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Nolvadex toxicity?

big_griff

New member
Hey bro's,
i heard some dude on here say that nolva is more liver toxic than any oral. is this total bullshit, cuz i've never heard it, and my liver is pretty banged up at the moment, and i'm about to hit up PCT...lol. anyways, thanks for tha help!
 
I think anything oral can have some damage to your liver.
However, nothing I have ever read has mentioned anything about Nolvadex being
very liver toxic. I would be very hesitant to believe what your buddy is telling you.
Anyone else have a better answer.
 
big_griff said:
Hey bro's,
i heard some dude on here say that nolva is more liver toxic than any oral. is this total bullshit, cuz i've never heard it, and my liver is pretty banged up at the moment, and i'm about to hit up PCT...lol. anyways, thanks for tha help!
Some studies and theories may say its toxic...

but never found a bodybuilder in the real life who got ill from it.
 
It has a low liver toxicity rate.....it does have a posative impact on the good cholesteral level though :)
 
: Annu Rev Pharmacol Toxicol. 2005;45:177-202. Links
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.
 
Carcinogenesis. 1995 Jul;16(7):1661-4. Links
DNA adducts caused by tamoxifen and toremifene in human microsomal system and lymphocytes in vitro.Hemminki K, Widlak P, Hou SM.
Center for Nutrition and Toxicology, Karolinska Institute, Huddinge, Sweden.

DNA-binding of tamoxifen and toremifene was studied in rat in vivo, in human and rat microsomes in vitro, and in cultured primary human lymphocytes by 32P-postlabelling. Only tamoxifen caused DNA adducts in rat liver. Both compounds induced adducts in both rat and human microsomal systems and in cultured lymphocytes. The levels of adducts in microsomes and lymphocytes were low, ca. 1 adduct/10(9) nucleotides. Toremifene showed lower binding in each system, and in lymhocytes adducts were only detected at a cytotoxic dose level.

PMID: 7614704
 
macrophage69alpha said:
Carcinogenesis. 1995 Jul;16(7):1661-4. Links
DNA adducts caused by tamoxifen and toremifene in human microsomal system and lymphocytes in vitro.Hemminki K, Widlak P, Hou SM.
Center for Nutrition and Toxicology, Karolinska Institute, Huddinge, Sweden.

DNA-binding of tamoxifen and toremifene was studied in rat in vivo, in human and rat microsomes in vitro, and in cultured primary human lymphocytes by 32P-postlabelling. Only tamoxifen caused DNA adducts in rat liver. Both compounds induced adducts in both rat and human microsomal systems and in cultured lymphocytes. The levels of adducts in microsomes and lymphocytes were low, ca. 1 adduct/10(9) nucleotides. Toremifene showed lower binding in each system, and in lymhocytes adducts were only detected at a cytotoxic dose level.

PMID: 7614704

I also did a pubmed search on this topic. What bothers me is they don't give dosages that toxicity becomes apparent. None of the studies that I read on Pubmed gave dosages that showed toxic effect. Nor did they give the dosage that was used in the study. But I know that there are a whole lot of people that are on tamoxifen. If liver toxicity was a magor problem they would be dropping like flies because they already have major health problems.
 
Studies may show some hepa-toxicity for nolvadex but women with breast cancer can be on it for up to 3 years so I'd be amazed if it were more toxic than oral AAS.
 
Bump.

Nolvadex is a Group 1 carcinogen. Do a google search for "known and probable carcinogens" and you'll see Tamoxifen listed right there among all kinds of other nasty things.

For this reason, I'll use Clomid for PCT and never use Nolvadex. I would rather not put any known carcinogen in my body and risk testicular cancer.

Did anyone ever wonder how Lance Armstrong got testicular cancer? (he has been a major user of testosterone for several decades now and it wouldn't be unreasonable to assume he used Nolvadex)
 
Bump.

Nolvadex is a Group 1 carcinogen. Do a google search for "known and probable carcinogens" and you'll see Tamoxifen listed right there among all kinds of other nasty things.

For this reason, I'll use Clomid for PCT and never use Nolvadex. I would rather not put any known carcinogen in my body and risk testicular cancer.

Did anyone ever wonder how Lance Armstrong got testicular cancer? (he has been a major user of testosterone for several decades now and it wouldn't be unreasonable to assume he used Nolvadex)

The very web page you directed us to states that tamoxifen increases the risk for uterine cancer but reduces the risk for breast cancer (it's actually a treatment for breast cancer).

Nolvadex and Clomid act very similarly (nolvadex being more effective at blocking estrogen in breast tissue receptors) so Clomid could be just as carcinogenic. But since Clomid is not a breast cancer treatment, women don't take it daily for years at a time the way they do with Nolvadex.

Besides, increasing your androgen level tenfold likely puts you at a much higher cancer risk (prostate, specifically) than using Nolvadex does.
 
So nolvadex is slightly more effective, but being a known carcinogen just kills the deal for me. Stating that clomid "could be just as carcinogenic" is pure speculation. The science is out there and nolvadex is a known carcinogen, per the American Cancer Society, while clomid is not.

Just because women use it for years to treat breast cancer doesn't make it ok for me either. 1. I'm not a woman 2. it is a necessary evil to fight off a more serious evil (breast cancer). Chemotherapy drugs are used to fight cancer and they're very hard on the body, but necessary to kill the cancer.
 
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