The history of SERM preparations begins in 1958, when MER25 (ethamoxytriphetol) was created. Dr. Leonard Lerner was a young endocrinologist employed at William S. Merrell in Cincinnati in the mid-1950s. He worked on non-steroidal estrogens. He noted that MER25 has a structure similar to triphenylene estrogens. During the tests, he noticed that the new compound showed no estrogen-specific activity in any animal species.
Instead, to his surprise, he noted anti-estrogenic activity. The compound was similar to triparanol, a drug from Merrell. It was supposed to reduce cholesterol levels, meanwhile it increased the level of desmosterol, which was responsible for the development of cataracts in women.
Many myths are associated with SERM – clomid and tamoxifen.
Unfortunately, misinterpretation of scientific research deepens confusion. It is claimed, for example, that SERM are completely safe and that no medicine is completely safe (tamoxifen may be the cause of thrombosis, deep venous thrombosis, venous thromboembolism and in extreme cases may cause visual disturbances, often caused by cataracts, corneal opacities and / or retinopathy). In patients treated with tamoxifen a 2-3-fold increased risk of venous thrombosis was observed. The stronger the drug, the greater the potential risk of complications. Another misconceived view is that tamoxifen is used to fight estrogen. The SERMES are right – they act indirectly, competently in relation to estrogens. This means that the SERM group will bind to the estrogen receptor, preventing the estrogen from binding in this place, thus limiting the movement of the estrogen-receptor complexes towards the cell nucleus. But there are studies that say that SERIES affect the activity of aromatase. Yes, only … they concern in vitro experiments, so their reference to the human system is negligible.
From the same backyard there are reports of muscle building and reduction of body fat by raloxifen. Jacobsen DE 6 and the partners conducted a randomized double-blind study and placebo. 198 women aged 70 (or more) years received 60 mg of raloxifene or placebo for 12 months. Before, after 3, 6 and 12 months, body composition, muscle strength and power were measured. It has been proven that ladies receiving raloxifene increased lean body mass by 0.83 kg, those in the placebo group by 0.03 kg. The amount of water increased by 600 g in the raloxifene group and decreased in the placebo group. There were no differences in muscle strength and strength.
The above study makes no sense.
Boneva-Asiova et al. 7 compared the TBF-215 machine (Tanita, Tokyo, Japan) with the DEXA measurement (Hologic QDR 4500 machine). Apparently the measurements did not differ significantly, but in skimmed people BIA method underestimated the amount of adipose tissue (in terms of% and kilograms), and in turn overstated the amount of lean body mass. With the increase in BMI, the spread between DEXA and BIA became more and more visible. With BMI over 35, the trend has reversed, the BIA method overstated the amount of body fat and understated muscle weight. In men, the correlation was higher. Is it possible to recommend raloxifene as a muscle growth and body fat reducing agent? Nothing similar.
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