Can i switch to Sustanon and and continue with it??

Hii

have used Test E for 4 months now, have some problems with my supplier...
The thing is that I have some Sustanon 250 in stock, would it a smart choice to start with the Sustanon??

Hey

thanks for the tips, but it was not the answer to my question.
I get it for free(=.

have some thoughts about the dosage 400-600mg weekly is it enough?

Would 250mg Test weekly work as a base with it?

Hello

Got an offer on some PRIMOBOLAN Tabs produced by HUBEI.
Wondering if anyone has experience of oral PRIMO is it worth??

thanks

just an allergic reaction, symptoms disappeared after the first week(=

Thanks guys for all the tips..
I am not drinking or smoking, its not that bad but noticed it the last days a bit itchy almost like small sticks..
Think that i will jump of it and try to check my blood.

Will send you a pm

Hi

Started my cycle this week, have used 20mg dbol daily since  Monday, i am now starting to get itching symptoms, my skin its itching often....its a typical symptom of liver toxication, so i will jump off it..
Wonder if someone has experience this??? May it be symptoms of other side effects like high estrogen???
For me this seems like liver toxication.,,,,

Haha, latiuss your picture tells everything you are nr1.
Haha nice pose, WOW how long have you train to develop that chicken breast of yours......
NO symmetry at all.....

He was the around the same weight as you , pic someone else with that weight, if you are 92kg with around 8% bodyfat you shuold look like a BB, or else you are big fail...
Post some info on your biceps and chest, back measurements..,,
So we can se how big you are and some pics, then i can compare you to me,.....
No pics and measurements how can i compare you with me!??

Someone who know wats he talking about great(=
Looks great man i would say 85kg.....
Most of the guys alos eats like the pros, if Jay cuttler eats 500g protein daily i would also do like him, but am i as big as he?
Its so funny when pepole tell you how to eat ,all is genetics and induvidual......

Lol, sure please i beg you post a pic on your current shape and your chest, biceps etc measurements.
You probably are a PRO, we can compare you with lots of great pros..i think that serge nubret was the same weight!!!!!!

Totaly agree with you....its no problem for me to gain to 90kg....FAT

Thats great!!!!  80-85 kg is dam good also depends on the bones structure, know lots of pepole who are 85kg but they are not that muscular, look at Mr Zane around 86kg

1,80cm

Was around 82kg after my cycle,my goal is to gain to 85kg Max and stay 6-8% bodyfat with proper symmetry.... That takes time!!!!!!
Homo??ask the bitches i bang everyday.....

haha next time i take it off... just kidding thanks(=

Starting my second cycle next week, will post some info about compunds that i will use ,diet training plan, goals etc.
I completed my first cycle last summer which consisted of Test Prop 100mg EOD 8weeks. I gained about 7-8 kilos, got pretty good results but also got a bit puffy. Since then I have continued to train hard and reach my goal to lean aout, around 8% bodyfat which went well bay the way.
My current weight (morning) is 71,5 kg a bit low , the goal is around 78-82 kg. Will try to stay  lean as possible and keep my diet strictly during throughout.

Diet plan

My daily  calorie intake 2300-2500 kcal, will increase if necessary, depending on results i get.

Protein: 32% Carbs: 43% Fat: 25%  to start with.

Meal 1: Eggs and spinach+ low fat yogurt and berries, multivits+omega 3.
Meal 2: Amino acids+ piece of fruit.
Meal 3: Beef+ brown rice+broccoli and salad low fat cheese.
Meal 4: Salmon+brown pastaand spinach+ almonds.
Meal 5: Amino acids+piece of fruit.
Meal 6: Chicken breast+ low fat cheese sallad, olive oil and almonds.
Meal 7: White fish+ sallad.

Just a  sample.

Supplements: Animal Pak multivits during meals+saw palmetto+milk thistle , Whey isolate post workout, Amino acids pre workout/during also beetwen meals.

CYCLE

Cycle lenght 12-14 weeks
The cycle will will consist of Test Enanthate 250mg e7d (base)+dbol 4-5weeks from start,  last 6 weeks i would start with Clenbuterol and add Tren A Winstrol or Anavar,depending on results.

Throughout cycle 14 weeks 250mg Test inject  Monday, Sunday, Saturday, Friday etc.

Week 1: 10mg dbol daily/70mg week.
Week 2: 20mg daily/140mg week.
Week 3: 30mg daily/210mg week.
week 4: 50mg daily/350mg week.

The dose will be adjusted according to the results and how my body reacts maybe its fine with 10mg daily if so il stay on for a longer time.

Week 9: Tren A 50mg eod+Maybe 25mg winstrol daily following weeks.
Week 10: Tren A 50mg edo
Week 12: Tren A 50mg eod.
Week 13: Tren A 50mg eod.
Week 14: Tren A 50mg edo.

If needed Clenbuterol will be added 20mcg,40mcg,60mcg two weeks off.

This is an sample everything will be adjusted after my results and how my body will react on the compounds, I may not even use Tren!!!!!

Will also try to post some pics during weeks!!!!

Got my magic tabs today "methandienone" 5mg
I am planing to kickstart my Test E cycle, with 20mg daily 1week then increase 10mg weekly up to 50mg(4weeks) if everything goes correctly..
Since the tablets are 5mg would it be better to split it,,,5mg 4 times daily with meals or just 10mg for breakfast and 10mg pre workout?
Breakfast 6AM Workout 7PM.

All personal tips and experience is appreciated.

Totally agree with you galeniko ,number of studies points on that(=

Found some supplements that's a bit interesting for my upcoming cycle, maybe worth giving them a chance...someone who tried???
Just mention that I will use Test+dbol .

1. http://www.aisportsnutrition.com/mstore/index.php/health/post-cycle-support-1/post-cycle-support.html
2. http://www.aisportsnutrition.com/mstore/index.php/root-category/testosterone/testopro.html
3. http://www.advancedmusclescience.com/products/hormonal-support-products/super-cycle%E2%84%A2/#nogo

Natural Approaches to Boost Testosterone and Suppress Estrogen

Nutrients function by increasing testosterone availability, often by affecting testosterone's interaction with SHBG or by decreasing its aromatization (conversion) into estrogen. Natural supplements can complement hormone replacement therapy. For people who choose not to (or should not) use hormone replacement therapy, nutrients can be a vital part of a comprehensive program to reduce the impact of aging on the systems of sex hormone production, regulation, and metabolism. Nutritional therapy also has a role in preventing diseases of the male reproductive tract, such as prostate cancer and benign prostatic hyperplasia (BPH). More specific information on these diseases can be found in the chapters "Prostate Cancer" and "Benign Prostatic Hyperplasia."

The following is a list of nutrients that are part of the Life Extension Foundation's comprehensive male hormone modulation program:

Zinc. Zinc is related to testosterone levels. In one animal study, rats subjected to an acute swimming test were either supplemented with zinc or placebo. The study showed that zinc supplementation led to significant increases in testosterone levels and may help in athletic performance (Kaya O et al 2006). Among humans, zinc supplementation in a group of male wrestlers prevented the depletion of testosterone after exertion (Kilic M et al 2006). Additional studies have suggested that zinc is important to the synthesis of testosterone (Ali H et al 2005).

Chrysin. A bioflavonoid called chrysin has shown potential as a natural aromatase inhibitor (Kellis JT Jr et al 1984). Chrysin can be extracted from various plants and is found in high concentrations in honey. Bodybuilders have used it as a testosterone-boosting supplement because, by inhibiting the aromatase enzyme, less testosterone is converted into estrogen. Although chrysin is a known inhibitor of aromatase, in one study it did not result in the expected increase in testosterone levels (Gambelunghe C et al 2003). This may be because of poor intestinal absorption of chrysin (Walle UK et al 1999). The Life Extension Foundation has identified a novel supplement called piperine that increases the bioavailability of chrysin.

Carnitine. Carnitine is an amino acid derivative that may be more active than testosterone in aging men who have sexual dysfunction and depression caused by an androgen deficiency (Cavallini G et al 2004). Both testosterone and carnitine improve sexual desire, sexual satisfaction, and nocturnal penile tumescence, but carnitine is more effective than testosterone in improving erectile function, nocturnal penile tumescence, orgasm, and general sexual well-being. Carnitine was better than testosterone at treating depression (Cavallini G et al 2004).

Muira puama. Muira puama is a South American folk medicine derived from a shrub, Ptychopetalum olacoides, which grows in the Amazon region of Brazil. Also called marapuama and "potency wood," it is considered an aphrodisiac and an effective treatment of impotence. Because of its purported libido-enhancing properties, muira puama has been the subject of two published clinical studies by Dr Jacques Waynberg, an eminent medical sexologist and author of 10 books on the subject.

The first study, conducted at the Institute of Sexology in Paris under Dr Waynberg's supervision, consisted of examining the effect of muira puama on 262 men who complained of lack of sexual desire or inability to attain or maintain erection. After receiving 1.5 grams (g)/day of muira puama for 2 weeks, 62 percent of the patients with loss of libido rated the treatment as having a dynamic effect, and 52 percent of patients with erectile dysfunction rated the treatment as beneficial (Wright JV et al 1999).

Dr Waynberg's second study, entitled "Male Sexual Asthenia," focused on sexual difficulties associated with asthenia, a deficiency state characterized by fatigue and loss of strength, both symptoms of a testosterone deficiency. The study population consisted of 100 men older than 18 years who complained of impotence and/or loss of libido. A total of 94 men completed the study, and their conditions were evaluated. Muira puama treatment led to significantly increased frequency of intercourse for 66 percent. Of the 46 men who complained of loss of desire, 70 percent reported intensification of libido. The stability of erection during intercourse was restored in 55 percent of patients, and 66 percent of men reported a reduction in fatigue. Other reported beneficial effects included improvement in sleep and morning erections (Waynberg J 1990).

Cruciferous vegetables. Cruciferous vegetables, such as broccoli and cauliflower, contain isothiocyanates and glucosinolates, which act as antioxidants and potent inducers of phase 2 proteins believed to suppress prostate cancer formation (Kris-Etherton PM et al 2002; Talalay P et al 2001).

Quercetin. Wine contains antioxidant polyphenols and quercetin. One study showed that red wine inhibited aromatase. The study attributed this effect to the quercetin and other ingredients (Eng ET et al 2002). In human colon cancer cells, quercetin has been shown to inhibit local synthesis of estrogen by inhibiting aromatase (Fiorelli G et al 1999).

Saw palmetto and nettle extracts. These two supplements are commonly used to reduce symptoms of BPH. In Europe, saw palmetto (Serenoa repens) has been used extensively as a drug for some time. Saw palmetto's clinical benefits for prostate enlargement include:

Found an very interesting article how to lower your estrogen activity (=

This situation suggests excessive aromatase activity, which converts free testosterone to estrogen. Inhibition of aromatase and reduction in aromatase-containing tissue (fat) is indicated. Suggestions include:

Take the following supplements:
Zinc—50 milligrams (mg)/day
Acetyl-L-carnitine—1000 to 2000 mg/day
Muira puama—850 mg/day
Chrysin—1500 mg/day
Piperine—10 mg/day to enhance absorption of chrysin
Quercetin—500 to 1000 mg/day
Lose weight to reduce aromatase activity.
Reduce or eliminate alcohol to enable the liver to better remove excess estrogen.
Review all current medications to see if they are interfering with healthy liver function. Common medications that affect liver function are nonsteroidal anti-inflammatory drugs (NSAIDs) such as naproxen, ibuprofen, acetaminophen, and aspirin; the statin class of cholesterol-lowering drugs; some heart medications; some blood pressure–lowering medications; and some antidepressants. Drugs being prescribed to treat the symptoms of testosterone deficiency (such as the statins and certain antidepressants) may actually aggravate the testosterone deficit, thus making the cholesterol problem or depression worse. However, do not discontinue any prescription medicine without consulting your physician.
If all of the above fail to increase free testosterone and lower excess estradiol, consider discussing with your physician the use of the aromatase inhibitor anastrozole at the very low dose of 0.5 mg twice per week.

I used Nolvadex and will also try Clenbuterol this time great products g2g!!!

Hey

Just read an interesting pos about the use of AIs during cycle , would be great to hear  your opinions!!!!!

Its well known (atleast I think it is) that estrogen is a carcinogen. In fact, its a Group 1 IARC classified estrogen, which means it a pretty potent one really. The risks of estrogen and carcinogenic activity are then again confirmed in 'estrogen only' conraceptive treatment(s). Although the data is somewhat confusing (as some data is on estrogen+progestagen treatment), the links to various forms of cancer rates increasing is pretty clear in my book.

To quote from a paper looking at the effects of estrogen only contraceptive treatment and estorgen+progestrogen contraceptive therapy:

"Four studies (one cohort study and three large case-control studies) reported increased risk of endometrial cancer with estrogen repla***ent therapy (Cushing et al. 1998, Shapiro et al. 1998, Persson et al. 1999, Weiderpass et al. 1999), and three of these studies reported strong positive associations between risk of endometrial cancer and duration of estrogen use."

"Two of four case-control studies found that estrogen-only repla***ent therapy was associated with an increased risk of breast cancer (Heinrich et al. 1998, Magnusson et al. 1999)."

"One study found that estrogen therapy was associated with ovarian cancer (Purdie et al. 1999)."

"In 2009, IARC concluded there was sufficient evidence of the carcinogenicity of estrogen-only therapy in humans based on increased risks of endometrial cancer and ovarian cancer and limited evidence based on increased risk of breast cancer (Grosse et al. 2009). The findings for ovarian cancer were based on two meta-analyses (Greiser 2007, Zhou 2008). Since then, another meta-analysis has estimated a significant overall increase in ovarian cancer risk related to duration of use of estrogen-only therapy (Pearce et al. 2009)."

"In rodents, steroidal estrogens caused benign and malignant tumors, as well as pre-cancerous lesions, in a variety of organs, including the mammary gland and female reproductive tract (IARC 1999). Estrogenic compounds generally caused endometrial, cervical, and mammary-gland tumors in mice, mammary- and pituitary-gland tumors in rats, and kidney tumors in hamsters"

I think you get my point...

Although there is mixed data in that study, the theory that estrogen is carcinogenic is overwhelming.




So what does that all tell us? It tells us that when exposed to estrogen (steroidal) that it can cause some serious problems. Yes, these studies are done on females (I didnt miss that), but women are a hell of a lot more tolerable to estrogen than men are. Males are not designed for increased levels of estrogens at all, womens are (during pregnancy for a start). Womens levels can hit 500pg/ml, the top end of males is 50pg/ml 10x lower.

Estrogen role in males is important. Its important for GH and IGF synthesis, bone density, lipid profile, glucose uptake and utilisation, AR sensitivity and activation, immuno function, anti-inflammitory effects and a host of other benifits. Without it, we (males) would't function properly.

There are studies for and against the importance of sex hormones on CHD and mortality, but the hypothsis is plausable. Why?

- Estrogens inhibit smooth muscle proliferation and decrease smooth muscle tone

- Their effects on lipid profiles

- High-affinity estradiol receptors are present in both vascular smooth muscle and endothelium

- Estrogens enhance the release of nitric oxide and prostacyclin from endothelial cells, thus inducing vasodilation

- Estrogens exert indirect effects on the cardiovascular system through their influence on lipoprotein metabolism and the coagulation, fibrinolytic, and antioxidant systems

So one can not see the importance estrogen have on the cardiovascular system, CHD, therefore mortality rates. Here is a good solid article on estrgens links to CHD, found here.



How else does estrogen negatively effect males?

Well, recent research has confirmed its role in the most common form of cancer in males - prostate cancer. The basics of which are shown here. These are very recent findings and more research is to be done. However, the links and risks are evident and whilst DHT was thought to play as the main role (10 years ago), estrogen and also prolactin (which worsesns prostate cancer) have been shown to have positive effects on expression and proliferation in cancerous prostate cells in vitro and vivo. On the plus side Tamoxifen has been shown to inhibti expression and proliferation, much like it does in female breast cancer patients.



When I see someone argue that an AI just isnt needed on a cycle, I think to myself, why is it not needed? Based on what? Because you haven't got gyno? The user may not experience side effects such as gyno, water retention, acne, but there estrogen level is sure as f*ck high.

Aromasin (Exemestane) at 10mg/ED will keep most people estrogen level under 50pg/ml on cycle IMO. It does me and I am sensitive to estrogenic side effects (very).

The common reason for not using an AI is, that it may limit gains made... But do they?

AI's have little impact on IGF-1 levels and Exemestane does not have any effects at all, as shown here. If IGF-1 was somewhat lowered, we also need to understand that exogenous testosterone and other anabolic steroids are going to increase IGF-1 and further negate these effects. To realise how little effect AI's have on IGF-1, read this study.To summarise; Nine young healthy men who received femara at 2.5 mg daily for 28 days had a 15% reduction in IGF-1, a 24% reduction in leptin, and a 14% increase in LDL (bad cholesterol).

As for Exemestane on lipid levels, it has far less impact than other AI's although it does not have the benificial effects of SERMs. Some data, such as this one, it has no "no clinically significant effect on the serum lipids". Another study stated, "Overall, exemestane has no detrimental effect on cholesterol levels and the atherogenic indices, which are well-known risk factors for coronary artery disease. In addition, it has a beneficial effect on TRG levels"

Here is one on young males thats slightly more applicable, this study states, "Plasma lipids and IGF-I concentrations were unaffected by treatment."

Finally, because of the LongFeedback Mechanism (google it), controlling estrogen means we can help control prolactin. So there is more of a reason to use an AI when using 19-Nors (if you experience increased PRL). I'd also keep a D2-agonist on hand though.