Milk Thistle in PCT – Tamoxifen (Nolvadex) Still a Liver Killer, Despite Hepatoprotective Effect of Silymarin or Ziziphus

Image 1: Silybum marianum, a medical plant that has been used to treat liver disease for >2,000 years and is a staple in many “post cycle therapy” supplements you can current purchase at your favorite supplement store.

Whether or not you are into “performance enhancing drugs” does not really matter. If you have browsed through the range of one of the myriad of on-line supplement vendors, you will have seen them: the “liver protectors”, “supplements for liver health”, or simply “post-cycle recovery” supplements. The most common ingredient, you will see on the labels of supplements listed in these or similar categories, is silymarin, a flavonoid complex consisting of silybin (the most active component), silydanianin and silychristin, which is either extracted or simply contained in a crude extract of the seeds of Silybum marianum, a flowering plant of the daisy family, the manufacturers put into their capsules. While scientists still debate whether and for which type of liver disease(s) the use of the obviously non-patentable (you know that this means that no big pharma company will be willing to acknowledge that it works ;-) flavonoid would be an appropriate treatment option (Loguercio. 2011), generations of bodybuilders may actually have saved their live(rs) from the toxic effect of a highly “underrated” liver-killer, the “bros” know as “Tamox” – the Selective Estrogen Receptor Modulator (SERM), Tamoxifen, which is the active ingredient in the “anti-breast-cancer drugs” Nolvadex, Istubal, and Valodex.

In a mouse model (using 60 male Balb/c mice), scientists from Malaysia and the Middle-East conducted a 4-week study on the toxicity of orally administered tamoxifen (20mg/kg; HED ~1.2mg/kg) and the potential protective effect of milk thistle or jujube (Ziziphus, a tree from the buckthorn family, and the ‘silymarin of the middle’ east; Shahat. 2011) extracts at 300mg/kg (HED ~24mg/kg; ~2g for an 80kg human). To this ends, the animals were randomly assigned to one out of four 6 groups (Al-Jassabi. 2011):

  1. control - no tamoxifen, no silymarin extract, no ziziphus
  2. silymarin control (SC) - no tamoxifen, 300mg/kg silymarin extract, no ziziphus
  3. ziziphus control (ZC) - no tamoxifen, no silymarin extract, 300mg/kg ziziphus
  4. tamoxifen control (TC) - 20mg/kg tamoxifen, no silymarin extract, no ziziphus
  5. tamoxifen silymarin (TS) - 20mg/kg tamoxifen, 300mg/kg silymarin extract, no ziziphus
  6. tamoxifen ziziphus (TZ) - 20mg/kg tamoxifen, no silymarin extract, 300mg/kg ziziphus

Now, if you look at the actual effects the admittedly high dose of tamoxifen that was administered to the animals (note: while a 100kg bodybuilder would have to take 160mg to achive the same exposure I have seen obviously idiotic recommendations on various boards which suggest starting off your PCT with doses in the 80mg+ range!), I suppose that those of you who have (for whatever reasons) already used Nolvadex & Co. will probably be shocked.

Figure 1: Changes in transaminase enzymes, lipid peroxidation and anti-oxidant enzymes in male mice after 4 weeks treatment with 20mg/kg tamoxifen per day (data calculated based on Al-Jassabi. 2011).

7-12x elevations in transaminase levels (ALT, GPT, GOT), >70% reductions in antioxidant enzymes (SOD, CAT, GSHpx), on average, and the incredible 68x elevation in lipid peroxidation after “only” four weeks of treatment should make every steroid user reconsider, whether a tamoxifen-based post-cycle protocol does not do more harm than good. After all, one of the most common causes of gynecomastia is liver cirrhosis (Swerdloff. 2011), and you will probably agree that taking a drug to “protect” yourself from the estrogen rebound after (or even in the course of a cycle) which has gynecomastia as a possible side-effect of a side-effect does not really make sense.

Moreover, scientific data on the efficiacy of tamoxifen in the treatment of male hypogonadism (which is basically what steroid users will experience at the end of a “cycle”) is pretty scarce, if not non-existent and from a “scientific point of view” clomifene citrate (clomid) would appear to be the SERM of choice, here (cf. Katz. 2011).

I hope that you notice the stupidity of the typical bro-scientific approach to taking B to counter the side-effects A, C to counter the side-effect B, D to counter the side-effects of C… and so on and so forth…, because, after all, even if C or D were silymarin or ziziphus, the use of these potent liver-protectants would still leave you with profoundly elevated transaminase levels and reduced anti-oxidant capacity (cf. figure 2):

Figure 2: Changes in transaminase enzymes, lipid peroxidation and anti-oxidant enzymes in male mice after 4 weeks treatment with 20mg/kg tamoxifen + 300mg/kg silymarin or ziziphus per day (data calculated based on Al-Jassabi. 2011).
And what’s more the lipid peroxidation would be significantly ameliorated by the use of 2g of silymarin (HED) per day, but still 13x over normal. If that is what you want, go ahead and terminate a harsh cycle with a harsher PCT, if not – select another method to get your HPTA (hypothalamic-pituitary-thyroid-axes) back in shape and use the milk thistle to counter potentially hepatoxic effects of the cycle itself.

Ah, and I don’t know if you have even remotely considered that: Not taking steroids would make any PCT and potential on- or off-cycle liver toxicity obsolete. The use of milk thistle extracts could yet nevertheless make sense! After all, the staff at ScienceDaily posted a short news-item on the anti-lung-cancer effects of silymarin, just this morning – so if your “drug of choice” is nicotine (not AAS), don’t forget to take your milk thistle ;-)

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