Thread: Next cycle, what you think?
07-17-2003, 05:49 PM #1
Next cycle, what you think?
I'm getting my next cycle ready, just wanted to know what you guys think. It looks like this:
Weeks 1-4 100mg Anadrol50 ED
Weeks 1-16 Sustanon 250 ED
Weeks 1-16 Deca 200mg EOD
Weeks 8-16 Fina 75mg EOD
Post cycle Clomid
Novaldex on hand, Proviron or Liquidex on hand
Clembuterol at end of cycle
HCG every 4 weeks @ 1250mg/day for 4 days
Let me know what you guys think. Thanks bro's.
07-17-2003, 05:53 PM #2
Is those are relatively high does, especially if this is your first cycle. Please post cycle experience, age, weight, height, training and etc... This will give the members on the board a base to help you plan you next cycle.
07-17-2003, 06:29 PM #3Member
- Join Date
- May 2003
- not too far from you
07-17-2003, 06:31 PM #4
whoa! extremely high dosages. no need for so much
07-17-2003, 06:43 PM #5
07-17-2003, 06:53 PM #6
07-17-2003, 07:06 PM #7
I have never run them, but all the posts I read say that you run a serious risk of dec/fina dick and prolactin problems. Maybe the test would help with the deca /fina dick, but it seems like prolactin levels might really soar if you are running both at the same time. I will bump for someone with more knowledge on the subject.
07-17-2003, 07:19 PM #8Junior Member
- Join Date
- Aug 2002
- ATL, ga
Let me know what happens after this cycle if you make it out ok
07-17-2003, 07:19 PM #9
I have done much research on this subject. Deca effects progesterone not prolactin. And yes Deca and Tren work great together.
There have been many debates on alo of other message boards about the possibility that ren may cause gyno due to it's REPORTED progesteronic activites. When you come right down to it, this is nonsense becuae tren does not aromatize into estrogen or any form of estrogen such as progesterone. Maby people link it to the same similar progesteronic traits as deca durabolin , but like I said since tren doesn't aromatize into estrogen is cannot contribute to the formation of gyno.
Now here is the flip side of the coin. While on tren you cannot get gyno, HOWEVER after your tren cycle is discontinued, unless you use post cycle anciallary therapy combined with nolvadex or arimidex to control estrogen levles, you can get gyno. Here's why:
As we all know tren is a very powerful anabolic compound, but it is also a very powerful androgenic compound. Milligram for milligram more powerful than test. Now while you are on a cycle of tren your androgen levles in your blood stream are elevated, well in order for your body to keep your endocrine levels normal, your body will raise normal estrogen levles to compensate. Now if you take nolvadex or arimidex while on a cycle this will keep your lowered estrogen levles in check, but for arguments sake , lets say becuase tren doesn't aromatize you don't take an anti-estrogen.
After your tren cycle is discontinued your androgen levels will drop rapidly due to the fact your LH has been shut down and not producing any natural testosterone . If you do not take any anti estrogens during your cycle your normal estrogen levles will be elevated and while your body is still expecting more tren to be injected, when it isn't your androgen levles will fall rapidly and your body will enter a catabolic phase where your nitorgen balance is off, protein synthesis is slowed and cortisol is allowed to run rampant and break down protein and hard earned muscle. Well during this phase if not controlld by clomid and and anti estrogen you elevated estrogen levles will then be free to attach to the estrogen receptor and from gyno is you are prone to it.
This is why people who are on tren belive they get gyno from tren. It isn't actually the tren that is causing it, it is the elevated estrogen levles your body raises naturally to compenstae from the elevated androgen levles from the cycle of tren. if youtake an anti estrogen during and after the cycle is finished then the chances of getting gyno are slim to none.
Now if you add testosterone to the cycle then you have your normal chances of getting gyno as test does aromoatize into excess estrogen. If you get gyno off a cycle of tren and test, the gyno is being from by the aromatzation of excess estrogen resulting from the test, not the tren.
Also as far a milligram dosages go, it really doesn't matter how much you have taken in the past or in the present, it all depends on the ration of androgens to estrogens in your endrocine system.
07-17-2003, 07:25 PM #10
I don't sugest this type of cycle but it can be done. He is really only about 1200mg test per week based on ester wieght and half lifes. Know that might be high for some but I have taken more with no problem.
07-17-2003, 07:29 PM #11
Strolling, I am not trying to start an argument, but I would like you to read a quote by Billy_Bathgate:
"Wow..so much misinformation in this thread lmfao!
Where to start...
Deca DOES NOT aromatize to Progesterone, but can to dihydronandrolone, which is a weak AR agonist. Deca is also weakend by the 5AR
Nandrolone is PR agonistic, and the PR can alter its structure. (This is where the myth of Deca>Progesterone comes from..not really, its more like a wanna be progesterone, but seems to act somewhat like progesterone). Progesterone is an E2 agonist, and believed by many also a prolactin agonist (this is why many take bromo or dostinex for deca and fina).
Both prolactin and progesteron receptors can be found in the mammary gland and can cause gyno, but it is rarer than from estrogen. IGF-1 can also cause gyno, and most AAS raise levels.
So if you take an anti-e, it can help. As I just said, Prog is an E2 agonist which could lead to gyno, lower the E2 lower the chances of that happening.
There is also the explanation (which seems rather fictional to me) that since anti-e slightly lower IGF-1, this can help fight gyno.
Since Prog may be a Prolactin agonist, Cabergoline (dostinex) may block that area.
Then there is the winstrol debate. Winny does bind with the PR and may block it. Problems is, nobody really knows wether nandrolone or winny has the highest affinity to it. Thats kinda a cross your fingers protection.
Bromo sucks. Dostinex is so much better.
Dostinex with Aromasin and you should have no worries about any gyno caused by 19nor substances.
Sorry if I dont post my sources, but this is pretty much common knowledge from the field I study and I just dont feel like it to be honest.
My advice, when lookin up answers, you have to stay away from biased sites. Especially ones on HRT...so much incorrect stuff its pathetic."
Sorry if this thread is getting off topic, but I think it is important for people to know this information if they are taking Deca or Tren .
The discussion can be found on The Final word on deca and ldex thread.
Last edited by sigrabbit; 07-17-2003 at 07:31 PM.
07-17-2003, 07:54 PM #12Junior Member
- Join Date
- Aug 2002
- ATL, ga
Does fina dry the water out of you like winny or eq?
07-17-2003, 08:19 PM #13
I don't feel like you are starting an argument. This board is meant to exchagne info and that is what we are doing but I still have to disagree to a point. I have read more info that says what bathgate said is wrong then is right. Myself not being in an medical profession I can only go my what I have read on the boards so of course I could be wrong but I have to side with the info I have read for now.
Nine males with gynecomastia were examined. The serum levels of LH, FSH, prolactin, testosteron, estradiol were determined, in some of the patients--progesterone. A stimulation with thyreoliberin was carried out to follow up prolactin reaction. The same examinations were performed with a control group of healthy males. Contrary to the healthy subjects, the patients with gynecomastia had a significantly higher levels of FSH and progesteron and testosteron was reduced with statistical signifigance. The basal level of prolactin in the patients with gynecomastia was not sifnificantly increased and no deviations in the parameters of prolactin reaction was observed after the stimulation by the thyreoliberin. On the base of those results progesteron in the males with gynecomstia is adimitted to be able to support the mammo--tropic effect of estrogens, together with the reduced androgens and the altered receptivity of the mammary glands. Prolactin is of no great importance for gynecomastia.
07-18-2003, 04:34 PM #14
To let you know, I'm 6'1" 220lbs 21 years old, and have done 1 cycle before consisting of sust250 and deca (200mg) one day on two days off, for weeks 1-15 also did 50mg d-bol ED weeks 1-5 and test prop 100mg EOD weeks 8-15. Had little to no side effects except for a couple pimples only on my face. No bloating at all, a little agression but usually only when there was a weight in my hand. Im thinking the Sust 250 ED weeks 1-16 is fine but Im open to what you guys think about how much Deca and Fina I should do. Maybe only 600mg Deca/week instead of EOD. And Ive never done Fina before but its so cheap that if it messes with my head or if i have alot of sides i'll just trash it. Let me know what you think. BUMP...
07-18-2003, 04:41 PM #15
". I have read more info that says what bathgate said is wrong then is right. Myself not being in an medical profession I can only go my what I have read on the boards so of course I could be wrong but I have to side with the info I have read for now."
Like what? Ill post some studies if thats what ya need to see. I wouldnt take everything you read on boards as truth.
07-18-2003, 05:27 PM #16
Well..I guess its prolactin is one thing you are disagreeing with so here ya go...Causes of gynaecomastia in young adult males and factors associated with idiopathic gynaecomastia.
Ersoz H, Onde ME, Terekeci H, Kurtoglu S, Tor H.
Karadeniz Technical University, Faculty of Medicine, Department of Endocrinology and Metabolism, Trabzon, Turkey. firstname.lastname@example.org
Gynaecomastia is a common clinical condition. Persistent pubertal or late onset idiopathic gynaecomastia is the leading cause of gynaecomastia in different series. The aim of this study was the assessment of the prevalence and characteristics of different causes of gynaecomastia in young adult males, and evaluation of the factors associated with idiopathic gynaecomastia. Fifty-three male patients (mean age 22.04 +/- 2.22, range 19-29), who had been admitted to our outpatient clinics with gynaecomastia as the main presenting symptom were enrolled in the study. Patients were evaluated with breast palpation, breast ultrasonography, anthropometric measurements and sex steroid levels. Secondary causes of gynaecomastia were ruled out. Thirty age-matched healthy individuals were also studied as healthy control group. Idiopathic gynaecomastia was diagnosed in 31 of 53 patients (58%), with 17 (32%) persistent pubertal and 14 (24%) late onset course. Other causes of gynaecomastia were hypogonadism in 13 cases (25%), hyperprolactinaemia in five (9%), chronic liver disease in two (4%), and drug induced (prolonged use of H2 antagonists) in two (4%). Patients with idiopathic gynaecomastia, either pubertal or late onset, were compared with the healthy control group in order to find out associated factors. Anthropometric measurements revealed a significant increase in body weight and body mass index (BMI) in the patient group compared with healthy controls (72.4 +/- 13.3 vs. 63.6 +/- 7.9 kg, p = 0.0086 and 25.2 +/- 4.0 vs. 21.5 +/- 2.7 kg/m2, p = 0.0001). Total skin fold thickness (SFT) of four different regions were also higher in the patient group (50.9 +/- 22.1 vs. 32.6 +/- 10.2 mm, p = 0.0006) indicating a higher body fat percentage. Total serum testosterone (4.76 +/- 1.31 vs. 5.70 +/- 1.06 microg/mL, p = 0.0038) and luteinizing hormone (LH) (4.80 +/- 1.92 vs. 7.32 +/- 1.90 mIU/mL, p < 0.0001) levels were significantly lower in the patient group while oestradiol levels were similar. There was a significant correlation between total testosterone and LH levels (r = 0.27, p = 0.0445). Total testosterone and LH levels were negatively correlated with BMI and total SFT. As a result most common form of gynaecomastia is idiopathic gynaecomastia either as persistent pubertal or late onset forms in young adult males. Idiopathic gynaecomastia is closely correlated with generalized obesity, reduced LH and testosterone levels which may be the result of increased conversion of testosterone to oestradiol in increased adipose tissue mass.
PMID: 12270030 [PubMed - indexed for MEDLINE]
Switch to quetiapine in antipsychotic agent-related hyperprolactinemia.
Keller R, Mongini F.
Dipartimento di Salute Mentale, Ospedale Amedeo di Savoia, Corso Svizzera 164, I-10149 Turin, Italy.
Novel antipsychotics (clozapine, risperidone, olanzapine, quetiapine) are effective in treating psychotic symptoms, also in neurological disease. Hyperprolactinemia is a side effect related to antipsychotics that can cause galactorrhea, gynecomastia , amenorrhea, anovulation, impaired spermatogenesis, decreased libido and sexual arousal, impotence, and anorgasmia, consequent to removal of tonic dopaminergic inhibition of prolactin secretion via hypothalamic dopaminergic receptor blockade in the tuberoinfundibolar tract. Hyperprolactinemia occurs more frequently during treatment with risperidone and olanzapine compared with clozapine and quetiapine. The therapeutic algorithm to antipsychotic-relatedhyperprolactinemia is the following: reduction in antipsychotic dose, addition of cabergoline, bromocriptine, amantadine, and/or switch to another antipsychotic. We propose switching to quetiapine in symptomatic hyperprolactinemia related to antipsychotics and describe five cases.
PMID: 12522680 [PubMed - indexed for MEDLINE]
: Minerva Pediatr. 2002 Dec;54(6):547-52. Related Articles, Links
[Hyperprolactinemia: from diagnosis to treatment]
[Article in Italian]
Rosato F, Garofalo P.
Divisione di Endocrinologia, A.O. <<V. Cervello>>, Palermo, Italy.
Hyperprolactinemia means the presence of abnormally high values of prolactin. It's the most common clinical hypothalamic-hypophysis disorder. Amenorrhea and anovulation are the most usual clinical findings but we can find milder alterations of gonadal function as oligomenorrhea or luteal phase alterations. Galattorrhea appears in approx 30% of patients, but its presence in women with ovulation disorders is highly suggestive of hyperprolactinemia. Subjects with primary amenorrhea and delayed puberty can present hyperprolactinemia. Male hyperprolactinemia can cause hypogonadism (decreased testosterone levels), libido decrease, infertility due oligospermia and gynecomastia while galactorrhea rarely occurs. Accurate anamnesis is very important for a correct diagnosis. It's necessary to exclude pregnancy and primary hypothyroidism. The use of many drugs can be associated with hyperprolactinemia but the most common causes are idiopathic hyperprolactinemia and hypophysis secreting adenoma. Diagnostic examinations are: PRL, FT3, FT4, TSH in case of hypothyroidism, testosterone in men, eventually sampling GH, IGF, ACTH, cortisol, free urinary cortisol. Dynamic tests are used just for idiopathic hyperprolactinemia, but today their meaning is widely discussed. CAT and MNR are necessary to observe hypotalamus, hypophysis and optic chiasm. Twenty years ago the sole option for prolactinoma patients was adenomectomy, today idiopathic hyperprolactinemia can be treated with drugs, while prolactinoma can be treated with a pharmacological, surgical or radiological therapy.
PMID: 12388943 [PubMed - in process]
Adv Contracept Deliv Syst. 1987;3(4):347-52. Related Articles, Links
Effect of pharmacological agents on male reproduction.
PIP: The main groups of drugs that affect male libido, potency, sperm production, structure and function are summarized and their mechanisms described when known. About 15% of the 200 most commonly prescribed drugs can have adverse effects on male reproduction. Sedatives, tranquilizers, hypnotics, antiandrogens and the common antihypertensive methyldopa can depress libido. Spironoacetone has been reported to impair libido, potency, sperm count and motility, although reversibly. The phenothiazines and tricyclic antidepressants may induce prolactin secretion and consequent gynecomastia. Narcotics and hallucinogens influence male sexual performance. Morphine and methadone decrease LH and testosterone, and increase prolactin. Cannabis, hashish and marijuana initially increase libido and potency, but chronic use causes sexual inversion. Chronic alcoholism also may upset testosterone metabolism, causing testicular atrophy. Cyclophosphamide, used for nephrotic syndrome, and nitrofurans, used as food preservatives, cause direct damage to seminiferous tubules. Synthetic oganochlorine pesticides, especially DDT, have also been reported to damage spermatogenic cells directly, when injected in mice. Steroids such as ACTH, hydrocortisone and dexamethasone may inhibit steroidogenesis in animals.
PMID: 12341906 [PubMed - indexed for MEDLINE]
: Endocrinology. 2002 Oct;143(10):4074-83. Related Articles, Links
Mammary gland development in transgenic male mice expressing human P450 aromatase.
Li X, Warri A, Makela S, Ahonen T, Streng T, Santti R, Poutanen M.
Department of Physiology, Institute of Biomedicine, University of Turku, Finland.
We recently generated a transgenic mouse strain that expresses the human aromatase gene under the ubiquitin C promoter (AROM+). We have previously shown that in these mice the serum estradiol concentration is highly elevated, whereas the testosterone concentration is decreased. In the present study we examined mammary gland development in AROM+ male mice at different ages and found that the mammary glands of AROM+ males undergo ductal and alveolar development morphologically resembling that of terminally differentiated female mammary glands, expressing mRNA for a milk protein gene (beta-casein). The male mammary glands also express multiple hormone receptors typical for female mammary gland: estrogen receptor alpha and beta, progesterone receptor, and PRL receptor. Furthermore, data showed activation of the Stat5 (signal transducer and activator of transcription 5) signaling pathway in the AROM+ male mammary gland. Interestingly, the phenotype observed is in part reversible. Treatment with finrozole, a specific aromatase inhibitor, caused an involution of the differentiated phenotype of the mammary gland, marked by the disappearance of alveolar structures and the majority of the tertiary side branches of the ducts. The present animal model is a valuable tool for better understanding the cellular and molecular mechanisms involved in the development of gynecomastia .
PMID: 12239119 [PubMed - indexed for MEDLINE]
Clin Pharm Ther. 2002 Feb;27(1):75-7. Related Articles, Links
Gynecomastia with sulpiride.
Kaneda Y, Fujii A.
Department of Neuropsychiatry, The University of Tokushima School of Medicine, Tokushima, Japan. email@example.com
OBJECTIVE: Neuroleptic agents have been associated with gynecomastia, but evidence for a causal link is insufficient. We describe a case of unilateral gynecomastia without galactorrhea in a 38-year-old man during sulpiride treatment for generalized anxiety disorder. The patient had been treated with sulpiride (100 mg/day) for about 5 months by a primary care physician. In this patient, no specific endocrine alterations were found, except for a marked increase in prolactin (PRL) level and slight decrease in testosterone (T)/estradiol (E2) ratio. Drug withdrawal led to a reduction of the lump. Sulpiride is a substituted benzamide with selective dopaminergic blocking activity. From the marked increase in PRL level and the slight decrease in T/E2 ratio observed during sulpiride therapy, it is proposed that sulpiride may induce gynecomastia by inhibiting hypothalamic-pituitary function directly, and/or indirectly through hyperPRLemia.
ehh thats enough
07-18-2003, 05:33 PM #17
07-18-2003, 05:59 PM #18
I like Billy's proposed cycle much better.
07-22-2003, 11:27 PM #19
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