Copper May Treat Als

[haidut]

The study of course tries to talk about how they have discovered a "special" (and likely patented) method of copper delivery to the cell, but the main message is that boosting copper levels in the cells increased lifespan of ALS rodents by 26%. Since copper is the crucial compound for cytochrome C oxidase, this study supports Ray's views on ALS being a bioenergetic disorder, with potentially straightforward treatment. Let's hope this research will have follow up.

http://oregonstate.edu/ua/ncs/archives/ ... 9s-disease

"...“The damage from ALS is happening primarily in the spinal cord and that’s also one of the most difficult places in the body to absorb copper,” Beckman said. “Copper itself is necessary but can be toxic, so its levels are tightly controlled in the body. The therapy we’re working toward delivers copper selectively into the cells in the spinal cord that actually need it. Otherwise, the compound keeps copper inert.”
“This is a safe way to deliver a micronutrient like copper exactly where it is needed,” Beckman said.
By restoring a proper balance of copper into the brain and spinal cord, scientists believe they are stabilizing the superoxide dismutase in its mature form, while improving the function of mitochondria. This has already extended the lifespan of affected mice by 26 percent, and with continued research the scientists hope to achieve even more extension."

 

[DaveFoster]

Very interesting. ALS seems to have a strong link to supraphysiological levels of testosterone, so this may be particularly beneficial alongside many of the androgenic effects of supplements such as zinc and Vitamin E.

Do you think that 2 mg of copper glycinate will still provide these benefits? I would be wary to go much higher for fear of neurotoxicity.

 

[haidut]

Very interesting. ALS seems to have a strong link to supraphysiological levels of testosterone, so this may be particularly beneficial alongside many of the androgenic effects of supplements such as zinc and Vitamin E.

Do you think that 2 mg of copper glycinate will still provide these benefits? I would be wary to go much higher for fear of neurotoxicity.

That dose actually was found to be optimal in a human study with nurses. They had 3 groups taking 2mg, 4mg, and 6mg copper daily. Both the 4mg and 6mg groups had symptoms of copper toxicity even though the 4mg group only had nausea and no change in blood tests. The 2mg group was doing fine and it improved their copper status and raised their ceruloplasmin.
Ray said that to him testosterone is almost as dangerous as estrogen, and he mentioned the connection between T and ALS as well. In my opinion the only two steroids worth raising exogenously are progesterone and DHT. Pregnenolone is also fine but most of it does not stay as pregnenolone but metabolizes downstream. As far as I know DHT may actually treat ALS. See below.
http://www.ncbi.nlm.nih.gov/pubmed/22606355
http://www.alsa.org/news/archive/new-als-research-findings.html

 

[DaveFoster]

That dose actually was found to be optimal in a human study with nurses. They had 3 groups taking 2mg, 4mg, and 6mg copper daily. Both the 4mg and 6mg groups had symptoms of copper toxicity even though the 4mg group only had nausea and no change in blood tests. The 2mg group was doing fine and it improved their copper status and raised their ceruloplasmin.
Ray said that to him testosterone is almost as dangerous as estrogen, and he mentioned the connection between T and ALS as well. In my opinion the only two steroids worth raising exogenously are progesterone and DHT. Pregnenolone is also fine but most of it does not stay as pregnenolone but metabolizes downstream. As far as I know DHT may actually treat ALS. See below.
http://www.ncbi.nlm.nih.gov/pubmed/22606355
http://www.alsa.org/news/archive/new-als-research-findings.html

That's very promising. So do you see any problem with using Proviron (DHT cream)? It seems like Privoron doesn't suppress the HPTA to the degree of Anavar, another DHT analogue, but I'll need to do some more research. I'd think that it would be dose dependent, similar to the estrogenic effect of high doses of DHEA.

I found this study on concerning exogenous DHT supplementation.

Varma TR, Patel RH.

Department of Obstetrics & Gynaecology, St. George’s Hospital Medical School London, U.K.

Two hundred fifty subfertile men with idiopathic oligospermia (count less than 20 million/ml) were treated with mesterolone (100-150 mg/day) for 12 months. Seminal analysis were assayed 3 times and serum follicle stimulating hormone (FSH) luteinizing hormone (LH) and plasma testosterone were assayed once before treatment and repeated at 3, 6, 9 and 12 months after the initiation of treatment. One hundred ten patients (44%) had normal serum FSH, LH and plasma testosterone, 85 patients (34%) had low serum FSH, LH and low plasma testosterone. One hundred seventy-five patients (70%) had moderate oligospermia (count 5 to less than 20 million/ml) and 75 patients (30%) had severe oligospermia (count less than 5 million/ml). Seventy-five moderately oligospermic patients showed significant improvement in the sperm density, total sperm count and motility following mesterolone therapy whereas only 12% showed improvement in the severe oligospermic group. Mesterolone had no depressing effect on low or normal serum FSH and LH levels but had depressing effect on 25% if the levels were elevated. There was no significant adverse effect on testosterone levels or on liver function. One hundred fifteen (46%) pregnancies resulted following the treatment, 9 of 115 (7.8%) aborted and 2 (1.7%) had ectopic pregnancy. Mesterolone was found to be more useful in patients with a sperm count ranging between 5 and 20 million/ml. Those with severe oligospermia (count less than 5 million) do not seem to benefit from this therapy.

PMID: 2892728 [PubMed – indexed for MEDLINE]One more…
Effect of non aromatizable androgens on LHRH and TRH responses in primary testicular failure.

Spitz IM, Margalioth EJ, Yeger Y, Livshin Y, Zylber-Haran E, Shilo S.

We have assessed the gonadotropin, TSH and PRL responses to the non aromatizable androgens, mesterolone and fluoxymestrone, in 27 patients with primary testicular failure. All patients were given a bolus of LHRH (100 micrograms) and TRH (200 micrograms) at zero time. Nine subjects received a further bolus of TRH at 30 mins. The latter were then given mesterolone 150 mg daily for 6 weeks. The remaining subjects received fluoxymesterone 5 mg daily for 4 weeks and 10 mg daily for 2 weeks. On the last day of the androgen administration, the subjects were re-challenged with LHRH and TRH according to the identical protocol. When compared to controls, the patients had normal circulating levels of testosterone, estradiol, PRL and thyroid hormones. However, basal LH, FSH and TSH levels, as well as gonadotropin responses to LHRH and TSH and PRL responses to TRH, were increased.

Mesterolone administration produced no changes in steroids, thyroid hormones, gonadotropins nor PRL.
There was, however, a reduction in the integrated and incremental TSH secretion after TRH.
Fluoxymesterone administration was accompanied by a reduction in thyroid binding globulin (with associated decreases in t3 and increases in t3 resin uptake). The free T4 index was unaltered, which implies that thyroid function was unchanged.

In addition, during fluoxymesterone administration, there was a reduction in testosterone, gonadotropins and LH response to LHRH.
Basal TSH did not vary, but there was a reduction in the peak and integrated TSH response to TRH. PRL levels were unaltered during fluoxymesterone treatment.

Mesterolone seems superior to fluoxymesterone due its lack of effects on TBG, but the researchers reported that even fluoxymesterone did not affect thyroid function. I'll see if I can do some more reading.

 

[haidut]

That's very promising. So do you see any problem with using Proviron (DHT cream)? It seems like Privoron doesn't suppress the HPTA to the degree of Anavar, another DHT analogue, but I'll need to do some more research. I'd think that it would be dose dependent, similar to the estrogenic effect of high doses of DHEA.

I found this study on concerning exogenous DHT supplementation.


Mesterolone seems superior to fluoxymesterone due its lack of effects on TBG, but the researchers reported that even fluoxymesterone did not affect thyroid function. I'll see if I can do some more reading.

I think small doses of DHEA are the best way to raise tissue levels of DHT. Topical is probably best for DHT conversion but oral works as well if each dose is kept under 5mg. And with DHEA, even if you raise DHT to supaphysiological levels there will be no HPTA suppression.

 

[Highserotonin90]

But if you are toxic and deficient at the same time, how can you safely integrate copper and above all its distribution?