What's up with the EGCG health potion trending on RPF?

Korven

I still check in on the RPF from time to time and the current obsession is a cocktail of EGCG and various vitamins + minerals, touted as a health potion to cure all ailments.

Has anyone here tried it and what has been your experiences?

It sounds totally ludicrous... but I am also a little intrigued

alex155

@Korven Chucky is completely fucked up

LucH

@Korven said in What's up with the EGCG health potion trending on RPF?:

the current obsession is a cocktail of EGCG and various vitamins + minerals, touted as a health potion to cure all ailments

Don't dream. They're part of the "solution" to stay fit and well if ...
Fine to optimize and compensate the lacks but nothing has been said about the right target. I mean: too much of a good thing is bad.
One example: Blockage of the enzyme succinate deshydrogenase by selenium supplement is known to disrupt the Krebs cycle, to alter brain functions and to enhance tumor proliferation. Details beneath.

RDA Supply for Selenium
Currently recommended nutritional supply (RDA) in adults is 55 micrograms/day.

Daily needs are 55 mcg (RDA). 1 mcg /kg of weight is optimal.
Diet (1) provides around 50 % of needs if you eat meat or legumes. A single nut from Brazil / Amazon covers needs (…).
In the event of pathology / detox, 200 - 300 mcg can be prescribed punctually.
“Too Much of a Good Thing is Bad!”
=> Selenium supplementation should not be taken every day (half-life). Except in particular cases, in the event of a detox for example, therefore punctually (2 to 300 mcg per day, in detox cure). But in this case, a contribution of curcumin would be desirable to reduce hepatic toxicity due to the impact on dehydrogenase enzymes.
Taking different forms of selenium is interesting, especially in the event of cancer prevention (recurrence).
If you exceed +/ 100 mcg/ L in the blood serum, you impact the operation of certain dehydrogenase enzymes, especially required in the Krebs cycle.

*) More details on this post, with sources and references.
Selenium: Too much of a good thing is bad. Forms and enzymes
https://mirzoune-ciboulette.forumactif.org/t1953-selenium-too-much-of-a-good-thing-is-bad#27971 (in French; translator needed but with references from studies in English)

*) Selenium in human health: Inverse U-shaped link with health!
Only one study – Select – indicates that the combination of Se and Vit E is counterproductive and harmful in cases of cancer. However, according to Luc’s pendulum, this study shouldn’t be taken into account because the form of vitamin E used in this study was 100% alpha-tocopherol. If you take of alone alpha-tocopherol (cheaper and easier to produce), this situation prevents the absorption of gamma-tocopherols. Vitamin E supplementation should always contain at least 2 tocos. And, personally, I don't take it every day. 400 IU 2x/week. 3x/week, in case of Covid virus. (The bug doesn’t like that; it stops its proliferation).
Why a Ʌ-shaped result?
Selenium administration resulted in a marked decrease in the activity levels of the liver succinate dehydrogenase, malate dehydrogenase, and lactate dehydrogenase while pyruvate dehydrogenase increased significantly. (2)
NB: Use the food grade meriva (for curcumin) to reach / penetrate the blood brain barrier.

Blockage of the enzyme succinate deshydrogenase is known to disrupt the Krebs cycle, to alter brain functions and to enhance tumor proliferation. This last point is however subject to discussion (diverging studies). Of course, a 12-week study is not able to establish a cause and effect result for a cancer since it takes more than 10 years to appear. Read further to see why it makes sense to avoid excess Se.
Practical consideration:

I take 100 mcg selenium (selenio-methionine) 2x/wk, on a usual manner. 200 mcg when making a detox (thus in cure).

Sources

Protective effect of curcumin during selenium induced toxicity on dehydrogenases in hepatic tissue. 2005 – PMID: 15881869
Succinate déshydrogénase
Enzyme used in the Krebs cycle and in the electron transport chain of oxidative phosphorylation (cellular respiration). Blockage of succinate dehydrogenase is known to cause serious illnesses (neurodegenerative diseases or tumors), with a very broad spectrum of symptoms typical of mitochondrial diseases.
The role of selenium in insulin resistance
BJPS. Larissa Cristina Fontenelle et al. 2018
https://www.scielo.br/j/bjps/a/GZsSGmGVwZYrt9CVCfvShZt/?lang=en&format=pdf
When ingested in sufficient amounts to maintain plasma concentrations in the range of 80-120 µg/L (Rayman, 2012), selenium acts as an antioxidant and insulin-mimetic nutrient, favoring the synthesis and action of insulin. However, when selenium intake results in plasma levels above 120 µg/L (Rayman, 2012), the cellular redox state may become dysregulated, which can compromise the chemical interactions.

I could do the same for other nutrients:

HD niacin with NAC
HD Vit E
Not HD Vit E and HD K at the same time
Frequent HD selenium (without Vit E)
Note: HD = High Dose.

ThinPicking

Hey now, hey now

@LucH said in What's up with the EGCG health potion trending on RPF?:

Don't dream

it's over

LucH

@ThinPicking said in What's up with the EGCG health potion trending on RPF?:

Hey now, hey now

Thanks for remind: aa. hat off.gif
https://youtu.be/bXzis29vA6k

cs3000

@Korven some benefits at low dose but its toxic in the 100s of miligrams over time, supplement doses
(& ironically low copper makes mammals more vulnerable to it)
(similar thing to high dose quercetin probably, where its chelating too much copper over time for diet to match. plus the ROS damage from excess)

https://pubmed.ncbi.nlm.nih.gov/25975988/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5943924/

But not great to go high copper to prevent that as can cause other problems from the excessive copper , "low" mg doses of catechins should have some benefits

Korven

@cs3000 Thanks for the warning, indeed looks like there are quite a few case reports of liver toxicity from EGCG.

I already knew this formula was insane (upwards of 1 g EGCG per day, 3 mg molybdenum and more) but I was kinda curious what people thought of it

CrumblingCookie

@cs3000
How would this study "Dietary Copper Reduces the Hepatotoxicity of (-)-Epigallocatechin-3-Gallate in Mice"
https://pubmed.ncbi.nlm.nih.gov/29295524/

"Following EGCG treatment, the survival rates were 12.5%, 50% and 100% in the Cu-deficient, -sufficient and Cu-super nutrition groups of mice, respectively."

"suggest that Cu can relieve EGCG hepatotoxicity, possibly by up-regulating ceruloplasmin activity, which can be used to promote EGCG applications."

fit in with any of the EGCG narratives of the latter binding iron and hence freeing up copper from iron-copper binding as currently discussed on the RPF?

It kind of says the opposite, i.e. EGCG application requiring additional copper for survival.

On the other hand the used dosage (EGCG, 750 mg/kg BW) seems gigantic and maybe there's another compensatory effect at play there fore bare survival.
Or the iron/copper binding molecules in mice could have slightly different structures than their human equivalents?

cs3000

@CrumblingCookie not aware of the narratives but human toxicity dose was 270mg & 400mg so didnt need that higher dose
some polyphenols chelate copper more than iron , copper can be damaging in high amounts but also vital for mitochondria so if someone over focuses on eliminating it their mitochondria suffers
(TSH starts to rise in some studies that use 100s of milligrams of some polyphenols too , maybe binding too much iron copper zinc so they cant be used for regular functions enough. i guess copper is especially vulnerable because lower amounts / intake. e.g too much quercetin is detrimental to complex IV activity in mitochondria alongside ceruloplasmin :

Quercetin is an iron & copper chelator
it lowers ceruloplasmin 50% , injected in mice at 50mg/kg mice dose
, In the present study a decreased activity of Complex IV in mice treated with quercetin is clear. This is well correlated with decreased levels of ceruloplasmin. {copper protein}
Our previous research [30] exposed that mild copper deprivation in mice is correlated with a decreased protein expression and activity of Complex IV at the level of OXPHOS supercomplexes along with a decrease in the ceruloplasmin levels

CrumblingCookie

@cs3000 said:

not aware of the narratives

In brief the current narratives of that RPF thread are that EGCG chelates iron from iron-copper complexes, which raises copper, which needs molybdenum to antagonize, chelate and excrete through increased uric acid through Mo-dependent xanthine oxidase, all of which needs vast amounts of vitamin B6 to replenish circulating copper with tissue copper, which needs vast amounts of biotin, which needs balancing with large amounts of vitamin B5 because of their shared transporter and lots of vitamin C, depending individually, to activate B vitamins and to keep iron and copper mobilized in circulation. All that so age-dependent iron and copper stores decrease and their alleged inhibitions are replaced with supplemented zinc ions to restore functions.

I've now had a brief look into ECGC + iron and it does appear to form (Ngal-)EGCG-iron complexes and alleviate iron-dependent injuries and ferroptosis. In this study, e.g. they beneficially used "only" 10mg/kg EGCG "EGCG activates Keap1/P62/Nrf2 pathway, inhibits iron deposition and apoptosis in rats with cerebral hemorrhage".
The cited mice study in which 750mg/kg EGCG was used is probably highly problematic. Probably the binding affinities and or the priorities regarding iron and copper shift and are different from much much lower high doses of EGCG as in 10mg/kg in rats.

CrumblingCookie

In this human study 300mg EGCG bound about 3-5mg (27%) of orally given iron but only 3% of intravenously given iron.
With only 150mg EGCG, curiously, there was 15% decreased retention of intravenously given iron. I.e. EGCG bound circulating iron but only when 150mg and not when 300mg EGCG were given at a time.
It's all a bit odd.
In this rat study the authors concluded "that green tea extract (GTE) ameliorates iron overload induced hepatotoxicity, apoptosis and oxidative stress in rat liver via inhibition of hepatic iron accumulation".

I'm now somewhat curious about this topic because of liver issues and taking any zinc causing extra nausea and headaches and insomnia.
By this currently trending RPF thread this should imply I had both too much iron and copper. Or mainly too much iron in case molybdenum doesn't improve such effects by zinc.
Which when I think about it becomes more interesting in the context of high ferroptosis observed in the causative chain of neurodegenerative diseases.