Why Primobolan is Primo
A. We could not find any androgen receptor binding studies for methenolone in our literature review.
It is unclear how websites report the androgenic to anabolic ratio.
B. Human Liver Function
a. Originally, methenolone enanthate and acetate (and nandrolone phenopropionate) were thought not to cause liver stress, unlike 17-alkylated steroids [1].
b. Methenolone enanthate appeared to improve albumin turnover in patients with liver cirrhosis [2].
C. Female Breast Cancer
a. Methenolone enanthate has been used (effectively) in the treatment of female breast cancer.
It was shown not to convert to estrogen and to cause virilization [3].
b. In a group of 28 women with cancer who received methenolone enanthate, 12 developed dyslipidemia, which worsened in these 12 upon discontinuation of the administration [4].
D. Anemia
a. The acetate version was used at 20mg to treat anemia in women [5].
b. In some anemias, it caused cholestatic jaundice at 1-2 mg/kg [6].

E. Human Metabolism
a. In men, after a single dose of methenolone acetate, methenolone was produced in the urine for up to 90 hours post-administration, amounting to 1.6% of the total oral dose.
b. Several other metabolites were found due to the oxidation of the 17-hydroxyl group and reduction of the A-ring [7].
c. The main metabolite is 3-alpha-hydroxy-1-methylene-5-alpha-androstan-17-one, which can be detected in urine for up to 5 days after a single ingestion of the drug [8].
d. Methenolone sulfate and other sulfate metabolites form key components of human methenolone metabolism [9].
F. Vision
a. There is a special US permit to use methenolone or nandrolone for the treatment of dry eye syndrome [10].

G. Erythropoiesis
a. Methenolone acetate has been shown to increase erythropoietic activity in bone marrow cells by increasing the sensitivity or number of erythroid cells [11].
b. Compared to testosterone, oxymetholone, and metholone, methenolone had a greater erythropoietic effect than testosterone (although metholone produced the most) [12].
This indicates that the masculinizing and erythropoietic effects act through different mechanisms.
c. One study showed that Halotestin (fluoxymesterone) and methenolone similarly increased hematopoiesis and blood iron absorption in rodents [13].

H. Bone Development
a. Like other AAS, methenolone enanthate was shown to increase bone development in growing female rodents and decrease it in male rodents [14].
b. It stunts the growth of young rodents [15].
c. In rodents, methenolone produced a favorable healing profile for fractured bones despite being less androgenic.
Initial calcium callus concentration increased less than with testosterone, but later recovery was similar [16].
d. DHT, fluoxymesterone (Halotestin), and methenolone cause mitosis in bone cells in vitro through the action of the androgen receptor, leading to bone cell division and proliferation [17].

I. Kidney Function
a. Even without improving muscle development, methenolone enanthate was shown to increase kidney weight in growing male rodents [18].

J. Cardiac Function
a. It has been shown to cause left ventricular hypertrophy in pubertal rodents, with a more pronounced effect in female rodents [19].
Primobolan (also known as Methenolone) is an anabolic steroid often used by bodybuilders and athletes to promote muscle growth and enhance athletic performance.
One of the unique features of Primobolan is its ability to lower estrogen levels in the body.
In this blog post, we will take a closer look at the relationship between Primobolan and estrogen.
Estrogen is a hormone produced primarily in the ovaries of women and the testes of men.
In both sexes, estrogen plays a crucial role in regulating the menstrual cycle, bone density, and cholesterol levels.
However, high levels of estrogen can lead to undesirable side effects such as water retention, gynecomastia (enlargement of breast tissue in men), and high blood pressure.
Anabolic steroids like Primobolan can affect estrogen levels in the body through their interaction with the aromatase enzyme.
The aromatase enzyme is responsible for converting androgens (such as testosterone) into estrogen.
Some steroids, like testosterone, are highly aromatizing and are easily converted to estrogen.
This can lead to high estrogen levels and associated side effects.

On the other hand, Primobolan has a low rate of aromatization, meaning it is less likely to be converted to estrogen.
This is because it has a double bond between the first and second carbon atoms, which makes it more difficult for aromatase to convert it to estrogen.
This is one of the reasons why Primobolan is often used by bodybuilders and athletes who want to avoid estrogen-related side effects.
In addition to its low aromatization rate, Primobolan also has anti-estrogenic effects.
It has been shown to bind to estrogen receptors, blocking the activity of estrogen in the body.
This can help reduce the risk of estrogen-related side effects and improve muscle hardness and definition.
However, it is important to note that Primobolan is still a potent steroid and can cause side effects if used improperly.
Like all steroids, it should only be used under the supervision of a licensed medical provider.
It is also important to follow proper dosing protocols and monitor estrogen levels to avoid the risk of side effects.
In conclusion, Primobolan is a unique steroid with the ability to lower estrogen levels in the body.
By reducing the risk of estrogen-related side effects, Primobolan can help bodybuilders and athletes achieve their goals of increased muscle mass and improved athletic performance.
However, it is important to use this steroid responsibly and follow proper dosing protocols to avoid the risk of side effects.
[References]
[1] MARQUARDT, GH, LOGAN, CE, TOMHAVE, WG, & DOWBEN, RM (1964). Failure of non-17-alkylated anabolic steroids to produce abnormal liver function tests. The Journal of Clinical Endocrinology & Metabolism, 24(12), 1334-1336.
[2] Knöbel, H., & Becker, K. (1975). Effect of an anabolic steroid (metenolone enanthate) on intravascular and extravascular albumin pools in liver cirrhosis. Zeitschrift fur Gastroenterologie, 13(6), 583-587.
[3] Notter, G. (1975). Treatment of disseminated carcinoma of the breast by metenolone enanthate. Acta Radiologica: Therapy, Physics, Biology, 14(6), 545-551.
[4] Garbrecht, M., Lehmann, U., O’Brien, S., Stolzenbach, G., & Müllerleile, U. (1981). Hyperlipoproteinemia during additional metenolone administration in the treatment of metastatic carcinoma of the breast. Deutsche Medizinische Wochenschrift (1946), 106(13), 400-403.
[5] Hamamoto, K., Ohno, T., & Ogawa, H. (1996). A case report of successful treatment with metenolone for myelodysplastic syndrome with CREST syndrome. [Rinsho ketsueki] The Japanese journal of clinical hematology, 37(4), 362-365.
[6] Palva, IP, & Wasastjerna, C. (1972). Treatment of aplastic anaemia with methenolone. Acta haematologica, 47(1), 13-20.
[7] Goudreault, D., & Massé, R. (1990). Studies on anabolic steroids—4. Identification of new urinary metabolites of methenolone acetate (Primobolan®) in human by gas chromatography/mass spectrometry. The Journal of steroid biochemistry and molecular biology, 37(1), 137-154.
[8] Björkhem, I., & Ek, H. (1983). Detection and quantitation of 3α-hydroxy-1-methylene-5α-androstan-17-one, the major urinary metabolite of methenolone acetate (Primobolan®) by isotope dilution—mass spectrometry. The Journal of steroid biochemistry, 18(4), 481-487.
[9] Fragkaki, AG, Angelis, YS, Kiousi, P., Georgakopoulos, CG, & Lyris, E. (2015). Comparison of sulfo-and gluco-conjugated urinary metabolites for the detection of methenolone misuse in doping control by LC–HRMS, GC–MS and GC–HRMS. Journal of mass spectrometry, 50(5), 740-748.
[10] Endo, K., Fujii, S., & Oki, K. (2018). U.S. Patent Application No. 15/563,108.
[11] Mori, M., Chiba, S., Suzuki, S., Kosaka, K., Miura, Y., & Takaku, F. (1974). Effect of methenolone acetate on erythropoietin responsive cells in rat bone marrow. Biochemical and Biophysical Research Communications, 60(1), 281-287.
[12] Duarte, L., Sánchez Medal, L., Labardini, J., & Arriaga, L. (1967). The erythropoietic effects of anabolic steroids. Proceedings of the Society for Experimental Biology and Medicine, 125(4), 1030-1032.
[13] Hotta, T., Hirabayashi, N., Utsumi, M., & Yamada, H. (1978). Basic study on the hematopoietic-activating function of androgens. In vivo effect of fluoxymesterone and methenolone.
[14] Bozkurt, I., Pepe, K., Ozdemir, M., Ozdemir, O., & Coskun, A. (2011). A morphological evaluation on the effects of methenolone enanthate on the femoral development in adolescent rats. Scientific Research and Essays, 6(7), 1634-1638.
[15] ÖZDEMİR, M., & Sefa, L. Ö. K. (2019). The Effects of Methenolone Enanthate Supplement with Exercise on Bone in Rats. Turkish Journal of Sport and Exercise, 21(2), 276-280.
[16] Frankle, M., & Borrelli, J. (1990). The effects of testosterone propionate and methenolone enanthate on the healing of humeral osteotomies in Wistar rats. Investigative Surgery, 3(2), 93-113.
[17] Kasperk, CH, Wergedal, JE, Farley, JR, Linkhart, TA, & Turner, RT (1989). Androgens directly stimulate proliferation of bone cells in vitro. Endocrinology, 124(3), 1576-1578.
[18] Holt, TL, Ward, LC, Thomas, BJ, Davey, JF, & Shepherd, RW (1990). The effects of an anabolic steroid, methenolone enanthate, on growth, body composition and skeletal muscle protein synthesis in growing rats. Nutrition research, 10(5), 535-545.
[19] Ozdemir, O., Bozkurt, I., Ozdemir, M., & Yavuz, O. (2013). Adverse effects of methenolone enanthate on the pubertal rat heart: a morphometric study. Experimental and Toxicologic Pathology, 65(6), 745-750.



