Progesterone (abbreviated as P4), also known as
pregn-4-ene-3,20-dione, is an endogenous steroid and progestogen sex hormone involved in
the menstrual cycle, pregnancy, and embryogenesis of humans and
other species. It belongs to a group of steroid hormones called the progestogens, and is the major progestogen in the body. Progesterone is also a
crucial metabolic intermediate in the production of other
endogenous steroids, including the sex hormones and the
corticosteroids, and plays an important role in brain function as a
It is on the WHO Model List of Essential Medicines, the most
important medications needed in a basic health system.
Micrograph showing changes to the endometrium due to progesterone
(decidualization) H&E stain.
Progesterone is the most important progestogen in the body, the
result of its action as a potent agonist of the nuclear
progesterone receptor (nPR) (with an affinity of KD = 1 nM). In addition, progesterone is an agonist of the more recently
discovered membrane progesterone receptors (mPRs), as well as a ligand of the PGRMC1 (progesterone receptor membrane
component 1; formerly known as the σ2 receptor). Moreover, progesterone is also known to be an antagonist of the σ1 receptor, a negative allosteric modulator of the nACh receptors, and a potent antagonist of the mineralocorticoid receptor (MR). Progesterone prevents MR activation by binding to this receptor
with an affinity exceeding even those of aldosterone and
glucocorticoids such as cortisol and corticosterone, and produces antimineralocorticoid effects, such as natriuresis,
at physiological concentrations. In addition, progesterone binds to and behaves as a partial
agonist of the glucocorticoid receptor (GR), albeit with very low
potency (EC50 >100-fold less relative to cortisol).
Progesterone, through its neurosteroid active metabolites such as
5α-dihydroprogesterone and allopregnanolone, acts indirectly as a
positive allosteric modulator of the GABAA receptor.
Progesterone and some of its metabolites, such as
5β-dihydroprogesterone, are agonists of the pregnane X receptor
(PXR), albeit weakly so (EC50 >10 µM). In accordance, progesterone induces several hepatic cytochrome
P450 enzymes, such as CYP3A4, especially during pregnancy when concentrations are much higher
than usual. Premenopausal women have been found to have greater CYP3A4
activity relative to men and postmenopausal women, and it has been
inferred that this may be due to the higher progesterone levels
present in premenopausal women.
Progesterone modulates the activity of CatSper (cation channels of
sperm) voltage-gated Ca2+ channels. Since eggs release progesterone, sperm may use
progesterone as a homing signal to swim toward eggs (chemotaxis).
As a result, it has been suggested that substances that block the
progesterone binding site on CatSper channels could potentially be
used in male contraception.
Progesterone binds extensively to plasma proteins, including
albumin (50-54%) and transcortin (43-48%). It has similar affinity for albumin relative to the PR.
Interactions with other steroid hormones
Progesterone has a number of physiological effects that are
amplified in the presence of estrogens. Estrogens through estrogen
receptors (ERs) induce or upregulate the expression of the PR. One example of this is in breast tissue, where estrogens allow
progesterone to mediate lobuloalveolar development.
Elevated levels of progesterone potently reduce the
sodium-retaining activity of aldosterone, resulting in natriuresis
and a reduction in extracellular fluid volume. Progesterone
withdrawal, on the other hand, is associated with a temporary
increase in sodium retention (reduced natriuresis, with an increase
in extracellular fluid volume) due to the compensatory increase in
aldosterone production, which combats the blockade of the
mineralocorticoid receptor by the previously elevated level of
Progesterone has key effects via non-genomic signalling on human
sperm as they migrate through the female tract before fertilization
occurs, though the receptor(s) as yet remain unidentified. Detailed characterisation of the events occurring in sperm in
response to progesterone has elucidated certain events including
intracellular calcium transients and maintained changes, slow calcium oscillations, now thought to possibly regulate motility. It is produced by the ovaries. Interestingly, progesterone has also been shown to demonstrate
effects on octopus spermatozoa.
Progesterone is sometimes called the "hormone of pregnancy", and it has many roles relating to the development of the fetus:
- Progesterone converts the endometrium to its secretory stage to
prepare the uterus for implantation. At the same time progesterone
affects the vaginal epithelium and cervical mucus, making it thick
and impenetrable to sperm. Progesterone is anti-mitogenic in
endometrial epithelial cells, and as such, mitigates the tropic
effects of estrogen. If pregnancy does not occur, progesterone levels will decrease,
leading, in the human, to menstruation. Normal menstrual bleeding
is progesterone-withdrawal bleeding. If ovulation does not occur
and the corpus luteum does not develop, levels of progesterone may
be low, leading to anovulatory dysfunctional uterine bleeding.
- During implantation and gestation, progesterone appears to decrease
the maternal immune response to allow for the acceptance of the
- Progesterone decreases contractility of the uterine smooth muscle.
- In addition progesterone inhibits lactation during pregnancy. The
fall in progesterone levels following delivery is one of the
triggers for milk production.
- A drop in progesterone levels is possibly one step that facilitates
the onset of labor.
The fetus metabolizes placental progesterone in the production of
See also: Breast development § Biochemistry
Progesterone plays an important role in mammary gland development
in females. In conjunction with prolactin, it mediates
lobuloalveolar maturation of the breasts during pregnancy to allow
for milk production, and thus lactation and breastfeeding after
childbirth. Estrogen is required for progesterone to mediate lobuloalveolar
maturation, as it induces expression of the PR in breast tissue. Moreover, it has been found that RANKL is a critical downstream
mediator of progesterone-mediated lobuloalveolar development. Knockout mice of RANKL show an almost identical mammary phenotype
relative to PR knockout mice, including normal mammary ductal
development but complete failure of the development of
Though to a far lesser extent than estrogen, which is the major
mediator of breast ductal development (via ERα, specifically), progesterone has been found to be involved in ductal development
as well. PR knockout mice or mice treated with the PR antagonist
mifepristone show delayed but otherwise normal ductal development
at puberty. In addition, mice modified to have overexpression of PRA display
ductal hyperplasia, and progesterone induces ductal growth in mouse mammary gland. Progesterone mediates ductal development mainly via the induction
of amphiregulin, the same growth factor that estrogen primarily
induces to mediate ductal development. These findings suggest that, while not essential for full ductal
development, progesterone seems to play a potentiating or
accelerating role in estrogen-mediated ductal development, at least
Progesterone also appears to be involved in the pathophysiology of
breast cancer, though its role, and whether it is a promoter or
inhibitor of breast cancer risk, has not been fully elucidated. In any case, while certain synthetic progestins with androgenic
effects such as medroxyprogesterone acetate and 19-nortestosterone
derivatives including norethisterone acetate, norgestrel, and
levonorgestrel have been found to significantly increase the risk
of breast cancer in postmenopausal women in combination with
estrogen as a component of hormone replacement therapy, the
combination of natural progesterone or the pure, non-androgenic
progestin dydrogesterone with estrogen has been found not to do so. In fact, progesterone or dydrogesterone added to estrogen appear
to decrease the risk of breast cancer relative to estrogen alone.
See also: Sexual motivation and hormones
Progesterone and its neurosteroid active metabolite
allopregnanolone appear to be importantly involved in sex drive in
Dr. Diana Fleischman, of the University of Portsmouth, and
colleagues examined the relationship between progesterone and
sexual attitudes. Their research was published in the Archives of
Sexual Behavior. They found that women who have higher levels of progesterone are
more likely to be open to the idea of engaging in sexual behaviour
with other women. Similarly, when heterosexual men are subtly reminded of the
importance of having male friends and allies, they report more
positive attitudes toward engaging in sexual behaviour with other
men. This pattern is particularly dramatic in men who have high
levels of progesterone.
Progesterone, like pregnenolone and dehydroepiandrosterone (DHEA),
belongs to an important group of endogenous steroids called
neurosteroids. It can be synthesized within the central nervous
system and also serves as a precursor to another major
Neurosteroids are neuromodulators, and are neuroprotective,
neurogenic, and regulate neurotransmission and myelination. The effects of progesterone as a neurosteroid are mediated
predominantly through its interactions with non-nuclear PRs, namely
the mPRs and PGRMC1, as well as certain other receptors, such as
the σ1 and nACh receptors.
Since most progesterone in males is created during testicular
production of testosterone, and most in females by the ovaries, the
shutting down (whether by natural or chemical means), or removal,
of those inevitably causes a considerable reduction in progesterone
levels. Previous concentration upon the role of progestogens in
female reproduction, when progesterone was simply considered a
"female hormone", obscured the significance of progesterone
elsewhere in both sexes.
The tendency for progesterone to have a regulatory effect, the
presence of progesterone receptors in many types of body tissue,
and the pattern of deterioration (or tumor formation) in many of
those increasing in later years when progesterone levels have
dropped, is prompting widespread research into the potential value
of maintaining progesterone levels in both males and females.
Studies as far back as 1987 show that female sex hormones have an
effect on the recovery of traumatic brain injury. In these studies, it was first observed that pseudopregnant female
rats had reduced edema after traumatic brain injury. Recent
clinical trials have shown that among patients that have suffered
moderate traumatic brain injury, those that have been treated with
progesterone are more likely to have a better outcome than those
who have not.
Previous studies have shown that progesterone supports the normal
development of neurons in the brain, and that the hormone has a
protective effect on damaged brain tissue. It has been observed in
animal models that females have reduced susceptibility to traumatic
brain injury and this protective effect has been hypothesized to be
caused by increased circulating levels of estrogen and progesterone
in females. A number of additional animal studies have confirmed that
progesterone has neuroprotective effects when administered shortly
after traumatic brain injury. Encouraging results have also been reported in human clinical
The mechanism of progesterone protective effects may be the
reduction of inflammation that follows brain trauma.
Damage incurred by traumatic brain injury is believed to be caused
in part by mass depolarization leading to excitotoxicity. One way
in which progesterone helps to alleviate some of this
excitotoxicity is by blocking the voltage-dependent calcium
channels that trigger neurotransmitter release. It does so by manipulating the signaling pathways of transcription
factors involved in this release. Another method for reducing the
excitotoxicity is by up-regulating the GABAA, a widespread inhibitory neurotransmitter receptor.
Progesterone has also been shown to prevent apoptosis in neurons, a
common consequence of brain injury. It does so by inhibiting enzymes involved in the apoptosis pathway
specifically concerning the mitochondria, such as activated caspase
3 and cytochrome c.
Not only does progesterone help prevent further damage, it has also
been shown to aid in neuroregeneration. One of the serious effects
of traumatic brain injury includes edema. Animal studies show that
progesterone treatment leads to a decrease in edema levels by
increasing the concentration of macrophages and microglia sent to
the injured tissue. This was observed in the form of reduced leakage from the blood
brain barrier in secondary recovery in progesterone treated rats.
In addition, progesterone was observed to have antioxidant
properties, reducing the concentration of oxygen free radicals
faster than without. There is also evidence that the addition of progesterone can also
help remyelinate damaged axons due to trauma, restoring some lost
neural signal conduction. Another way progesterone aids in regeneration includes increasing
the circulation of endothelial progenitor cells in the brain. This helps new vasculature to grow around scar tissue which helps
repair the area of insult.
Vitamin D and progesterone separately have neuroprotective effects
after traumatic brain injury, but when combined their effects are
synergistic. When used at their optimal respective concentrations, the two
combined have been shown to reduce cell death more than when alone.
One study looks at a combination of progesterone with estrogen.
Both progesterone and estrogen are known to have antioxidant-like
qualities and are shown to reduce edema without injuring the
blood-brain barrier. In this study, when the two hormones are
administered alone it does reduce edema, but the combination of the
two increases the water content, thereby increasing edema.
The clinical trials for progesterone as a treatment for traumatic
brain injury have only recently begun. ProTECT, a phase II trial
conducted in Atlanta at Grady Memorial Hospital in 2007, the first
to show that progesterone reduces edema in humans. Since then,
trials have moved on to phase III. The National Institute of Health
began conducting a nationwide phase III trial in 2011 led by Emory
University. A global phase III initiative called SyNAPSe®, initiated in June
2010, is run by a U.S.-based private pharmaceutical company, BHR
Pharma, and is being conducted in the United States, Argentina,
Europe, Israel and Asia. Approximately 1,200 patients with severe (Glasgow Coma Scale
scores of 3-8), closed-head TBI will be enrolled in the study at
nearly 150 medical centers.
Progesterone enhances the function of serotonin receptors in the
brain, so an excess or deficit of progesterone has the potential to
result in significant neurochemical issues. This provides an
explanation for why some people resort to substances that enhance
serotonin activity such as nicotine, alcohol, and cannabis when
their progesterone levels fall below optimal levels.
- To examine the effects of progesterone on nicotine addiction,
participants in one study were either treated orally with a
progesterone treatment, or treated with a placebo. When treated
with progesterone, participants exhibited enhanced suppression of
smoking urges, reported higher ratings of "bad effects" from IV
nicotine, and reported lower ratings of "drug liking". These
results suggest that progesterone not only alters the subjective
effects of nicotine, but reduces the urge to smoke cigarettes.
- Sex differences in hormone levels may induce women to respond
differently than men to nicotine. When women undergo cyclic changes
or different hormonal transition phases (menopause, pregnancy,
adolescence), there are changes in their progesterone levels. Therefore, females have an increased biological vulnerability to
nicotine's reinforcing effects compared to males and progesterone
may be used to counter this enhanced vulnerability. This
information supports the idea that progesterone can affect
- Similar to nicotine, cocaine also increases the release of dopamine
in the brain. The neurotransmitter is involved in the reward center
and is one of the main neurotransmitters involved with substance
abuse and reliance. In a study of cocaine users, it was reported
that progesterone reduced craving and the feeling of being
stimulated by cocaine. Thus, progesterone was suggested as an agent
that decreases cocaine craving by reducing the dopaminergic
properties of the drug.
- During pregnancy, progesterone is said to decrease irritability.
- During pregnancy, progesterone helps to suppress immune responses
of the mother to fetal antigens, which prevents rejection of the
- Progesterone raises epidermal growth factor-1 (EGF-1) levels, a
factor often used to induce proliferation, and used to sustain
cultures, of stem cells.
- Progesterone increases core temperature (thermogenic function)
- Progesterone reduces spasm and relaxes smooth muscle. Bronchi are
widened and mucus regulated. (PRs are widely present in submucosal
- Progesterone acts as an antiinflammatory agent and regulates the
- Progesterone reduces gall-bladder activity.
- Progesterone normalizes blood clotting and vascular tone, zinc and
copper levels, cell oxygen levels, and use of fat stores for
- Progesterone may affect gum health, increasing risk of gingivitis
- Progesterone appears to prevent endometrial cancer (involving the
uterine lining) by regulating the effects of estrogen.
- Progesterone plays an important role in the signaling of insulin
release and pancreatic function, and may affect the susceptibility
to diabetes or gestational diabetes.
- Progesterone may play a role in male behavior, such as in male
aggression towards infants.
Prometrium 100 mg Oral Capsule
The use of progesterone and its analogues have many medical
applications, both to address acute situations and to address the
long-term decline of natural progesterone levels. Because of the
poor bioavailability of progesterone when taken orally, many
synthetic progestins have been designed with improved oral
bioavailability and have been used long before progesterone
formulations became available. Progesterone was approved by the United States Food and Drug
Administration as vaginal gel on July 31, 1997, an oral capsule on May 14, 1998 in an injection form on April 25, 2001 and as a vaginal insert on June 21, 2007. Progesterone is marketed under a large number of different brand
names throughout the world.
Progesterone, when taken orally, has very poor pharmacokinetics,
including low bioavailability (only about 10-15% reaches the
bloodstream) and a half-life of only about 5 minutes, unless it is micronized. As such, it is sold in the form of oil-filled capsules containing
micronized progesterone for oral use (Utrogestan, Prometrium,
Microgest), termed oral micronized progesterone (OMP). Progesterone is also available in the forms of vaginal or rectal
suppositories or pessaries (Cyclogest), transdermally-administered gels or creams (Crinone, Endometrin,
Progestogel, Prochieve), or via intramuscular or subcutaneous injection of a vegetable oil
solution (Progesterone, Strone).
Transdermal products made with progesterone USP (i.e., "natural
progesterone") do not require a prescription. Some of these
products also contain "wild yam extract" derived from Dioscorea
villosa, but there is no evidence that the human body can convert
its active ingredient (diosgenin, the plant steroid that is
chemically converted to produce progesterone industrially) into progesterone.
The route of administration impacts the effects of progesterone.
OMP has a wide inter-individual variability in absorption and
bioavailability. In contrast, progestins are rapidly absorbed with
a longer half-life than progesterone and maintain stable levels in
the blood. The absorption and bioavailability of OMP is increased
approximately two-fold when it is taken with food.
Progesterone has a relatively short half-life in the body. As such,
OMP is usually prescribed for twice or thrice-daily administration
or once-daily administration when taken by injection. Via the oral route, peak concentrations are seen about 2-3 hours
after ingestion, and the half-life is about 16-18 hours. Significantly elevated serum levels of progesterone are maintained
for about 12 hours, and levels do not return to baseline until at
least 24 hours have passed.
OMP is prescribed in divided doses of 25-400 mg/daily, but in the range of 100-300 mg per day most commonly. Oral doses
of 100-200 mg will result in serum progesterone levels greater than
10 ng/mL. Notably, a portion of progesterone is converted into
5α-dihydroprogesterone and allopregnanolone (a conversion that is
catalyzed by the enzymes 5α-reductase and 3α-hydroxysteroid
dehydrogenase (3α-HSD) and occurs in the liver, reproductive
endocrine tissues, skin, and the brain), which are neurosteroids and potent potentiators of GABAA receptors. It is for this reason that common reported side effects of
progesterone include dizziness, drowsiness or sedation, sleepiness,
and fatigue, especially at high doses. As a result, some physicians may instruct their patients to take
their progesterone before bed. Both oral and intramuscularly injected progesterone produce
sedative effects, indicating that first-pass metabolism in the
liver is not essential for the conversion to take place. Moreover, the sedative effects occur in both men and women,
indicating a lack of sex-specificity of the effects.
There are several notable drug interactions with progesterone.
Selective serotonin reuptake inhibitors (SSRIs) may increase the
GABAA receptor-related central depressant effects of progesterone by
enhancing its conversion into 5α-dihydroprogesterone and
allopregnanolone via activation of 3α-HSD. Progesterone potentiates the sedative effects of benzodiazepines
and ethanol. Notably, there is a case report of progesterone abuse alone with
very high doses. 5α-Reductase inhibitors such as finasteride and dutasteride, as
well as inhibitors of 3α-HSD such as medroxyprogesterone acetate,
inhibit the conversion of progesterone into its inhibitory
neurosteroid metabolites, and for this reason, may have the
potential to block or reduce its sedative effects.
Progesterone is a weak but significant agonist of the PXR, and has
been found to induce several hepatic cytochrome P450 enzymes, such
as CYP3A4, especially when concentrations are high, such as with
pregnancy range levels. As such, progesterone may have the potential to accelerate the
clearance of various drugs, especially with oral administration
(which results in supraphysiological levels of progesterone in the
liver), as well as with the high concentrations achieved with
sufficient injection dosages.
Progesterone, when taken orally, undergoes gastrointestinal
(especially hepatic) metabolism to form hydroxylated metabolites,
which in turn are metabolized into sulfate and glucuronide
derivatives. Enzymes involved in the hepatic metabolism of progesterone
include, particularly, CYP2C19 and CYP3A4, as well as CYP2C9.
Transdermal progesterone is about 5-7 times stronger than oral
progesterone. This is due to the fact transdermal administration bypasses
first-pass metabolism. As such, 20-30 mg/day transdermal progesterone is equivalent to
about 100-200 mg/day oral progesterone.
With vaginal and rectal administration, a 100 mg dose of
progesterone results in peak levels at 4 hours and 8 hours after
dosing, respectively, with the levels achieved being in the serum
luteal phase range. Following peak serum concentrations, there is a gradual decline in
plasma levels, and after 24 hours, serum levels typical of the
follicular phase are reached.
With intramuscular injection of 10 mg progesterone suspended in
vegetable oil, maximum plasma concentrations (Cmax) are reached at
approximately 8 hours after administration, and serum levels remain
above baseline for about 24 hours. Doses of 10 mg, 25 mg, and 50 mg via intramuscular injection
result in mean maximum serum concentrations of 7 ng/mL, 28 ng/mL,
and 50 ng/mL, respectively. With intramuscular injection, a dose of 25 mg results in normal
luteal phase serum levels of progesterone within 8 hours, and a 100
mg dose produces mid-pregnancy levels. At these doses, serum levels of progesterone remain elevated above
baseline for at least 48 hours.
Due to the high concentrations achieved, progesterone by
intramuscular injection at the usual clinical dose range is able to
suppress gonadotropin secretion from the pituitary gland,
demonstrating antigonadotropic efficacy.
Progesterone can also be administered alternatively via
subcutaneous injection, with the aqueous new formulation Prolutex
being intended specifically for once-daily administration by this
route. This formulation is rapidly absorbed and has been found to result
in higher serum peak progesterone levels relative to intramuscular
oil formulations. In addition, subcutaneous injection of progesterone is considered
to be easier, safer (less risk of injection site reactions), and
less painful relative to intramuscular injection.
For comparative purposes, mid-luteal serum levels of progesterone
are above 5-9 ng/ml, plasma levels in the first 4 to 8 weeks of pregnancy are 25-75
ng/ml, and serum levels at term are typically around 200 ng/ml. Production of progesterone in late pregnancy is approximately 250
mg per day, 90% of which reaches maternal circulation.
Prevention of preterm birth
Vaginally dosed progesterone is being investigated as potentially
beneficial in preventing preterm birth in women at risk for preterm
birth. The initial study by Fonseca suggested that vaginal
progesterone could prevent preterm birth in women with a history of
preterm birth. According to a recent study, women with a short cervix that
received hormonal treatment with a progesterone gel had their risk
of prematurely giving birth reduced. The hormone treatment was
administered vaginally every day during the second half of a
pregnancy. A subsequent and larger study showed that vaginal progesterone was
no better than placebo in preventing recurrent preterm birth in
women with a history of a previous preterm birth, but a planned secondary analysis of the data in this trial showed
that women with a short cervix at baseline in the trial had benefit
in two ways: a reduction in births less than 32 weeks and a
reduction in both the frequency and the time their babies were in
intensive care. In another trial, vaginal progesterone was shown to be better than
placebo in reducing preterm birth prior to 34 weeks in women with
an extremely short cervix at baseline. An editorial by Roberto Romero discusses the role of sonographic
cervical length in identifying patients who may benefit from
progesterone treatment. A meta-analysis published in 2011 found that vaginal progesterone
cut the risk of premature births by 42 percent in women with short
cervixes. The meta-analysis, which pooled published results of five large
clinical trials, also found that the treatment cut the rate of
breathing problems and reduced the need for placing a baby on a
- Progesterone is used for luteal support in Assisted Reproductive
Technology (ART) cycles such as In-vitro Fertilization (IVF).
- Progesterone is used to control persistent anovulatory bleeding. It
is also used to prepare uterine lining in infertility therapy and
to support early pregnancy. Patients with recurrent pregnancy loss
due to inadequate progesterone production may receive progesterone.
- Progesterone is also used in nonpregnant women with a delayed
menstruation of one or more weeks, in order to allow the thickened
endometrial lining to slough off. This process is termed a
progesterone withdrawal bleed. The progesterone is taken orally for
a short time (usually one week), after which the progesterone is
discontinued and bleeding should occur.
- Progesterone can be used to treat catamenial epilepsy by
supplementation during certain periods of the menstrual cycle.
- Progesterone is being investigated as potentially beneficial in
treating multiple sclerosis, since the characteristic deterioration
of nerve myelin insulation halts during pregnancy, when
progesterone levels are raised; deterioration commences again when
the levels drop.
- Progesterone also has a role in skin elasticity and bone strength,
in respiration, in nerve tissue and in female sexuality, and the
presence of progesterone receptors in certain muscle and fat tissue
may hint at a role in sexually dimorphic proportions of those.[copyright violation?]
- Antiprogestins and selective progesterone receptor modulators
(SPRM)s, such as mifepristone, can be used to prevent conception or
induce medical abortions (note that methods of hormonal
contraception do not contain progesterone but a progestin).
- Progesterone is starting to be used in the treatment of the skin
condition hidradenitis suppurativa.
- Progesterone is sometimes employed as a component of hormone
replacement therapy for trans women.
Sample of Progesterone.
Progesterone was independently discovered by four research groups.
Willard Myron Allen co-discovered progesterone with his anatomy
professor George Washington Corner at the University of Rochester
Medical School in 1933. Allen first determined its melting point,
molecular weight, and partial molecular structure. He also gave it
the name Progesterone derived from Progestational Steroidal ketone. The drug was originally administered by injection because it
rapidly inactivated after oral use 
- When you supplement with Nandrolone-Decanoate, as is with all
anabolic steroids, your natural testosterone production will be
suppressed; in this case it will be completely suppressed from one
single dosing. A single 100mg injection of Nandrolone-Decanoate is
all it takes to suppress all testosteron production. For this
reason, it is imperative that you supplement with some form of
exogenous testosteron when you supplement with the Nandrolon
compound. Failure to do so will result in a low testosteron
condition, and this is simply not good for your health. Further,
testosterone is a fantastic, highly versatile and generally
well-tolerated anabolic steroid your body is very familiar with and
will only enhance your total results.
- Nandrolon-Decanoate does aromatize to a degree; approximately 20%
the rate of testosterone. Further, this is a steroid that carries a
progestin nature and by these traits can lead to Gynecomastia. With
the use of an Aromatase Inhibitor, Gynecomastia can be avoided;
Arimidex and Letrozole will both do the trick. Further, an
Aromatase Inhibitor will aid in combating water retention that can
occur with this steroid.
- When supplementing with Nandrolon-Decanoate, 8 weeks of total use
should be the minimal time frame of use. Any use less than 8 weeks
will provide very little as this is such a slow acting steroid, and
will simply be a waste of time. To maximize your results, 10-12
weeks of total use will be far more optimal, with 16 weeks
generally being the maximal time frame of use.
- Whenever you decide to discontinue anabolic steroid use, you do
not want to end use while still supplementing with
Nandrolon-Decanoate. As a steroid with a very long activity time,
if you end use with a large amount still freshly in your system it
can make recovery a tremendously difficult process. In most cases,
all Nandrolone-Decanoate use should end at least 2 weeks before all
anabolic steroid use comes to a halt; many will find 4 weeks to be
Nandrolon Decanoate Dosage Recommendations for Bodybuilding Cycles
Numerous individuals may find it really difficult to come up with
the proper Nandrolone Decanoate dosage to take in their cycle.
There is limited information online that gives accurate advice and
many of the articles suggest lower doses than what should be used.
Uses often decide to overcompensate with testosterone and
shortchange their Deca doses due to the fact that the hormone is so
suppressive to natural testosterone production. In order to achieve
positive results, you will need to keep total hormonal balance. To
avoid any problems, you have to keep your estrogen levels in normal
limits and offer the body the necessary quantity of testosterone.
Numerous individuals are unaware of the possible results of using
some particular Nandrolone Decanoate doses. Many bodybuilders use
this steroid in the off-season bulking cycles so as to promote
muscle size and growth. In case bulking is not the main target of
the bodybuilder, lower Nandrolone Decanoate doses can be really
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Off-season Nandrolon Decanoate Doses:
It is enough to take 300-400mg of Nandrolon Decanoate per week in
the off-season. For this, you will need to take one injection each
week. To increase the efficiency of the steroid, the majority of
bodybuilders will split the injection into 2 small equal size
injections per week. This task will reduce the total injection
volume. You can increase your dosage in case you tolerate 300-400mg
without any problems. Even though there is no need for high
dosages, we need to know that most men will support 60mg per week
without any major problems. It is enough to stick with 400mg. It is
more likely to experience negative side effects in case you
increase the dosage. In some cases, the negative effects may
outweigh the positive effects, even though this may differ from one
person to another.
Dosages for Cutting Before a Contest
The Nandrolon hormone may be identified in numerous competitive
bodybuilding contest cycles, even though the majority of
bodybuilders don`t consider Nandrolon Decanoate to be a cutting
steroid. People may find this steroid to be really useful, even
though it does not offer the conditioning effects of Trenbolone,
Anavar or Winstrol. People may obtain numerous benefits by taking
200-300mg Nandrolon Decanoate doses on a weekly basis. Even though
this steroid has a powerful ability in preserving lean tissue,
there is another benefit that is far more important.
During the demanding cutting cycle of the bodybuilding domain, the
body needs a lot of relief, which can be provided by a low
Nandrolone Decanoate doses. The hard dieting combined with hard
training session can really tire the body. Apart from offering a
powerful therapeutic relief, low Nandrolon Decanoate doses will
also improve muscular endurance throughout the demanding training
Other Uses of Nandrolon Decanoate Cycles
Numerous individuals don`t view Nandrolon Decanoate as adequate for
improving athletic performance due to the fact that it is primarily
regarded as a bulking steroid. Many athletes prefer these steroid
due to the fact that they understand it`s potential. It will not be
any problem in case the athlete does not need to grow. You will
never grow in case you do not consume high quantity of calories and
take important Nandrolon Decanoate doses. The individual will take
the Deca Dorabolin doses simply to obtain a therapeutic relief in
this situation. This is the main goal, even though the steroid also
improves the muscular endurance. It will be enough to consume
100-200mg of Nandrolon Decanoate on a weekly basis. To obtain the
true benefits, you need to stick with the 200mg dose. View the best
Deca Durabolin stacks and cycle dosages here.
How Long Should your Cycle Be?
After you have selected your dosage for Nandrolon Decanoate, the
next step will be to establish the entire time frame of usage.
Considering the important Decanoate ester attached to the steroid,
we can state that Nandrolon Decanoate acts really slowly.
Therefore, this is not recommended for short term usage. You will
have to use the steroid for a minimum of 8 weeks in order to reap
the benefits, regardless of the doses that you select. However,
most men will usually take the steroid for 10-12 weeks. This is the
perfect time frame, even though some may go up to 16 weeks.
Sexual Side Effects from Nandrolone Use
Nandrolon Decanoate Dosage CycleIn case you encounter any sexually
related side effects, such as erectile dysfunction or los of
libido, you often make improper adjustments. Most individuals will
likely presume the fact that their testosteron dose has dropped
below normal levels. These individuals will usually increase the
testosteron level, regardless if their Nandrolon Decanoate doses
are at the low end range. While this may work in some cases, the
problem will get worst in most of the situations.
You may consider the fact that your hormone levels are unbalanced
in case you have experiencing some problems. You are simply
aggravating the problem in case you add more testosteron. You can
experience sexually related side effects in case you don`t manage
to control your estrogen levels. Your estrogen levels should be
neither too high nor too low in order to avoid any sexually related
However, what is the perfect way to solve this issue? You just need
to make sure you have sufficient testosterone in your body. The
next step will be to maintain a normal estrogen level in your body.
You will definitely avoid all side effects if you manage to respect
these two aspects. Click here to find Deca Durabolin for Sale.
Nandrolon Decanoate, Dianabol and Testosteron Cycle
In case you replace the testosteron, Nandrolon Decanoate and Dbol
cycle with sustanon, this cycle can be used without the help of a
Week Testosteron Cypionate Deca Durabolin Dianabol Ostarine MK-2866
1 600mgs/week 400mgs/week 50mgs/day 25mgs/day 25mgs/day 7caps/day
2 600mgs/week 400mgs/week 50mgs/day 25mgs/day 25mgs/day 7caps/day
3 600mgs/week 400mgs/week 50mgs/day 25mgs/day 25mgs/day 7caps/day
4 600mgs/week 400mgs/week 50mgs/day 25mgs/day 25mgs/day 7caps/day
5 600mgs/week 400mgs/week 50mgs/day 25mgs/day 25mgs/day 7caps/day
6 600mgs/week 400mgs/week 50mgs/day 25mgs/day 25mgs/day 7caps/day
7 600mgs/week 400mgs/week -OFF- 25mgs/day 25mgs/day 7caps/day
8 600mgs/week 400mgs/week -OFF- 25mgs/day 25mgs/day 7caps/day
9 600mgs/week 400mgs/week -OFF- 25mgs/day 25mgs/day 7caps/day
10 600mgs/week 400mgs/week -OFF- 25mgs/day 25mgs/day 7caps/day
11 600mgs/week 400mgs/week -OFF- 25mgs/day 25mgs/day 7caps/day
12 600mgs/week 400mgs/week -OFF- 25mgs/day 25mgs/day 7caps/day
The half-life of Nandrolone Decanoate Nearly six days, however it
requires about 21 days to become released out of your organism.
Actually, several sportsmen have positive for the metabolite months
following their final injection, therefore always be cautious with
your Nandrolone decanoate dosage per week and give yourself lots of
time before a potential test might occur.
Quick Detail :
Nandrolon Decanoate / Nandro Deca / DECA / Durabolin
Nandrolon Decanoate Chemical Name: 4-estren-17beta-ol-3-one
Durabolin Synonyms: 19-nortestosterone 17-decanoate;
DECA Molecular Formula: C28H44O3
Nandrolone Decanoate Molecular weight: 428.65
Durabolin CAS NO.: 360-70-3
DECA EINECS: 206-639-3
DECA Assay: 99% min.
Nandrolon Decanoate Appearance: white or oyster white to pale
yellow crystalline powder
Durabolin Usage: pharmaceutical material, Steroid hormone,
Anabolin. Is a male hormone, anabolic hormones drugs.
Durabolin Standard: USP28; BP2003
Storage: Shading, Confined Preservation
Package: Discreet Packing ways for your choice.
Delivery: Deliver out within 24 hours after payment.
Payment: West Union, T/T, Money Gram.
Deca Durabolin,also known as Nandrolon Decanoate, is perhaps the
second-best known injectable anabolic androgenic steroid after
Testosteron. Used for bulking.Nandrolon is the base hormone, but it
is better known under the trade name Deca Durabolin, which contains
Nandrolon Decanoate. This popular preparation takes the nandrolon
hormone and adds a decanoate ester chain. This ester chain is
attached during the manufacturing process and it serves dual
purposes. The main purpose is to make the hormone oil soluble, so
it can be put in an amp or multi-dose vial. The second purpose of
this ester chain is to slow-release the steroid by keeping deca
from interacting with androgen receptors until the ester chain is
cleaved off by enzymes in your body. Since nandrolon decanoate
cannot attach to an androgen receptor until enzymes in your body
have cleaved off the decanoate ester, it causes the steroid to
slow-release into your system over many days. For medical use, the
ester's main function is to allow the hormone to be injected only
once every 3 weeks. However, bodybuilders may inject deca durabolin
weekly or as often as every three days.
Nandrolon decanoate can be used for the treatment of osteoporosis,
for the palliative treatment of selected cases of disseminated
mammary carcinoma in women and as an adjunct to specific therapies
and dietary measures in pathologic conditions characterized by a
negative nitrogen balance.
Nandrolon decanoate is an injectable sort of the anabolic steroid
nandrolon. The decanoate ester supplies a slow release of nandrolon
from the site of injection, continuation for up to 3 weeks.
Nandrolon 200 USP injection provides nandrolon decanoate. In human
trials nandrolone has been shown to positively influence calcium
metabolism and to increase bone mass in osteoporosis. The
esterification of the 17-beta-hydroxyl group increases the duration
of the action of nandrolon. Nandrolon esters in oil injected
intramuscularly are absorbed slowly from the lipid phase, thus
Nandrolon 200 can be administered at intervals of 3-4 weeks.
Nandrolon 200 contains nandrolone decanoate in a 10ml solution for
injection (200mg nandrolon decanoate / ml). Nandrolon 200 is a
yellowish oily solution for intramuscular injection.
Deca for 5 grams 25 ml @ 200mg/ml
5 grams powder
16.25ml sesame oil
1.25ml BA 5%
3.75ml BB 15%
|Hot Sale Semi-finished Steroid Liquid||Concentration|
|Testosteron Enanthate(Primoteston)||250mg/ml / 300mg/ml|
|Testosteron Cypionate||250mg/ml / 300mg/ml|
|Testosteron Sustanon 250||200mg/ml / 250mg/ml|
|Testosteron Supertest 450||450mg/ml|
|Nandrolon Decanoate (DECA)||200 / 250 / 300mg/ml|
|Drostanolone Propionate (Masteron)||100mg/ml|
|Boldenon Undecylenate (Equipoise)||200mg/ml / 300mg/ml|
|Methenolon Acetate (Primobolone)||100mg/ml|
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