimulate Cp gene activity in any of the organs, except SAT (Fig 3B).
Moreover, in SAT, the expression of the genes that are involved in the metallation of Cp, i.e., Ctr1 (encodes universal high affinity Cu(I) importer) [28], Atp7a and Atp7b (encode Cu(I)/Cu(II)-transporting P1 type ATPases [29] that supply copper atoms to GPI-Cp and sCp, respectively), was significantly increased (Fig 3B).
In addition, the expression level of the Dmt1 gene (encodes divalent metal transporter) [30] was increased by a factor of two. Thus, the expression of the genes that are typically responsible for blood copper status was increased in SAT cells of the Ag-rats. These data allowed us to hypothesize that SAT was a suitable candidate (or one of the candidates) organ that could compensate for the hepatic holo-Cp deficiency in the Ag-rats.

So might need to have a certain amount of bodyfat for proper copper utilization when it's impaired ,
being way too lean = less ability to make ceruloplasmin if adjustments need to be made?
due to overload of a metal here as the bodyfat didnt accumulate silver, but works outside of that also

Until recently, white adipose tissue was only considered an energy storage organ. At present, it is viewed as an endocrine organ that secretes factors (adipokines, including Cp [41]) with autocrine, paracrine, and endocrine functions [50]. Perhaps, our work revealed new aspects of the physiological role of adipose tissue in mammalian copper homeostasis. It is possible that the blood Cp level during inflammation [51], tumor growth [17], pregnancy and lactation [52] is increased not only due to Cp gene activation in the liver, but also because the white fat cells produce holo-Cp more intensively.

Thus,
subcutaneous fat can almost substitute for the liver with respect to the control of the holo-Cp level in blood. SAT may be a part of a system that controls the copper balance in the mammalian body, which may be used to elucidate the relationships between tumor growth, obesity and copper metabolism. Investigating the inter-organ regulation of copper metabolism in response to changing copper status may help us identify new antineoplastic approaches based on decreasing the bioavailable copper level

Ceruloplasmin Is a Novel Adipokine Which Is Overexpressed in Adipose Tissue of Obese Subjects and in Obesity-Associated Cancer Cells

^ mechanism works in humans without inducing metal overload
We searched for novel adipokines that were overexpressed in adipose tissue of obese subjects as well as in tumor cells derived from cancers commonly associated with obesity. For this purpose expression data from human adipose tissue of obese and non-obese as well as from a large panel of human cancer cell lines and corresponding primary cells and tissues were explored. We found expression of ceruloplasmin to be the most enriched in obesity-associated cancer cells. This gene was also significantly up-regulated in adipose tissue of obese subjects. Ceruloplasmin is the body's main copper carrier and is involved in angiogenesis.

We demonstrate that ceruloplasmin is a novel adipokine, which is produced and secreted at increased rates in obesity. In the obese state, adipose tissue contributed markedly (up to 22%) to the total circulating protein level.
1686235614861.png

wanna see the difference between nonobese and lean , looks like it scales
Ceruloplasmin in the circulation is believed to be primarily produced by the liver [15], [19]. However, the present data suggest a hitherto unknown contributing role of adipose tissue
We previously observed a rapid reduction in plasma ceruloplasmin activity in lean Zucker (Fa/Fa) rats fed a marginal copper (Cu)-deficient diet compared to similarly fed obese Zucker (fa/fa)
 
Last edited:

Don

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Messages
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i stopped taking copper supplements with my zinc 4 weeks ago. i only take an average of about 10-15mg per day.

i wonder what's the truth about copper, how important is it really, and it's there anything like copper toxicity ?

i have a tendency to attention deficit, low zinc, IBS, and they always warry about copper toxicity, but it's it really such a thing as copper toxicity ? or is it only vitamin a toxicity, lack of antioxidants, lack of zinc, with copper being accused ?
Jason Hommel says there is no such thing as copper toxicity as the body has pathways to remove it. He has an interesting copper group on FB
 

purple pill

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Jason Hommel says there is no such thing as copper toxicity as the body has pathways to remove it. He has an interesting copper group on FB
I joined his fb group briefly a while back, alot of people on the group where coming back saying they were have serious reactions to the copper supplementation but were constantly told "its just detox symptoms, carry on"... quite the echo chamber of copper being the be all end all of all problems....never seemed to find many success stories. 🤷‍♂️
 

Don

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Messages
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I joined his fb group briefly a while back, alot of people on the group where coming back saying they were have serious reactions to the copper supplementation but were constantly told "its just detox symptoms, carry on"... quite the echo chamber of copper being the be all end all of all problems....never seemed to find many success stories. 🤷‍♂️
fair enough. I see quite a few who "say" they benefit but agree a one solution for everything seems a bit of a dream.
 

Ismail

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Messages
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The statement mission of the Root Cause Protocol:

The RCP is designed to:

1. increase bioavailable COPPER (Ceruloplasmin) in order to...
2. decrease unbound IRON and...
3. decrease the MAGNESIUM burn rate in order to...
4. repair cellular mineral imbalance - the ROOT CAUSE of virtually ALL health challenges.

RCP Handbook (The Root Cause Protocol | Handbook Download)

I always found this concept quite fascinating as I have been struggling with low ceruloplasmin/copper mixed with iron dysregulation and magnesium deficiency symptoms for nearly 2 years, but for me, the RCP approach did not work out.

I think Ray‘s health philosophy could (theoretically) help us achieve the goals of the RCP, without following the protocol per-se.

This is just a hypothesis, that I have not yet tested out. But it might be interesting nonetheless.

In the following I want to present the peatarian perspective.

1. How to raise ceruloplasmin:

We know that thyroid hormone regulate ceruloplasmin and serum copper levels by controlling hepatic export and transport protein synthesis.

„In the present paper we show that serum copper levels are regulated by thyroid hormone, which stimulates the synthesis and the export of the hepatic copper-transport protein ceruloplasmin into the serum.“
(Serum copper as a novel biomarker for resistance to thyroid hormone)

In subclinical hypothyroid subjects, mean serum ceruloplasmin levels were found to be significantly lower in comparison to healthy subjects (p<0.0001).“
(Analysis and establish a correlation between serum ceruloplasmin, serum apelin level and thyroid profile in patients with hypothyroidism and healthy controls | International Journal of Research in Medical Sciences)

„Here we describe a 3-year-old Caucasian girl who was admitted to our Clinic due to pericardial effusion, muscle weakness and weight gain. At clinical examination, she presented with bradycardia, pale and round face, pseudohypertrophy of calf muscles and no pitting edema of the limbs. Routine blood investigations showed high serum aspartate and alanine aminotransferase levels, low serum ceruloplasmin without clinical signs of Wilson's disease, dyslipidemia. Thyroid function tests revealed a picture of severe hypothyroidism associated with HT. After the replacement treatment with L-T4, thyroid-stimulating hormone serum levels gradually decreased, with concomitant resolution of pericardial effusion and normalization of ceruloplasmin levels.“
(Hypoceruloplasminemia: an unusual biochemical finding in a girl with Hashimoto's thyroiditis and severe hypothyroidism - PubMed)

„Compared to euthyroid participants, patients with clinical hypothyroidism had statistically significant (P < 0.05) lower levels of serum copper and ceruloplasmin. The scenario was the opposite in the case of Grave's hyperthyroidism patients. Our study found statistically significant (P < 0.05) higher serum copper and ceruloplasmin levels in Grave's hyperthyroidism patients.
(Study of copper and ceruloplasmin in hypothyroidism and Grave's hyperthyroidism as compared to euthyroidism: Hospital-based case–control study Bhat VG, Patra R, K. Raju D S, Mohandas G V, Rao N L, - J Indian Prosthodont Soc)

Ray also recommended regular consumption of copper-rich foods like oysters, shellfish and liver.

A deficiency of copper causes our tissues to retain an excess of iron, so foods such as shrimp and oysters which contain abundant copper should be used regularly." - Ray Peat, PhD



The RCP recommends getting the serum copper to 100 mcg/dl and the serum ceruloplasmin to 30 mg/dl.
("Ideal" Values for Lab Tests - The Root Cause Protocol)

Ray said that the middle of the reference range for ceruloplasmin would be a good level. So roughly 30-40 mg/dl.

2. How to lower the iron footprint?

Ray recommended a low iron diet. He also recommended dairy (calcium) and coffee consumption with iron-rich meals to reduce iron absorption.

„Iron causes cell aging.

Drinking coffee with iron rich foods can reduce iron's toxic effects.

Use shrimp and oysters, etc., to prevent the copper deficiency which leads to excess storage of iron.

Avoid food supplements which contain iron.

Take about 100 units of vitamin E daily; your vitamin E requirement increases with your iron consumption.“
— Ray Peat PhD

He also wrote that a lower iron saturation is protective against cancer (I think he thought <25% was good, but I couldn’t find a quote, so I‘m not 100% sure)

This is in alignment with the RCP. The RCP also recommends a ferritin level between 20-50.

The RCP recommends lowering iron with blood donation.

Ray said:

„Blood transfusions damage immunity, and excess iron has been suspected to be one of the causes for this. People who regularly donate blood, on the other hand, have often been found to be healthier than non-donors, and healthier than they were before they began donating.“

3. How to restore magnesium levels?

Ray said that a hypothyroid person does not retain magnesium well and that a lot of benefits from thyroid supplementation come from increased magnesium retention.

„Magnesium is rapidly lost from cells in hypothyroidism.“ - Ray Peat PhD

„These data indicate that thyroid hormone has a direct stimulatory action on the cellular transport of magnesium. The ability of thyroid hormone, as well as altered extracellular concentrations of magnesium, to influence the cellular transport of magnesium is indicative of a regulated process involving either active transport or facilitated diffusion. A probable but not invariable result of the hormonal stimulation of magnesium transport appears to be a preservation of normal cellular concentrations of magnesium despite a tendency to depletion of extracellular magnesium in hyperthyroidism and to an excess of extracellular magnesium in hypothyroidism.“
(Magnesium Transport in Patients with Thyroid Disease)

„You can get enough magnesium from ordinary food if your thyroid let‘s you retain it“ (YouTube: „Ray Peat on magnesium from foods. Thyroid retaining magnesium.“)

4. How to restore mineral balance?

Ray said that thyroid/CO2 regulates mineral balance. So increasing thyroid activity or taking a thyroid supplement should restore mineral balance.

Ray also recommended the consumption of milk, eggs, oysters, shrimp, liver, orange juice and ripe fruits for adequate mineral intake.


View: https://m.youtube.com/watch?v=74oLBrVddFs

The RCP on other hand recommend HTMA testing for mineral balancing.

The big difference between the two remain:

• RCP avoids vitamin D. Ray thinks that vitamin D is helpful.
• RCP does not recommend a high calcium intake. Ray thinks it’s essential for keeping PTH in check.
• RCP avoids hormone therapy. Ray thinks it‘s sometimes necessary to overcome a problematic environment.
• RCP focuses on the adrenals. Ray focuses on the thyroid to ease off the adrenals from compensating for low thyroid function.
• RCP focuses on addressing liver function through diet and supplements. Ray thinks that a hypothyroid person has almost inherently a sluggish liver function.

Thank you for this, very helpful.

I’ve followed Morley’s work for a while now, and noticed how he referenced Dr Peat a couple of times, however the way you’ve put the similarities and differences like this is extremely helpful.

Always learning something new; didn’t know Dr Peat recommended calcium/dairy with iron rich meals, always thought it was coffee only - incidentally does anyone know if decaf coffee is also as effective?

Thank you again 🙏
 
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youngsinatra

youngsinatra

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Thank you for this, very helpful.

I’ve followed Morley’s work for a while now, and noticed how he referenced Dr Peat a couple of times, however the way you’ve put the similarities and differences like this is extremely helpful.

Always learning something new; didn’t know Dr Peat recommended calcium/dairy with iron rich meals, always thought it was coffee only - incidentally does anyone know if decaf coffee is also as effective?

Thank you again 🙏
He was once asked by Danny if he would..
a. consume calcium/dairy
b. consume coffee
c. take aspirin
..to lower iron absorption in a given meal

and he said that a-b-c would be his priority to lower iron
 

moa

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From my personal experience and all the people I‘ve texted with, who struggled with mysteriously low copper (and/or non-responsive low iron) blood levels (without genetic diseases) I think that copper-iron metabolism is one of the most complicated aspects of human physiology, which (to me) is still barely comprehensible.

From experience I can say that copper supplementation rarely raises ceruloplasmin. It does raise serum copper acutely, but the body rapidly removes copper from the blood and moves it into the liver, to store it relatively safely there. Free circulating copper is quite damaging in the blood stream. So we most likely have enough copper in our liver, but then we need adequate adrenal and thyroid function to fuel the enzymes that make ceruloplasmin.

And no, I don’t believe at all that vitamin A is a missing piece that is needed to „load copper into ceruloplasmin“ aka „make copper bioavailable“.

There is an animal study where the vitamin A deficient animals have the highest ceruloplasmin.

If anything, excess vitamin A lowers thyroid hormone function (by impairing iodine->thyroxine synthesis), which impairs adrenal function and liver function. All organ systems that are needed to regulate copper utilization and metabolism.

I think good copper/ceruloplasmin status is very important for proper iron metabolism (which is necessary for oxygenation and mitochondrial respiration)

Copper toxicity (excess) will likely impair the liver‘s detoxification (Copper quickly causes liver stagnation / impaired bile flow from my experience) and also place a burden on the adrenals by momentarily activating the sympathetic nervous system when freely circulating in the blood stream.

I have/had vitamin a toxicity. i do have sometimes sluggish bile flow too. my blood iron is very high, just a bit more than normal range.

i was zinc deficient last year.

I'm not sure how to supplement with zinc and copper any longer, I'm confused, with copper i have stomach pain, with zinc i don't.

i feel quite tired, confused and a bit anxious.
 
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youngsinatra

youngsinatra

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I have/had vitamin a toxicity. i do have sometimes sluggish bile flow too. my blood iron is very high, just a bit more than normal range.

i was zinc deficient last year.

I'm not sure how to supplement with zinc and copper any longer, I'm confused, with copper i have stomach pain, with zinc i don't.

i feel quite tired, confused and a bit anxious.
Ray did not recommend supplementing with those metals in general. You can get plenty through the diet.

How is your pulse and body temperature? Have you ever checked your thyroid labs? I’m asking because Hypervitaminosis A can cause hypothyroidism.
 
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youngsinatra

youngsinatra

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Hypothyroidism can cause hypervitaminosis A too right?
Correct. But only indirectly, by slowing down liver function and bile flow and thus vitamin A excretion. (which is limited)
 
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moa

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Ray did not recommend supplementing with those metals in general. You can get plenty through the diet.

How is your pulse and body temperature? Have you ever checked your thyroid labs? I’m asking because Hypervitaminosis A can cause hypothyroidism.
Yes, if i eat more oysters, but not something easy to eat. liver i don't eat any longer cause of too much vitamin a.

pulse is 83, has always been 83 at rest during the day. body temp is usually good, but my TSH was almost 4 in the lab test, i don't know the t3 levels.

so i guess TSH is higher to try compensate for the high vitamin a ? Ray said that TSH alone is bad regardless of if you are hypothyroid or not based on pulse.
 

moa

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i also have stomach pain now, because i are copper i think. it's better but still, either stomach or duodenum.

is it possible to have liver flush of toxins causing duodenum and stomach pain just because the liver is producing more bile (because i took some taurine, glycine, copper, etc).

i day this because i used to have quite puzzle stools before, and the past few weeks, even though i stopped taurine (but not coffee) i have much more brown darker stools than usually, and i have this stomach pain without knowing if it's related also to toxic liver bile or it's just because i took copper on empty stomach ?

home test of occult blood in stools came negative, cause i was worried but it's only dark because of bile it seems. Coffee is really strong bile stimulator.
 
Last edited:

cs3000

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you might find this interesting,
bodyfat plays a decent role in copper mobilization :

body has mechanisms for adjusting ceruloplasmin generation in other places than the liver when levels drop

So might need to have a certain amount of bodyfat for proper copper utilization when it's impaired ,
being way too lean = less ability to make ceruloplasmin if adjustments need to be made?
due to overload of a metal here as the bodyfat didnt accumulate silver, but works outside of that also
& taking estrogen inhibiting supplements when trying to mobilize copper (or having crashed estrogen i.e from low testosterone) can be detrimental
https://www.biomed.cas.cz/physiolres/pdf/43/43_219.pdf
1686296210583.png

but tipping over too high shifts copper from the liver to the brain Effect of estrogen on serum and tissue levels of copper and zinc - PubMed
 
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youngsinatra

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& taking estrogen inhibiting supplements when trying to mobilize copper (or having crashed estrogen i.e from low testosterone) can be detrimental
https://www.biomed.cas.cz/physiolres/pdf/43/43_219.pdf
View attachment 51596
but tipping over too high shifts copper from the liver to the brain Effect of estrogen on serum and tissue levels of copper and zinc - PubMed
Yes. Estrogen seems quite essential for ceruloplasmin production. I have seen studies where estradiol raised ceruloplasmin and lowered hepatic copper.

That’s probably why it has been said that adrenal health (proper DHEA levels -> estradiol) is so crucial for ceruloplasmin synthesis.

I definitely feel worse from estrogen-lowering substances.

I am very excited to see my blood work, when it’s done. I just came back from the private lab.
(I have tested all the steroid hormones, full iron panel, CBC, ceruloplasmin, copper, zinc, vitamin D)
 

cs3000

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Yes. Estrogen seems quite essential for ceruloplasmin production. I have seen studies where estradiol raised ceruloplasmin and lowered hepatic copper.

That’s probably why it has been said that adrenal health (proper DHEA levels -> estradiol) is so crucial for ceruloplasmin synthesis.

I definitely feel worse from estrogen-lowering substances.

I am very excited to see my blood work, when it’s done. I just came back from the private lab.
(I have tested all the steroid hormones, full iron panel, CBC, ceruloplasmin, copper, zinc, vitamin D)
aye same here Copper deficiency halves serum dehydroepiandrosterone in rats
(this led me to DHEAs role in wound healing / colitis actually ty)
curious to see what stands out and if theres improvement from taking that thyroid product
 
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EMF Mitigation - Flush Niacin - Big 5 Minerals

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