Getting massive gains from/and climaxing without ejaculation

Mizguy, thanks for pointing that out. I made a goof. Like you say, Copper definitely is not the most prevalent mineral in the human body. It is however the third most prevalent trace mineral. More importantly, however, for our purposes, it is the most prevalent trace mineral found in connective tissues like the ones you can find in your cock.
D.B. Milne and F.H. Nielsen, AM J Clin Nutr 1996; 63; 358-364. This is a comprehensive study you may want to peruse at your leisure. I will provide a summary for you written by:
A.S. Gissen
As regular readers of our newsletter already know, coppers importance in our nutrition is a popular topic on these pages. Long ignored by all but a handful of dedicated minimum human nutrition researchers, copper is inexpensive and unglamorous. In animal nutrition, however, where the ill effects of copper deficiency are well established, copper is liberally added to diets, and copper deficiency is a scientific curiosity usually caused by poor animal management. One of the problems of accurately determining the minimum human requirement for dietary copper is the lack of a sensitive test to detect deficiencies of copper which are not severe enough to cause the unmistakable symptoms of anemia, leukopenia, and skeletal demineralization found in severe copper deficiency. Numerous short-term studies of copper deprivation in human subjects have provided evidence to support the belief that copper deficiency may cause long term negative consequences, namely cardiovascular disease. Most of these studies have utilized young men or women over short periods of time. Now a new study has been published that examined the effects in postmenopausal women of a diet low in copper over a four-month period.

This study was designed to test the hypothesis that copper-containing enzymes in blood cells are more sensitive indicators of copper status than plasma copper levels. The women were fed a copper-depleting diet containing .57 milligrams of copper daily for 105 days, followed by a copper-repletion period of 35 days during which the women consumed 2.57 milligrams of copper daily. Plasma copper and ceruloplasmin did not change significantly during copper depletion. This was in spite of significant changes in several enzymes in circulating blood cells that are directly related to oxygen metabolism or antioxidant function, including cytochrome c oxidase, superoxide dismutase, and glutathione peroxidase. In the authors words, These enzymes seem to change before other indicators that have been associated with severe copper deficiency in animals, such as plasma copper, cholesterol, or hemoglobin concentrations. This provides strong evidence that the traditional measures of copper status are not particularly useful at detecting the subclinical deficiency we are most likely to develop. Because most of our understanding of human copper requirements are based on these inaccurate measures, these findings will force a re-evaluation of decades of copper research.

Among the changes found, platelet cytochrome c oxidase activity seems to be a sensitive indicator of changes in human copper status. Low tissue cytochrome c oxidase has already been shown to be an early and consistent finding in copper deficient animals. In this study, platelet cytochrome c oxidase activity dropped by almost one-half after 9 weeks of copper deprivation. During the 35 day repletion phase its activity only partially recovered. As the authors point out, Defects in cytochrome c oxidase activity may cause neurologic, cardiac, and muscle disease when the activity is only about 50% of normal. In many ways this resembles the deficiency symptoms of one of cytochrome c oxidases partners in energy production within cells, coenzyme Q10. Additional research with rats has shown that the cytochrome c oxidase activity in platelets correlates well with liver copper stores, the benchmark measure of copper status. The fact that 35 days of copper repletion with slightly more than the RDI of copper didnt restore cytochrome c oxidase activity to pre-depletion levels is troublesome. This activity didnt drop significantly until after 8 weeks of depletion, and then dropped markedly over the next five weeks. Apparently five weeks of almost 2.6 milligrams of copper daily doesnt provide enough excess copper beyond the bodys actual requirement to significantly replete copper stores. Incidentally, of the 13 women who began the low-copper-intake phase of the study, three were withdrawn and supplemented with copper after the detection of a significant increase over control values in the number of ventricular premature discharges, a heart rhythm abnormality. One could easily speculate that this is only the tip of the iceberg in relation to the relevance of copper deficiency to the incidence of heart rhythm abnormalities.

In the case of erythrocyte superoxide dismutase, a decline in its activity was observed during copper depletion. During the period of copper repletion its activity failed to recover to pre-depletion levels. This lack of recovery of erythrocyte superoxide dismutase activity, coupled with the decrease in cytochrome c oxidase activity, adds evidence to the belief that current copper recommendations for humans may be understated. The researchers write that, It is likely that the response of these enzymes to copper repletion after copper depletion is influenced by the amount of copper fed, the duration of depletion and repletion, and the rates of cell turnover. They then provide evidence from other studies in which superoxide dismutase activities were lowered during copper deprivation. Recoveries of activity were documented when either 3 mg or 4.3-6.4 mg copper per day was fed for greater than 30 days, but not when less than 2.6 mg per day was fed for periods of up to 42 days. Erythrocyte glutathione peroxidase, a selenium-containing antioxidant enzyme, was also sensitive to changes in copper intake. Although it, too, significantly decreased during copper depletion, it was restored to normal levels during the copper repletion phase of the study. Like superoxide dismutase, glutathione peroxidase is an important antioxidant enzyme. While the long-term effects of this are unknown, the importance of these two enzymes in protecting us from free-radical damage cannot be overlooked.

One of the interesting findings from this study was that coagulation factors V and VIII, which contain copper and have structural similarities to ceruloplasmin (the main copper-containing protein in plasma), are sensitive to changes in copper intake. Surprisingly, copper depletion caused factor VIII activity to significantly increase to almost twice the normal range. Factor VIII is a procoagulant, and an elevation of factor VIII activity is often seen in hypercoagulation and thrombotic disease, important risk factors for vascular disease. An increase in factor VIII activity is consistent with the increased incidence of thrombotic events observed in copper-deficient animals. This adds an additional cardiovascular risk factor to go with the electrocardiogram abnormalities, lowering of antioxidant enzymes, and promotion of atherosclerosis already known to be associated with copper deficiency. It seems likely that copper deficiency has relevance to many patients with hypercoagulation and thrombotic disorders, as well as atherosclerosis in general. While taking aspirin to prevent abnormal blood clotting is widely practiced and recommended, adequate copper supplementation seems even more logical, beneficial, and necessary for overall cardiovascular health.

While the work of these and other researchers will eventually result in a better understanding of copper metabolism in humans, their results also force us to take a new look at how we view copper deficiency and requirements in humans. One of the most important discoveries was that, unlike other animal models of copper deficiency, low copper intakes did not induce the changes in serum cholesterol and hematology generally found in copper-deficient animals. Because of this the authors suggest that, These results indicate that a paradigm shift may be needed in evaluating copper status in adult humans. Taken in its entirety, the findings of this research should provide a wake-up call for the nutritionally concerned.

It is already well-documented that most of us get only about 1 milligram of copper daily from our diets, well below the recommendation of up to 3 milligrams daily. In fact, subclinical copper deficiency is believed to be a common cause of illness in this country. The problem, up until now, has been proving the existence of subclinical copper deficiency in otherwise healthy human subjects. It is likely that the finding of several sensitive indicators of copper status, including the functional activities of platelet cytochrome c oxidase, glutathione peroxidase, and clotting factor VIII, will make it possible to more fully quantify the incidence of copper deficiency in the general population. More importantly, it will make it possible for the first time to accurately determine the optimal copper requirement for diverse population groups with different copper needs based on sensitive indicators of copper status. Because of the vital roles copper plays in ensuring our health, this will be an important advancement in human preventive nutrition. It is also one of many examples of how far we have yet to go in determining our optimal dietary requirements.

http://skinbiol ogy.com/copper- … ging-metal.html

Here is another interesting read we could discuss.

I read that and I agree to disagree :-P

He’s been spoken to and if your content at this point then lets try to move on.
Aside from your dissagrements you both have something to offer the forum so if you can just avoid each other then all’s good.

Exchange pms. You’ll become good friends.

Interesting stuff chubby. Makes you wonder though why copper supplementation didn’t restore the negative effects. Personally I wouldn’t mess with self medication by copper (risk to high for supposed reward) but to each their own. Good luck with your journey.

Mizguy12, I’m thinking your reticence to engage in a regime of topical colloidal copper applications may be ill informed. When you have a little time you should read clear through that last link I posted, paying particular attention to the section titled “Should I worry about copper excess.”

One of the fascinating things about copper is the precision with which this essential mineral is regulated in the body. In one study of copper transport in the blood, scientists tried to create an elevated level of copper in plasma, injecting dogs and healthy human volunteers with high doses of copper. To their amazement, all excess copper magically disappeared from the blood shortly after injection!

For example, 50 mg of copper injected in healthy human volunteers (which amounts to 25 times the recommended 2 mg of copper a day) completely cleared from the blood in just 4 hours (Gubler et al 1953).

In experimental settings, researchers gave healthy volunteers 4-8 mg of copper a day for 1 to 3 months without any adverse effects. Due to the efficient mechanism of copper homeostasis, even this high dosage didn’t change the plasma concentration (Harvey et al 2003, Turnlund et al 2005).

In a multicenter European study performed in 2000, researchers investigated the effect of extra copper on oxidative processes in the blood cells of middle aged people. Again, they were amazed that even 7 mg/day of copper taken during the 6 week period did not produce any increase in oxidative damage. On the contrary, it improved anti- oxidant defense (Rock et al 2000).

The only dietary source of copper that a person should worry about is in contaminated water, since it supplies inorganic copper not bio-complexes of copper. If you drink water that contains 4-8 mg of copper per liter as your only water source for several weeks, you may experience nausea and other gastric symptoms. However, such problems occur only in Third World countries, where water quality is low. In the United States drinking water does not contribute much to copper intake (Araya et al 2001).

As you can see, our bodies are well equipped with a system of copper balancing proteins and peptides that regulate copper absorption and elimination, swiftly correcting copper excess. Even though copper toxicity may occur (if we ingest too much copper salts or drink copper-loaded water or work in the copper industry), for the majority of us, the issue of copper deficiency is much more worrisome than that of copper excess.

A 6-12 weeks time frame is pointless.

Link the studies you quote please.

What is the advantage in taking copper transdermal?

I read along the way somewhere that there is the possibilitie that the body is not taking anymore through the skin when it has “enough”.
Im pretty sure it was in relation to iodine (so called “nascent” iodine, which felt more pleasurable then any other iodine taken on skin for me). And didnt absorb after added dosages!
Or even taking a swim in the ocean (salts) will “refresh” the tissue transdermaly. A Magnesium bath, which is considered transdermal readily, has obvious, for me positive, effects. Better hang and overall feel. But no matter how long Im reasonably in the bath I wont absorb all the magnesium.
(saturated skin maybe..)

By the way, give a read to this

‘J Am Coll Nutr. 2009 Jun;28(3):238-42.
The risks of copper toxicity contributing to cognitive decline in the aging population and to Alzheimer's disease.
Brewer GJ1.
Author information
Abstract

It is a pleasure and an honor to contribute a paper to a special issue of the Journal of the American College of Nutrition honoring Stanley Wallach and Pearl Small. In this brief review I advance the hypothesis that copper toxicity is the major cause of the epidemic of mild cognitive impairment and Alzheimer’s disease engulfing our aging population. This epidemic is recent, exploding in the last 50-60 years. The disease was virtually unknown 100 years ago. And it involves only developed countries that use copper plumbing. Something in our environment associated with development is poisoning the minds of our aged. The epidemic is associated with the use of copper plumbing, and the taking of copper in multi-mineral supplements. Food copper (organic copper) is processed by the liver and is transported and sequestered in a safe manner. Inorganic copper, such as that in drinking water and copper supplements, largely bypasses the liver and enters the free copper pool of the blood directly. This copper is potentially toxic because it may penetrate the blood/brain barrier. I review a web of animal and human data that tightens the noose around the hypothesis that copper toxicity is causing the epidemic of Alzeimer's disease and loss of cognition in our aging population.

The risks of copper toxicity contributing to cognitive decline in the aging population and to Alzheimer’s disease - PubMed

Chuby,

I was simply trying to be polite. I am afraid that you may be misinformed. Please allow me to quote directly from each of the articles you have quoted

From pg 409 - “Attempts to study blood copper changes, at intervals after the ingestion of copper sulfate or copper acetate … met with failure because of the emetic action of these inorganic compounds.”

That means they couldn’t study the copper intake because the subjects VOMITED IT OUT. Two paragraphs later they were attempting to study copper intake and KILLED A DOG with copper.

From pg 166 - “When the volunteers were on the high-Cu diet, 40 (SD 11) % of the
absorbed dose was excreted 14 d after the dose was given. The volunteers were not, however, in balance (0·75 mg/d was retained). It is not clear from our study or others (Turnlund et al. 1989; 1998) how long, if at all, it would take to restore Cu balance on such a high-Cu diet.”

It didn’t change the plasma concentration because it has been known since the 50s that copper is not found in the serum, it is stored in the liver where it can cause severe toxicity both acutely and over time.

“The decreased oxidizability of red blood cells did not result from increased (Cu,Zn)SOD activity and may occur through other mechanisms such as changes in membrane antioxidant content.”

Actually they stated that the increase in anti-oxidants wasn’t caused by copper.

From pg 137 - “Although exposure to copper results almost exclusively from food and water intake, acute copper toxicity … is usually the consequence of contaminated foodstuffs or bevarages… or from accidental or deliberate consumption of …copper”

It appears that those problems occur also if you deliberately consume copper.

So please do as you will, but I am going to leave the copper alone. Its not worth the risk.

Mix guy, I don’t have the time to go through all you’ve written, but let me just go over your first point, or what ever it was. Ingesting copper sulfate or copper acetate has no relevance to the statement of fact presented by the author. There is a major difference between “injecting” copper, and “ingesting” copper sulfate or copper acetate.

I think your PE routine, and in particular the cock sock which sounds like it could be the best ADS and clamping wrap of all time, is probably more responsible for the huge gains than the copper supplementation. Of course good nutrition is necessary for any tissue growth, especially in the presence of a particular deficiency, but this copper debate is getting ridiculous.

Clearly chuby knows what he’s doing, has done a lot of research on it, and is not taking it in toxic levels, or even near toxic levels. He brought it up only to give a thorough account of his PE regimen, not to carelessly lead people down a dangerous path. And on the other side, clearly supplementing with any heavy metal has inherent risks vs benefits, and taking toxic levels of copper or any metal is poisonous.

Can we get back to the all day erection cock sock and endless orgasms discussion? I’ve already ordered some neoprene. Intuitively I see no reason I can’t get it to work through a lot of trial and error. If the pressure gradient is just right, it will cause a non-stop erection.

I noticed you said all the wraps are 2.5 mm thickness, except the last which is 4 mm. What’s the reasoning behind having the last one thicker?

You also said they are decreasing in length with each additional sock you add on. So I’m envisioning the first cock sock goes the full length of the shaft. Second one goes half the length. Third goes about 30%. And fourth and fifth are perhaps 1.0” - 1.5” bands that act more like a clamp / elastic ring. Have I got the right idea?

Also wondering how to get them to go further down the shaft (like into the ball sack area is what I assume you’re doing) and whether that mechanic is responsible for your huge base girth in the photo. I’m curious what effect clamping that far down has had on your overall shape over the years.

BD

I would like nothing better than to take bearded Dragon’s advice. You, sir, seem like a very reasonable fellow.

I have done a lot of experimenting with different types, grades and thicknesses of neoprene. Some are much better for our purposes than others. The reason for the thicker neoprene sock at the end is that to some degree it acts like a exoskeleton, or perhaps better put, it creates, if built to contour your base sufficiently well, a suction and rigidity that holds your organ to that shape while also applying pressure as it attempts to become more fully engorged. The whole sock when fitted into place acts a little bit like a suction cylinder and compression bandage in one. This is why the fit is so crucial. There is a type of neoprene that aids this effect. You will find it on some wet suites. It is more rubbery and spongy. I wouldn’t use this type for any but the final layer on the base, as it does not hold a stitch well, but you should experiment to see what works best for you.
Did I really say that about sizes? Hmmm. Anyway, let’s say you have a non bone pressed 5 12 inches to where your gland starts on top. That is how long the top side of your sock should be. The bottom side, the side with seam - where you sew it together, should be longer, so that it curls and wraps up tight to the under side of your gland. And it should also be a bit longer as it reaches down toward your rectum. The next one should be slightly longer, about the same as your bone pressed length. And slightly larger in circumference. The third one should be slightly longer still, a bit longer than your bone pressed, and again slightly bigger. I say “longer” than your bone pressed length because you should find that as you roll this on, with the two previous starting to wrap your base, you can actually get a hold of more cock than you thought you had. You may find it helpful after having rolled the first sock on to put a cable clamp lightly on the base while you roll the next one on, and of course remove it just before the final roll of the proceeding sock. And so on.
The next three are to fully capture your base. They will become larger as you go just like the first three. These all have to mimic the shape of your base. This is a tricky operation and will take you some time, probably, to work it out. Maybe not though, now that you all have me to explain this shit to you. The first one should be about two inches in width at the top, and curl back down around the base to about three inches at the bottom.. Probably reduce all of the measurements if your unit is smaller. The next one, a bit bigger in all direction. The last one should reach all the way to nearly your rectum. Your ball sack should hopefully be long and stretchy enough so that your nuts are just peeking out the very bottom of this arrangement. I should probably also point out that the opening at the base, where your buts are hanging out, is angles nearly 90 degrees in relation the direction your shaft is naturally pointed when erect.
If you’ve gotten this far, here is where the real fun begins. But I’m going to save this for latter, until somebody does actually get this far. I have a feeling, however, that you won’t be needing me to have fun if you do make this far. The sensation is phenomenal.

You are absolutely right BD, the last three act like large, elastic clamps. But also like a suction cylinder as well.
Yea, and I’m pretty sure this is responsible for the how and why of my base girth. Well, not just this, I mean if you saw my clamping,.. Well I told you already. Without the sock,though, I could never have started such a clamping routine. As for the shape change. I didn’t even know that part of my organ existed when I first started. It simply never became engorged. The rest of my organ has remained the same shape, just bigger.
I hope you guys all find some success with this. It may be useful to note that I had already built up amazing toughness before I started this practice. And one last thing. Be sure to have some power in you before rolling it on the first time. It helps to find the process a wee bit arousing.

Chuby, they had to inject it because the people were throwing up what they ingested. Which goes back to what I have been saying from the beginning, be careful with ingesting copper. Good luck with your story, can’t wait to see the pics of the cock sock in action.