We usually say tamoxifen is an antiestrogen, able to block the estrogen recptor and prevent any action(antagonist)which in part is true. But it also acts like estrogen, therefore able to stimulate estrogen receptors in certain estrogen dependent tissues (agonist). Therefore tamoxifen is really a mixed agonist/antagonist. Tamox , and related drugs, are termed SERMS for Selective Estrogen Receptor Modulators. SERMS block the action of estrogen in certain tissues, while mimicking the actions of estrogen in others. This is made possible because estrogen receptors (although basically similar) vary in chemical structure depending on the tissue. Estrogen molecules act on a number of tissues in the body including the breast, uterus (of course not applicble to men), brain, bone, liver and heart.
We all know these drugs block estrogen dependent cell proliferation in breast tissue(antagonist). They also seem to provide the benefits of estrogens in tissues such as the liver, heart and bones, leading to favorable lipid profile (decreased LDL and total cholesterol), and prevent bone resorption and subsequent bone break down. This is one advantage the SERMS have over the aromatase inhibitors, which function to prevent the formation of estrogen entirely. This is why you will usually see that arimidex and relatives have a negative effect on lipid profiles.
But the clinical side effects of tamox are well known because this drug has been around for awhile allowing the opportunity for many post-marketing (phase IV) clinical studies. Probably the most significant are CYP450 enzyme inhibition (namely CYP3A4), thromboembolism, and ocular toxicity.
I find an interest in enzyme inhibition/induction. So since we know tamox is metabolized in the liver(and other tissues) by the CYP450 mixed function oxidase system this could lead to significant drug-drug interactions. If you are taking a drug such as tamox, which is an enzyme inhibitor and you add another drug that is also metabolized by the same enzyme (CYP3A4), what do you think could happen? If a drug is an enzyme inhibitor, it decreases the ability of the enzyme to metabolize drugs used by this enzyme. So you may see an increase in plasma levels of the added drug possibly leading to toxicity. So be aware if you are taking other drugs that are also metabolized by the same enzyme. And > 50% of all drugs are metabolized by the CYP3A4 enzyme. I did a related spew before:
http://boards.elitefitness.com/forum/showthread.php?s=&threadid=197180&highlight=antibiotics
in there is also a link to a great list of drugs metabolized by the different CYP450 enzymes. Worth taking a look at.
The thromboembolism should not be of too much concern unless there are other risk factors associated(predisposition etc). Tamox stimulates clotting factor production in the liver. AAS suppress certain clotting factors.
The ocular toxicity is well established. Corneal microdeposits, visual chagnes, retinopathy and even cataracts. This I would be concerned with. The studies documenting oculotoxicity are many, but they mostly involved women taking tamox as a chemo for breast cancer and used the drug for lengths of 1-5 years even longer. I know alot of people compalin of visual changes/disturbances while on clomiphene and tamox. So this may be something to think about. I could not answer your question that if taking it for 4 months will definately produce oculotoxicity, but there is always the possibility that even intermittent repeated exposure may be a factor in the long run. Sorry to rant! Peace
