Zinc: strong aromatase inhibitor - MUST READ!!

[gainerxxl]

I´m very active on a big german anabolics dicussion board, which has a great member, who´s a medical doctor. He´s really into steroids and knows his stuff like few others. About a year ago, he suggested to use zinc supplements at high dosages when cycling test. I didn´t buy it at first, nor did most of the other members.

Now, one year later, everybody uses zinc at 100-150mg/day as their only anti-E. It works great up to 750mg Test/week, by inhibiting aromatase activity as well as 5-alpha reductase (less DHT=less hair loss=good for prostrate) to a surprising degree.
This actually makes zinc an aromatase inhibitor, not an anti-E.

On my first cycles of only 250mg test-E/week (second cycle 250 every 5 days) I experienced some bloat, sore nipples and buildup of fatty tissue around my nipples, I had to use Nolva to get rid of that.

Now I use up to 750mg of test/week along with 150mg of a high quality zinc supplement and I don´t even bloat one bit, my nipples are fine, and so is my prostrate.
It is used by hundreds of Juicers in Germany now, almost everybody reports great success.

On top of that, it´s proven to be non toxic at those dosages, it helps to clear up skin (due to DHT reduction, I guess) and it costs next to nothing. It´s properties make it a must for post cycle recovery as well, the studies I will present clearly show that.

I was sceptical and so will you, but please give it a try, you´ll be surprised.
I did some research and found lots of studies that indicate an inhibition of aromatase and 5-alpha reductase. Most were performed on rats, but there´s some on humans, but I couldn´t find any about large dosages of test and zinc supplementation.

You can give me Karma, when you actually try it, you´ll see it works!

 

[gainerxxl]

Dietary zinc deficiency alters 5 alpha-reduction and aromatization of testosterone and androgen and estrogen receptors in rat liver.

Om AS, Chung KW.

Department of Food and Nutrition, College of Home Economics, Hanyang University, Seoul, Korea.

We studied the effects of zinc deficiency on hepatic androgen metabolism and aromatization, androgen and estrogen receptor binding, and circulating levels of reproductive hormones in freely fed, pair-fed and zinc deficient rats. Hepatic conversion of testosterone to dihydrotestosterone was significantly less, but formation of estradiol from testosterone was significantly greater in rats fed the zinc-deficient diet compared with freely fed and pair-fed control rats. There were significantly lower serum concentrations of luteinizing hormone, estradiol and testosterone in rats fed the zinc-deficient diet. No difference in the concentration of serum follicle-stimulating hormone was observed between the zinc-deficient group and either control group. Scatchard analyses of the receptor binding data showed a significantly higher level of estrogen receptor in zinc-deficient rats (36.6 +/- 3.4 fmol/mg protein) than in pair-fed controls (23.3 +/- 2.2 fmol/mg protein) and a significantly lower level of androgen binding sites in rats fed the zinc-deficient diet (6.7 +/- 0.7 fmol/mg protein) than in pair-fed control rats (11.3 +/- 1.2 fmol/mg protein). There were no differences in hepatic androgen and estrogen receptor levels between freely fed and pair-fed controls. These findings indicate that zinc deficiency reduces circulating luteinizing hormone and testosterone concentrations, alters hepatic steroid metabolism, and modifies sex steroid hormone receptor levels, thereby contributing to the pathogenesis of male reproductive dysfunction.



[Effect of zinc deficiency on apoptosis of spermatogenic cells of rat tostis]

[Article in Chinese]

Li J, Xu P, He Z.

Department of Anatomy, Chinese People's Armed Police Force Medical College, Tianjin.

OBJECTIVE: To study the changes of testis apoptosis in zinc deficient rats will promote the understanding of the molecular mechanism of zinc deficiency in the development and function of testis. METHODS: 16 Wistar rats were divided randomly into zinc control group (ZC) and zinc deficiency group (ZD). The serum and testis zinc contents were measured with atomic absorse method; the apoptosis of spermatogenic cells was studied with in situ nick translation (ISNT) technique. RESULTS: Under zinc deficient status, the zinc contents of the serum and testis were obviously decreased (P < 0.05). The apoptosis number of spermatogenic cells was significantly increased (P < 0.01). CONCLUSION: The adequate amount of zinc is essential to the development of testis, whereas zinc deficiency can harmfully affect it. This effect is perhaps carried out in different ways, but the increasing apoptosis numbers of spermatogenic cells might be one of molecular miechanisms of the effect of zinc defficiency on testis development.

PMID: 10923414 [PubMed - indexed for MEDLINE]

 

[newpump]

Any specific types of Zinc to use gainer? Like I know with ALA I prefer r-ALA - is all zinc built equal?

 

[gainerxxl]

Dietary Zinc Deficiency Alters 5 Alpha-Reduction and Aromatization of Testosterone and Androgen and Estrogen in Rat Liver," Ae-Son Om and Kyung-Won Chung, published in the April 1996 Journal of Nutrition, 126[4]: 842-848.
Ae-Son Om and Kyung-Won Chung are from the Department of Anatomical Sciences in the University of Oklahoma College of Medicine. They had done a previous study in 1990 on why alcoholics and coke addicts develop feminine characteristics. In this study, they had found that the hepatic aromatization of androgens to estrogens is enhanced by alcohol ingestion and cocaine administration. Both alcohol and cocaine also lower an individual's zinc levels, sometimes beyond simple depletion and into actual deficiency. In their new work, they sought an anatomical/biological explanation of why this occurred.
The researchers included three populations of rats in their study. The first group was fed a zinc-deficient diet; the second were fed a controlled but adequate diet of zinc; and the third group was comprised of free feeders.
After a pre-determined time, the scientists measured the rat’s Testosterone and estrogen levels and measured and counted their androgen and estrogen receptor sites.
Among the zinc deficient rats, they found the androgen receptor sites had reduced in number and size by 40%. At the same time, the estrogen receptor sites increased by 60%! The liver's conversion of Testosterone to estrogen was significantly greater in the rats on the zinc deficient diet. The same rats that had the decrease in androgen receptor sites showed significantly reduced amounts of luteinizing hormone and Testosterone.
Having a zinc-deficient diet evidently increased the aromatization of Testosterone and the formation of estradiol, the primary estrogen hormone.
Another study that seems to confirm my need to eat crow is "Androgen Receptors in the Ventral Prostate Gland of Zinc Deficient Rats,"Life Science, January 27, 1986, 38 [4]: 351-356. This study involved two groups of rats; one group fed a zinc deficient diet for three months, and one group fed a controlled (zinc adequate) diet for the same amount of time. Analysis of the data revealed that the number of androgen binding sites of the zinc deficient rats' prostates was 31 fmol/mg cytosal protein. This was significantly lower than the 84 fmol/mg protein of the controls.
Do the math! Divide 31 by 84 and you have a 63% reduction in the number of androgen binding sites!
To synopsize, if some of the Testosterone has nowhere to go — nowhere to bind — it’ll continue to circulate in the blood, finally being aromatized in the liver and producing estrogen, which could lead to gynecomastia.
So it appears that the simple addition of adequate zinc to your diet will increase Testosterone and the number of receptors for Testosterone, in addition to reducing estrogen and the number of receptors for estrogen, as well as preventing decreases in LH from happening.

 

[gainerxxl]

Zinc status and serum testosterone levels of healthy adults.

Prasad AS, Mantzoros CS, Beck FW, Hess JW, Brewer GJ.

Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan, USA.

Zinc deficiency is prevalent throughout the world, including the USA. Severe and moderate deficiency of zinc is associated with hypogonadism in men. However, the effect of marginal zinc deficiency on serum testosterone concentration is not known. We studied the relationship between cellular zinc concentrations and serum testosterone cross-sectionally in 40 normal men, 20 to 80 y of age. In four normal young men (27.5 +/- 0.5 y), we measured serum testosterone before and during marginal zinc deficiency induced by restricting dietary zinc intake. We also measured serum testosterone in nine elderly men (64 +/- 9 y) who were marginally zinc deficient before and after 3 to 6 mo of supplementation with 459 mumol/ d oral zinc administered as zinc gluconate. Serum testosterone concentrations were significantly correlated with cellular zinc concentrations in the cross-sectional study (lymphocyte zinc versus serum testosterone, r = 0.43, p = 0.006; granulocyte zinc versus serum testosterone, r = 0.30, p = 0.03). Dietary zinc restriction in normal young men was associated with a significant decrease in serum testosterone concentrations after 20 weeks of zinc restriction (baseline versus post-zinc restriction mean +/- SD, 39.9 +/- 7.1 versus 10.6 +/- 3.6 nmol/L, respectively; p = 0.005). Zinc supplementation of marginally zinc-deficient normal elderly men for six months resulted in an increase in serum testosterone from 8.3 +/- 6.3 to 16.0 +/- 4.4 nmol/L (p = 0.02). We conclude that zinc may play an important role in modulating serum testosterone levels in normal men.

PMID: 8875519 [PubMed - indexed for MEDLINE]

Experimental zinc deficiency in man. Effect on testicular function.

Abbasi AA, Prasad AS, Rabbani P, DuMouchelle E.

Dietary zinc intake was restricted (2.7 to 5.0 mg daily) for 24 to 40 weeks in five male volunteers. Their mean age was 57 years. Oligospermia (total sperm count less than 40 million per ejaculate) was induced in four out of five subjects. A decrease in the sperm count occurred during zinc restricion and the early phase of zinc repletion before body stores of zinc were restored to normal. The duration of oligospermia in the four subjects ranged from 6 to 14 months. Oligospermia was reversed after zinc supplementation in physiologic amounts. The baseline sperm concentration and total sperm count per ejaculate in all five subjects dropped significantly (p < 0.05) after zinc restriction and returned to normal 6 to 12 months after zinc supplementation. The decrease in sperm count coincided with decline in Leydig cell function and was reversed after zinc supplementation in low doses. Our study has demonstrated that dietary restriction of zinc can affect testicular function adversely. This effect of zinc deficiency, however, is a reversible process and can be corrected by proper supplementation with zinc.



Zinc Deficiency

Zinc inhibits the levels of aromatase in the body. If zinc levels are inadequate, the levels of aromatase rise. Zinc is also necessary for normal pituitary functions. Without zinc, the pituitary gland cannot release the luteinizing and follicle stimulating hormones that stimulate the testes to produce testosterone. An interesting note; while zinc is necessary for testosterone production, testosterone is necessary to maintain levels of zinc in body tissues.

 

[bazilbb]

it would b great if u tell us what natural food, veggies, fruits etc. has ZINC in good quantity in them.........

 

[CLOBRO]

What I don't get is that if some DHT blockers like proscar/propecia cause gyno and zinc is a dht blocker, how is zinc an aromatase inhibitor?
Zinc is supposed to work well to keep testosterone levels up too. Am I missing a piece of the puzzle?

DHT helps to regulate estrogen from Patrick Arnold:
Anti – Estrogen effects of DHT

One important function of DHT in the body that does not get much discussion is its antagonism of estrogen. Some men that take proscar learn this the hard way – by developing a case of gynecomastia. By reducing DHT’s protection against estrogen in the body, these men have fallen victim to its most dreaded ramification – bitch tits!

How does DHT protect against estrogen? There are at least three ways that this likely occurs. First of all, DHT directly inhibits estrogens activity on tissues. It either does this by acting as a competitive antagonist to the estrogen receptor or by decreasing estrogen-induced RNA transcription at a point subsequent to estrogen receptor binding.

Second of all, DHT and its metabolites have been shown to directly block the production of estrogens from androgens by inhibiting the activity of the aromatase enzyme. The studies done in breast tissue showed that DHT, androsterone, and 5alpha-androstandione are potent inhibitors of the formation of estrone from androstenedione. 5alpha-androstandione was shown to be the most potent, while androsterone was the least.

Lastly, DHT acts on the hypothalamus / pituitary to decrease the secretion of gonadotropins. By decreasing the secretion of gonadotropins you decrease the production of the raw materials for estrogen production – testosterone and androstenedione (DHT itself cannot aromatize into estrogens). This property of DHT comes into particular utility when it is administered exogenously, and this is to be discussed in further detail in the next section.

DHT, estrogen, and the prostate

When it comes to sex hormones, few things are as misunderstood by the general consumer as the relationship of the prostate to DHT. The inaccurate and overly simplistic attitude that DHT is responsible for prostate hypertrophy, and even prostate cancer predominates amongst most people.

The real situation is, of course, much more complex. One must understand that there are marked differences between healthy prostate growth (developmental growth), prostate growth due to BPH, and cancerous prostate growth.

The first period of prostate growth, deemed developmental growth, is connected to puberty and the testicular secretion of androgens. This takes the prostate from its prepubertal dormancy to the normal sized, healthy, and functional prostate gland of an adult. During the early and mid adult years the prostate stays at this stage, despite the constant high levels of androgens in the body. However, if androgens are blocked in the body then the adult prostate will shrink in size. This can occur by castration, or even by blockade of 5-AR (recall that DHT is the active androgen in the prostate).

Later in life, there is often a second stage of growth. This growth is deemed benign prostate hypertrophy (BPH) and this growth occurs in a wholly different hormonal environment than that of developmental growth. Evidence is mounting that the existence of a high estrogen / androgen ratio – a condition common in older men – is highly correlated to the development of BPH.

Experimental studies have shown the inability of androgens with saturated A rings (DHT related) to induce an initial condition of prostate hypertrophy. These compounds are non-aromatizable. Aromatizable androgens on the other hand, such as testosterone or androstenedione can induce hyperplasic modifications of the prostate of monkeys, but these effects are reversed by the addition of an aromatase inhibitor.

So apparently, estrogen is a causative factor in BPH or, probably more accurately, estrogen in the presence of a minimum, permissive amount of androgen.

None of this may come as news to many of you, but I bet that very few of you know that DHT can actually be used to treat BPH!! How can it do that? It basically does this by replacing the testosterone in the body, which then has the effect of reducing the amount of estrogen in the body. As I started to explain before, DHT is a strong androgen that will signal the pituitary to decrease the production of gonadotropins. The decrease in gonadotropins will then cause less testosterone to be produced which will in turn cause the estrogen levels to drop. The resulting change in the hormonal milieu (high DHT, low estrogen) then apparently results in a regression of BPH.

The clinical application of this theory is discussed in US patent 5,648,350 "Dihydrotestosterone for use in androgenotherapy". The following illustrates the results:

"In 27 subjects in which the plasma DHT level was controlled, so as to modulate the administered doses, said levels have been increased to 2.5 to 6 ng/ml. There resulted a decrease in gonadotrophy as well as in the plasma levels of testosterone which exceeded at least 1.5 ng/ml (from 0.5 to 1.4 according to the case); as to the estradiol plasma levels, these decreased by 50%.

Among this group of subjects, the volume of the prostate diminished significantly, as was evaluated by ultrasound and by PSA (Prostate Specific Antigen). The mean volume of the prostates was from 31.09.+-.16.31 grams before treatment and from 26.34.+-.12.72 grams after treatment, for a mean reduction of 15.4%, the treatment having a mean duration of 1.8 years with DHT (P=0.01)."

This kind of flies in the face of the traditional thinking concerning BPH now doesn’t it?

Conclusion

People have a natural tendency to classify things as either good or bad, with no gray areas. DHT (like estrogen) has recently been on everyone’s bad list, and is often considered to be a hormone that serves no function in the body except to cause harm. As you can see, this view is far from the truth. In my opinion, the widespread use of 5-AR inhibitors such as Proscar as a prophylactic agent for people that really don’t need it should be reconsidered. So give DHT a break. I now pronounce June "DHT Appreciation Month". Thank you.

by Pat Arnold

 

[Silent Method]

Too much zinc...

Nutrient
Zinc

Toxic Dosage
75 mg

Symptoms and Diseases
Gastrointestinal irritation, vomiting, adverse changes in HDL/LDL cholesterol ratios, impaired immunity. Nausea, anemia, bleeding in stomach, premature birth and stillbirth, abdominal pain, fever. Can aggravate marginal copper deficiency. May produce atherosclerosis.

The toxic dosage can change acording to what kind of zinc supplement is used as well as the individual. Athletes can utilize more zinc than others, but I'd be very weary of high end doses.

 

[Triple J]

Some recommended sources of high quality zinc supplements would be helpful!! I think ZMA is a good quality zinc, but overpriced!! So I take zinc gluconate and zinc picolinate that I got at Vitamin World cheap, but I don't really trust Vitamin World. Should I try somethig else? Will increase my dose anyway- thanks.

 

[gainerxxl]

Re: Too much zinc...

The toxic dosage can change acording to what kind of zinc supplement is used as well as the individual. Athletes can utilize more zinc than others, but I'd be very weary of high end doses.

Zinc at dosages up to 200mg/day are proven to be non toxic, even for prolonged periods of time. Studies showed no adverse effects of high dose zinc supplementation in healthy males, you only have to take some copper with it, if you take very much zinc for very long periods. Zinc somewhat interferes with copper uptake. Most Multi Vitamin/mineral supps contain copper anyways.

I´ll dig up the studies, zinc is not toxic, especially when taken for a short time during a cycle.

Best zinc is zinc-chelate or zinc piccolinate. KAL produces a great zinc supplement, it´s called zink 100+ and costs about 12 Bucks for 100 Tabs with 100mg zinc per tab in high quality chelate form.