Clomid, the generic name for ClomipheneCitrate, is a synthetic estrogen. At home it's also known as clomiphene.
Another common name for it is Serophene, which helps women with low fertility ovulate.
Most anabolic steroids, especially androgens, inhibit the body's own testosterone production.
As you come to the end of a steroid cycle, natural testosterone production is usually low or close to zero, and blood steroid levels are dropping.
This leads to a catabolic rate: the body is in a catabolic state where, if nothing is done, most of the muscle tissue gained during the cycle is about to be lost.
Clomid stimulates the hypothalamus, which in turn stimulates the anterior pituitary gland (also known as the posterior pituitary) to release gonadotropins.
Gonadotropins are follicle-stimulating hormone (FSH) and luteinizing hormone (LH-AKA interstitial cell stimulating hormone (ICSH)). FSH stimulates the testes to produce more testosterone, while LH stimulates them to produce more testosterone. This feedback mechanism is known as the hypothalamic-pituitary-testicular axis (HPTA) and causes the body's own testosterone production and blood levels to rise. To some extent compensates for the reduction in exogenous steroids, which is critical in reducing muscle loss after the cycle ends.
However, not all steroids cause the feedback mechanism to turn off, and everyone's situation is different. You need to consider when and how you use steroids to determine if you need to use Clomid.
Clomid is also an anti-estrogen, a weaker synthetic estrogen that binds to estrogen receptors in cells, preventing them from entering the bloodstream. This reduces negative effects such as male breast development and water retention, which can be side effects caused by testosterone. It has a weak anti-female effect, but you don't need it if you're taking androgen steroids, or if you don't have female breasts.
Arimidex (anastrozole) and Nolvadex (tamoxifen) have more potent anti-female effects.
Important: Clomid does not stimulate the release of natural testosterone, as is commonly thought, but rather reduces estrogen suppression due to steroid cycling. It works in a similar way to Nolvadex (tamoxifen) blocking estrogen receptors on the nipple to counter breast development in women, by blocking estrogen receptors in the hypothalamus and pituitary gland to reduce estrogen inhibition. This causes LH levels to return to normal, or even above normal, and natural testosterone levels to return to normal. Inhibition of HPTA is caused by high androgen, estrogen, or progesterone levels.
Androgen levels begin to decline at the end of the steroid cycle, and Clomid doses are typically initiated according to the drug with the longest half-life in the system. This also explains why people often find it more difficult to recover after using dika because the presence of progesterone is not affected by Clomid.
We know that both Clomid and Nolvadex (which are chemically very similar) are ineffective for reducing progesterone associated GYno, so it's reasonable to assume that Clomid has no effect on progesterone levels.