So whats the verdict on Rebound XT vs. Nolva?
- 05-17-2005, 01:03 AM
So whats the verdict on Rebound XT vs. Nolva?
Yes i searched and read all the threads on this, but i still cant get a clear answer. I did one cycle of SD and used Nolva for PCT, then everyone hyped up RXT (big suprise) and it was supposedly replace Nolva completely. So i figured no more bad tasting Nolva and RXT from here on... Now it seems like it messes your lipids real bad, and specially after SD this aint good. What do you guys think, stick with nolva?
- 05-17-2005, 01:09 AM
Well, RXT is working great so far.
Not only are people recovering, they often continue to gain strength during PCT.
I'm sure you'll find that is the consensus, and considering one bottle is good enough for PCT, it's a pretty good deal. Personally, this is my favorite DS product....abve and beyond anything.
05-17-2005, 10:38 AM
Rebound XT is a great product that works as advertised. You'll generally find no AI, be it Rebound, 6-Oxo or letro or arimidex, will help lipid profiles too much. They block the formation of estrogen, estrogen is essential for getting lipids back to normal. Nolva on the other hand just blocks estrogen in certain tissues, but still acts like estrogen in others. PCT after an oral cycle should always include nolva and/or clomid, regardless of the incorporation of an AI into PCT.
05-17-2005, 11:43 AM
05-17-2005, 12:08 PM
Originally Posted by CDB
Umm, not completely true. 6-OXO does not lower lipids at moderate dosages.
There also another post in which PA indicates that one of the reasons 6-OXO may be awarded a patent is that its a novel suicide inhibitor in that at moderate dosages it can raise T while not decreasing E. I would guess that this is why 6-OXO at moderate dosages does not damage lipid profiles. Otherwise, yes, for the most part any AI or suicide inhibitor that lowers estrogen is not healthy with regards to lipid profiles.
05-17-2005, 08:47 PM
05-18-2005, 11:10 AM
Rebound is an AI whereas Nolva is a SERM, so we are not exactly talking about the same thing. Also, it is known that Nolva can be harsh on your liver in a different way than merely ****ing up your lipids. The damage from Nolva is more long term, and harder to control especially if you run alot of cycles. Personally, even with Sdrol I would run Rebound, and take K-RALA as well as high doses of fish/flax oil.
05-18-2005, 11:12 AM
Do you have anything to back this up? What kind of damage are you talking about? thxOriginally Posted by Redeemer
05-18-2005, 11:20 AM
I've seen a couple people mention taking RXT as well as Nolva for PCT. I initially ordered RXT just because it was suggested in the product description but then I heard my rats would do better with nolva so I ordered that as well. Since I have both products already, would I see better results by taking both of them. How would I do this and at what dose?
05-18-2005, 11:23 AM
Same thing I was pondering. If RXT is letting some people still gains strength even on PCT, then I'd think nolva and RXT would be a great stack....although I'm only speaking outa my ass...lol. I'm about to buy a bottle and run just one cap/day along with my current nolva to see how I fare.Originally Posted by DuiLee
05-18-2005, 11:36 AM
I didn't mean say AIs will lower lipids in and of themselves, though they generally can, just that they aren't that good for restoring lipid profiles after an oral cycle. For that you need estrogen or a SERM like nolva. I don't think the dosing for 6-oxo where it supposedly doesn't effect estrogen levels is effective for PCT from an oral cycle, though I guess that depends on the oral. Maybe milder ones like MOHN, but then the milder the oral generally the lower the effect on lipids and the need to address that issue PCT.Originally Posted by bow
05-18-2005, 11:42 AM
well here are some personal facts: after 12 weeks 1-test cyp, 4ad cyp, tren, 4 weeks m1t, 8 weeks m-dien,mohn my total test was 160. after 5 weeks nolva and fenugreek (no hcg) my test was 611! i'd say that nolva works pretty damn good! for pct comparison b/t nolva and rebound i'd like to see some blood work indicating toal test before and then after pct.
05-18-2005, 11:44 AM
05-18-2005, 01:11 PM
I used SD for 4 weeks and then RXT for pct. I kept all my gains. I was very impressed with RXT. I was also using 20mg a day while on cycle. I was running a CKD during the 4 weeks so I gained 8lbs and lost 5% BF. Strenght also increased and has remained to this day with only a slight drop off in strength, and I do mean slight.
05-18-2005, 02:07 PM
05-18-2005, 02:21 PM
05-18-2005, 06:47 PM
05-18-2005, 08:13 PM
05-18-2005, 11:34 PM
05-19-2005, 12:03 AM
agree 100%, my bloodwork proved that.Originally Posted by CDB
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05-19-2005, 02:10 PM
05-20-2005, 09:28 AM
The role of metabolic activation in drug-induced hepatotoxicity.
Park BK, Kitteringham NR, Maggs JL, Pirmohamed M, Williams DP.
Department of Pharmacology and Therapeutics, University of Liverpool, Sherrington Buildings, Liverpool, Merseyside L69 3GE, United Kingdom. [email protected]
The importance of reactive metabolites in the pathogenesis of drug-induced toxicity has been a focus of research interest since pioneering investigations in the 1950s revealed the link between toxic metabolites and chemical carcinogenesis. There is now a great deal of evidence that shows that reactive metabolites are formed from drugs known to cause hepatotoxicity, but how these toxic species initiate and propagate tissue damage is still poorly understood. This review summarizes the evidence for reactive metabolite formation from hepatotoxic drugs, such as acetaminophen, tamoxifen, diclofenac, and troglitazone, and the current hypotheses of how this leads to liver injury. Several hepatic proteins can be modified by reactive metabolites, but this in general equates poorly with the extent of toxicity. Much more important may be the identification of the critical proteins modified by these toxic species and how this alters their function. It is also important to note that the toxicity of reactive metabolites may be mediated by noncovalent binding mechanisms, which may also have profound effects on normal liver physiology. Technological developments in the wake of the genomic revolution now provide unprecedented power to characterize and quantify covalent modification of individual target proteins and their functional consequences; such information should dramatically improve our understanding of drug-induced hepatotoxic reactions.
CYP17 polymorphism as a risk factor of tamoxifen-induced hepatic steatosis in breast cancer patients.
Ohnishi T, Ogawa Y, Saibara T, Nishioka A, Kariya S, Fukumoto M, Onishi S, Yoshida S.
Department of Tumor Radiology, Kochi Medical School, Oko-cho, Nankoku, Kochi 783-8505, Japan. [email protected].
Oral administration of tamoxifen, an endocrine therapy for breast cancer, often induces hepatic steatosis (THS, tamoxifen-induced hepatic steatosis) as a complication, which can progress to non-alcoholic steatohepatitis (NASH). The development of this complication is strongly associated with three clinical risk factors; specifically, insulin resistance, central obesity, and hypertriglyceridemia, however a genetic predisposition to THS has yet to be investigated. The aim of this study is to determine whether genetic polymorphism of the P450c17alpha enzyme coded for by the CYP17 gene, responsible for regulating serum estrogen, has an association with THS. After obtaining informed consent from 180 eligible breast cancer patients treated with tamoxifen, DNA was collected and analyzed by restriction fragment length polymorphism assay and classified into alleles defined as A1 and A2. The absence or presence and extent of THS was evaluated by calculating the liver/spleen (L/S) ratio based on Hounsfield units with a CT scanner. Administration of tamoxifen led to THS (L/S ratio <0.9) in 57 (31.7%) of 180 patients while the remaining 123 (68.3%) patients did not develop THS. A significant difference in the distribution of CYP17 genotypes was observed between patients who developed THS and those who did not (P=0.021). A significantly higher frequency of the A2 allele was seen in the THS group (odds ratio, 1.90; 95% confidence interval, 1.21-2.99). Our study provides the first evidence that CYP17 polymorphism participates in the development of THS, and sheds light on the genetic causes of this side effect and genetic differences between tamoxifen-treated individuals.
And the following is another possible reason not to take it, but don't put too much stock in the study, it was done on post menopausal women:
Tamoxifen and megestrol acetate for postmenopausal breast cancer: diverging effects on liver proteins, androgens, and glucocorticoids.
Lofgren L, Wallberg B, Wilking N, Fornander T, Rutqvist LE, Carlstrom K, von Schoultz B, von Schoultz E.
Department of Surgery, St Gorans Hospital, SE-112 81 Stockholm, Sweden. [email protected]
AIM: To compare the effects of tamoxifen and megestrol acetate on liver proteins, androgens, and glucocorticoids during adjuvant treatment for postmenopausal breast cancer. METHODS: A subgroup of women within a large prospective multicenter trial were followed with blood sampling every 3 mo during 2 yr. Women were randomized to receive either continuous tamoxifen 40 mg/d or repeated sequential treatment with tamoxifen and megestrol acetate (MA) 160 mg/d. RESULTS: We found profound and distinct differences between the two regimens. Tamoxifen increased steroid-binding proteins (SHBG and CBG) and suppressed circulating androgens and IGF-I. In contrast, the metabolic effects of tamoxifen were clearly antagonized by MA. There was a rise in IGF-I and marked suppression of steroid-binding proteins. Levels of free testosterone were reduced by 70%. MA also caused apparent adrenal suppression. CONCLUSION: The different effects on anabolic/catabolic balance and adrenal function may relate to certain clinical effects during treatment.
- Clinical Trial
- Multicenter Study
- Randomized Controlled Trial
05-20-2005, 02:24 PM
05-21-2005, 03:54 AM
The toxic effects of tamixofen are in cancer patients who are using years on end and its still not well established. My guess is that AI's might have similiar effects after years of use.
In other words, don't put to much stock it in at all.
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05-21-2005, 06:35 AM
I took RXT with Nolva during PCT a few months back, dropped the Nolva after 3 weeks, and boy did I feel like I was still "On" it was crazy.
I thought for sure that the three bottles of Nolva I had would gather dust.....until I started my next cycle and rebound wasn't doing a damn thing to keep my nipples from feeling puffy and sore. A day or two of Nolva cleared things up like it always does. I'll use RXT in conjunction with Tamox but thats about it.
Last edited by mmorpheuss; 05-21-2005 at 07:52 AM.
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