Raloxifene Dosage
Raloxifene is one of the latest anti-estrogens available on the market for the treatment of estrogen-related conditions.
Its two most prominent indications are osteoporosis and estrogen-responsive breast cancer.
Like other similar SERMs such as Nolvadex (Tamoxifen), bodybuilders primarily use it as an ancillary drug outside of its medical indications to address or prevent estrogen-related side effects and issues when using anabolic steroids.
Raloxifene is not as popular as Nolvadex for these purposes.
However, studies show growing evidence that Raloxifene is nearly or equally as effective for these purposes [1] [2] [3].
Although Raloxifene does not have as much research and clinical data as more established SERMs like Nolvadex, it is rapidly gaining popularity and attention within the bodybuilding and anabolic steroid-using communities.
Many in that community consider Raloxifene a somewhat safer alternative, though this claim is currently unsubstantiated.
The dosage of Raloxifene for treating and preventing estrogen-related side effects from anabolic steroid use is generally higher than that of traditional SERMs like Nolvadex.
Therefore, higher doses of Raloxifene are necessary to prevent and control estrogenic side effects.
In the context of anabolic steroid use, Raloxifene is primarily used to treat gynecomastia and offers little to no benefit for other estrogenic side effects.
This is because, as mentioned in the profile introduction, Raloxifene does not lower total estrogen levels in the body but only blocks the activity of estrogen in specific tissues.
This is a common characteristic of all SERMs and is the inherent way they all function.
Any attempt to use Raloxifene to treat other estrogenic side effects like bloating or water retention will inevitably fail.
Anabolic steroid users must keep this in mind.
Aromatase inhibitors are better suited for these purposes.
In addition to its anti-estrogen applications, Raloxifene has shown significant use as a compound for stimulating endogenous testosterone.
Studies have shown that a dose of 120mg/day of Raloxifene increased serum testosterone levels by 20% [4].
While the level and magnitude of this endogenous testosterone stimulation are not as efficient as Nolvadex, it is sufficient for use as a viable ancillary during Post Cycle Therapy (PCT).
Before delving into more detail, it is important to inform the reader of one crucial point.
SERMs or anti-estrogens should only be used when absolutely necessary, and their use should be discontinued immediately once the need for them has passed (e.g., gynecomastia or lack of androgen production).
Medical Raloxifene Dosage
Evista (Raloxifene) is FDA-approved for the treatment and prevention of osteoporosis by reducing bone resorption and promoting bone formation (bone creation) through its estrogenic action in bone tissue.
Administration for these purposes is primarily directed at post-menopausal women.
This is where osteoporosis is most prominent.
Its use for this purpose is also associated with the treatment of estrogen-responsive breast cancer in post-menopausal women.
Here, Raloxifene’s estrogen-antagonistic action serves to prevent the cancer-promoting effects of estrogen in breast tissue.
The standard medical dose of Raloxifene for the treatment of osteoporosis and female breast cancer is one 60mg tablet per day.
A single 60mg dose of Raloxifene can be administered with or without food.
Raloxifene Dosage During Anabolic Steroid Use.
Specifically, Raloxifene cannot be categorized into the three tiers (beginner, intermediate, and advanced) typically described and listed for other compounds and drugs.
This is because Raloxifene is not used specifically for performance enhancement but as an ancillary drug to prevent or mitigate various estrogenic side effects when using aromatizable anabolic steroids.
In many cases, Raloxifene can be used to increase endogenous testosterone secretion in men.
This compound can be used as an ancillary drug during the Post Cycle Therapy (PCT) phase after an anabolic steroid cycle.
However, its standalone use for this purpose alone is uncommon and is unlikely to produce any noticeable performance-enhancing effects.
For the purpose of preventing/reducing gynecomastia during a cycle:
Raloxifene is typically used either as a preventative measure to avoid the development of gynecomastia during an anabolic steroid cycle that includes aromatizable anabolic steroids, or as an interceptive agent immediately following the onset of gynecomastia.
For both conditions, the Raloxifene dosage is the same: 30-60mg per day for the duration of the anabolic steroid cycle.
The most common starting point is 30mg per day.
It is crucial to inform the reader that the use of Raloxifene can negatively impact performance, muscle, and strength gains during an anabolic steroid cycle.
Like Nolvadex, Raloxifene has also been shown to reduce serum levels of IGF-1 (Insulin-like Growth Factor 1) in the body.
IGF-1 is known to be a very important mediator of muscle growth, crucial for increasing nitrogen retention, protein synthesis, and new muscle cell growth (hyperplasia) [5].
Other studies have reported a statistically significant decrease in IGF-1 levels when measuring pre- and post-administration levels in patients receiving Raloxifene [6].
In conclusion, SERMs like Raloxifene and Nolvadex have a detrimental effect on muscle growth by reducing plasma levels of important hormones (such as IGF-1) required for it.
Therefore, it is recommended that Raloxifene only be administered for the necessary duration to mitigate estrogen-related side effects during the use of aromatizable anabolic steroids (i.e., for PCT or gynecomastia control/reduction).
While short-term use of Raloxifene may not have a significant impact, long-term use can negatively affect muscle growth and performance.
One study investigating long-term Raloxifene use found that subjects had significantly lower IGF-1 levels at the 24-month mark post-administration compared to the control group [7].
Another study examining the effects of Raloxifene and Tamoxifen (Nolvadex) in men reported that Raloxifene did not significantly reduce IGF-1 compared to Nolvadex [8].
One study in which patients with acromegaly were administered 120mg of Raloxifene split into two daily doses showed a 16% reduction in IGF-1 levels [9].
While most studies using Raloxifene have shown a statistically significant decrease in IGF-1 levels, some have not.
Therefore, prospective users considering anabolic steroids should carefully consider this effect of Raloxifene administration.
Female Raloxifene Dosage
Since Raloxifene is primarily used by men seeking to mitigate and/or prevent the development of gynecomastia and to stimulate endogenous testosterone production, there is little to no need for Raloxifene among female users.
Women do not specifically require these functions.
For women, Raloxifene should only be used when there is a medical indication for it.
Using Raloxifene in women without a medical need can lead to additional physiological complications due to the nature of its estrogen agonistic/antagonistic effects in relation to the female endocrine physiology.
Raloxifene Dosage for Increased Endogenous Testosterone Secretion and PCT (Post Cycle Therapy)
The effects of Raloxifene administration on endogenous testosterone production in men are quite well-documented.
This occurs through Raloxifene’s estrogen-antagonistic effects on the hypothalamus and pituitary gland.
This leads to a significant release of FSH and LH (the two hormones that signal the testes to begin or increase testosterone production and secretion).
This is no different from how most SERMs exhibit these effects in men.
For this reason, Raloxifene and its related SERMs, such as Nolvadex and Clomid, are known to be very essential components of a PCT program for hormonal recovery following an anabolic steroid cycle.
However, it should be noted that one previously mentioned study (Birzniece et al., 2010) on the testosterone-stimulating effects of Raloxifene compared to Nolvadex revealed that Raloxifene is markedly deficient in stimulating testosterone production in men compared to Nolvadex.
Other studies have also pointed to Raloxifene’s clear disadvantage in stimulating endogenous testosterone production in men compared to Nolvadex (and even Toremifene) [10].
Therefore, when choosing between Raloxifene and Nolvadex for testosterone stimulation, it should be clearly understood that Nolvadex is the preferred drug of the two.
Nolvadex has proven time and again, both historically and today, to be the superior (and likely cheaper) choice over other SERMs not only for stimulating endogenous testosterone secretion but also for combating gynecomastia.
The dosage of Raloxifene for stimulating endogenous natural testosterone production is ideally 30-60mg per day, though a dose of 60mg per day is more common for this purpose.
Proper Administration and Timing of Raloxifene
The limitations (or lack thereof) of Raloxifene administration are very flexible.
Raloxifene doses can be administered before, during, or after meals.
It can also be taken in the morning or evening, depending on the user’s preference.
Instead of splitting the Raloxifene dosage throughout the day, the entire daily dose can be taken all at once.
This is because Raloxifene’s long half-life (27.7 hours) eliminates the need to split or divide doses.
Expected Results from Raloxifene Administration
Raloxifene is an effective solution for preventing and mitigating problematic estrogenic side effects, particularly gynecomastia.
It holds an advantage over other SERMs like Nolvadex in that it maintains or even increases bone density and strength through its estrogenic action in bone tissue.
Nolvadex exhibits an antagonistic effect on bone.
Furthermore, because Raloxifene is quite effective at stimulating endogenous natural testosterone production in men, it can be concluded that it can be utilized very effectively for restoring endogenous testosterone production after a cycle.
Medical References
[1] Lawrence SE1, Fautz KA, Vethamuthu J, Lawson ML. Beneficial effects of raloxifene and tamoxifen in the treatment of pubertal gynecomastia. J Pediatr. 2004 Jul;145(1):71-6.
[2] Malozowski S. Treatment of adolescents with gynecomastia. J Pediatr. 2005 Apr;146(4):576; author reply 576-7.
[3] Nordt CA, DiVasta AD. Gynecomastia in adolescents. Curr Opin Pediatr. 2008 Aug;20(4):375-82. doi: 10.1097/MOP.0b013e328306a07c.
[4] Effects of raloxifene on gonadotropins, sex hormones, bone turnover and lipids in healthy elderly men. Eur J Endocrinol. 2004 Apr;150(4):539-46.
[5] Signore C1, Dubrock C, Richie JP, Prokopczyk B, Demers LM, Hamilton C, Hartman TJ, Liao J, El-Bayoumy K, Mani A. Supplementation with omega-3 fatty acids and raloxifene in women at high risk for breast cancer: an interim feasibility and biomarker analysis of a clinical trial. Eur J Clin Nutr. 2012 Aug;66(8):878-84. doi: 10.1038/ejcn.2012.60. Epub 2012 Jun 6.
[6] da Silva BB, Moita DS, Pires CG, Sousa-Junior EC, dos Santos AR, Lopes-Costa PV. Evaluation of insulin-like growth factor-I in postmenopausal women with breast cancer treated with raloxifene. Int Semin Surg Oncol. 2007 Jul 23;4:18.
[7] Lasco A1, Gaudio A, Morini E, Morabito N, Nicita-Mauro C, Catalano A, Denuzzo G, Sansotta C, Xourafa A, Macrì I, Frisina N. Effect of long-term raloxifene treatment on breast density in postmenopausal women. Menopause. 2006 Sep-Oct;13(5):787-92.
[8] Birzniece V, Sata A, Sutanto S, Ho KK. Neuroendocrine regulation of growth hormone and androgen axes by selective estrogen receptor modulators in healthy men. J Clin Endocrinol Metab. 2010 Dec;95(12):5443-8. doi: 10.1210/jc.2010-1477. Epub 2010 Sep 15.
[9] Dimaraki EV, Simmons KV, Barkan AL. Raloxifene administration decreases serum IGF-1 in male patients with active acromegaly. Eur J Endocrinol. 2004 Apr;150(4):481-7.
[10] Tsourdi E, Kourtis A, Farmakiotis D, Katsikis I, Salmas M, Panidis D. The effect of selective estrogen receptor modulator administration on the hypothalamic-pituitary-testicular axis in men with idiopathic oligozoospermia. Fertil Steril. 2009 Apr;91(4 Suppl):1427-30. doi: 10.1016/j.fertnstert.2008.06.002. Epub 2008 Aug 9.
