2 replies to this topic

[HBRU]

Despite unquestionable essentiality of copper, unregulated copper ions may increase oxidative damage. It is known that amyloid precursor protein (APP) implicated in development of Alzheimer's disease (AD) can convert Cu (II) into Cu (I) potentially increasing oxidative damage [19]. However, it remains unclear whether copper accumulation in senile plaques of AD patients is a cause or a consequence of pathological processes observed in AD. According to Exley followed by Bolognin et al., only aluminum, but not copper or iron, is capable of triggering amyloid precipitation and APP and tau181 protein overproduction [20, 21]. The study by Kawahara et al. showed that copper and carnosine attenuate neurotoxicity of another compound involved in neurodegeneration—prion protein [22]. Bishop and Robinson observed that amyloid beta protein may be neuroprotective when combined with copper. According to these authors, amyloid beta injected simultaneously with copper was not toxic, while iron and zinc complexed with amyloid beta were more toxic than amyloid beta alone [23].

 

Since copper accumulates in senile plaques of AD patients, some authors proposed dietary restriction of copper or intake of copper chelators as a preventive therapy for the elderly. However, several studies demonstrated that AD patients have reduced, not elevated, brain and cerebrospinal fluid copper level [24, 25]. Currently, many authors suggest mild copper deficiency as a causative factor in AD and possibly other neurodegenerative disorders [26, 27]. In a placebo-controlled, double-blinded, randomized clinical trial, oral copper supplementation (8 mg/day) in 68 AD patients had a beneficial effect on relevant AD biochemical markers. The authors concluded that long-term intake of copper can be excluded as a causative factor in AD and may in fact be protective [28]. In addition, several studies revealed molecular mechanisms underlying beneficial effects of copper in AD, such as an inhibition of beta-amyloid peptide production [29].

 

The Human Tripeptide GHK-Cu in Prevention of Oxidative Stress and Degenerative Conditions of Aging: Implications for Cognitive Health - PMC (nih.gov)

[HBRU]

carnosine aids copper absorpion,

copper + carnosine + glycine + lysine ------> cheap intracellular ghk-cu

 

Eating a lot of zinc depletes copper from the body (and vice versa). As zinc is known to boost testosterone levels, many men tend to supplement with high-dose zinc supplements on a daily basis, without taking in any copper to balance that zinc-induced depletion (optimal ratio of zinc and copper is considered to be between 10:1 and 10:2).

If you supplement with 30 mg’s of zinc per day, then you should also take 3-6 mg’s of copper to balance out the zinc-induced copper depletion.

a) In this old in-vitro study, the researchers saw that when isolated hypothalamic cells were altered to chelated copper complexes, gonadotropin-releasing hormone (GnRH) increased by a nice 68%. As GnRH is basically the hormone that starts the whole cascade of events that lead to testosterone production, even a slight boost in it should increase testosterone levels. To what degree this happens when chelated copper is orally ingested? Hard to say.

b) This Indian study wanted to take the above experiment further, and they decided to inject copper chloride straight into the guts of living male Wistar rats for 26 consecutive days, with varying doses (1000 mcg, 2000 mcg, and 3000 mcg/kg).

They found out that the 1000 mcg dose significantly increased testosterone levels via luteinizing hormone (LH) stimulation. Which supports the findings of the first study above.

However, the 2000 mcg and 3000 mcg doses started to become toxic for the rats, and on the higher dosed groups, testosterone was actually decreased. Several human studies have also found out that when copper intake gets too high, it becomes unhealthy and toxic, but lower intake is absolutely essential for the health of the human body (study, study, study).

c) Then there’s this other quite old in-vitro study, which found out that when isolated hypothalamic neurons were altered to chelated copper, luteinizing hormone (LH) release increased by 45%. As LH is the hormone that stimulates testosterone synthesis inside the ballsack, these findings furthermore support the theory that copper should increase testosterone production.

Copper and Testosterone: Chelated & Androgenic (anabolicmen.com)

 

--------------------------------------------------------------------------------------------------------------

 

As for CANCER, good Cu levels keep Iron low... and high Iron is bad for cancer

 

Copper, like iron, is required for normal erythropoiesis; copper deficiency causes an iron-deficiency-like anemia [ 1 ]. Moreover, copper homeostasis is closely linked with iron metabolism, since iron and copper have similar physiochemical and toxicological properties.

 

Iron-copper interactions were described decades ago; however, molecular mechanisms linking the two essential minerals remain largely undefined. Investigations in humans and other mammals noted that copper levels increase in the intestinal mucosa, liver and blood during iron deficiency, tissues all important for iron homeostasis. The current study was undertaken to test the hypothesis that dietary copper influences iron homeostasis during iron deficiency and iron overload. We thus fed weanling, male Sprague-Dawley rats (n = 6-11/group) AIN-93G-based diets containing high (~8800 ppm), adequate (~80) or low (~11) iron in combination with high (~183), adequate (~8) or low (~0.9) copper for 5 weeks. Subsequently, the iron- and copper-related phenotype of the rats was assessed. Rats fed the low-iron diets grew slower than controls, with changes in dietary copper not further influencing growth. Unexpectedly, however, high-iron (HFe) feeding also impaired growth. Furthermore, consumption of the HFe diet caused cardiac hypertrophy, anemia, low serum and tissue copper levels and decreased circulating ceruloplasmin activity. Intriguingly, these physiologic perturbations were prevented by adding extra copper to the HFe diet. 

 

High-Iron Consumption Impairs Growth and Causes Copper-Deficiency Anemia in Weanling Sprague-Dawley Rats | PLOS ONE

 

 

Edited by HBRU, 15 November 2023 - 07:42 AM.

[HBRU]

I believe poor anti aging result in the anti-aging-community in the past was caused by low Cu levels (and so low GHK-CU) this was doe to fear of this CRUCIAL mineral... if you read both Imminst and Longecity topics in the past they full of people fearing copper....

 

Even if low copper levels is (and was) linked with gray hairs....