What You Should Know
Also known as
Nucific Bio X4 -4 in 1 Probiotic
DHEA, Pradesterone, Hydroxyandrosterone, -3β-hydroxy-5-androstene-17-oneNot to be confused with
DMAE (structurally related compound of the hill), DMAA (doping)
Things to consider
DHEA can not be approved by all sports federations (currently on the list of prohibited substances by the WADA [1]), check to see if it is on the list of banned substances
At least one previous report (1998 [2]) pointed out that the quality control in the DHEA supplements were not satisfactory. Current status of the industry is not known, but it would be wise to seek reliable suppliers
Taking (the recommended dose, active and quantities, and other details)
DHEA supplements seem to be effective in more than 40 people in the dose range of 25-50 mg, while prolonged use of 100mg Oabdo to be safe in this population group. While the use of DHEA in young people for the purpose of improving people's testosterone is not clear, it tends to be used for this purpose in 200mg.
Eleven. Source
DHEA was discovered as the first metabolism in the urine in 1934 by Adolf and Hans Dannenbaum Buteiiandt Germany, stressed that metabolism in the urine and serum 1943 isolate in 1954. [3]
Dehydroepiandrosterone or DHEA, is the most abundant circulating steroid in humans and the second as a substrate (precursor) to other androgens such as testosterone and dihydrotestosterone (DHT) and estrogen such as 17β-estradiol and estrogen. [4] There is a relatively balanced set of DHEA and its sulfated conjugate, DHEAS (dehydroepiandrosterone sulfate, the most abundant steroid in the blood circulation) for further metabolism in more effective molecules.
As a complement, it is directed towards the relief of symptoms associated with the pool decreased DHEA (either aging where reduces DHEA after the age of 30 to 40, or adrenal insufficiency, where the decline in the synthesis of DHEA) and is sometimes used when the user wants to increase DHEA gathering medium and metabolism, such as testosterone , for a short period of time.
1.2. Structure
DHEA is the official name -3 for β-hydroxy-5-androstene-17-one and has a backbone similar to the skeleton of cholesterol, except without the side chain (separation in the first pass metabolism, cholesterol pregnenolone) is replaced by the remnants of side chain with a ketone group (oxygen double bond in the upper right of the structures below).
1.3. Property
The molecular formula is C19H28O2 DHEA, and has a molecular weight of 288.43. [3]
2. biological importance
Bio X4 synthesis and metabolism
Dietary cholesterol is converted to pregnenolone by the enzyme CYP11A1, and then converted into DHEA through CYP17 (P450c17) also known as enzyme 17alpha-hydroxylase 17,20 lyase. [5] becomes DHEAS to DHEA via sulfotransferases and can be converted again through sulfatase, and create a "pool" large interchangeably DHEA: DHEA circulating in your body to process subsequent metabolism [6] synthesis DHEA refers usually occur in the adrenal cortex (small renal glands above) due to high localized expression. Said second enzyme (CYP17), [7] [8] However, it can be synthesis DHEA occurs in the testes, [7] the ovaries, [9] and the brain, where circulating DHEA levels are manufactured locally from independent rest of the body can reach concentrations 6-8 times higher than the regular serum. [10]
DHEA is naturally cholesterol through two enzymes, and are very translation of the adrenal gland, but not limited to
Since DHEA: DHEA DHEAS gathering tends to be converted into androstenedione directly by enzyme 3β-HSD and then can take multiple paths. Androstenedione can be directed towards the hormone androgen stronger 5α- dihydrotestosterone (DHT) by any of the testosterone transformation then become a pillar of the 5α reductase enzyme, or as a substrate for the enzyme 5α reductase (become 5α -androstenediona) and then converted to DHT. It requires either one road passes through the 5α reductase enzyme and one pass through the enzyme 17β-HSD (conversion of androstenedione to testosterone and androstenedione 5α-DHT). [6] [5]
If one of these androgens has mentioned after the substrate of the enzyme 5α reductase, instead it can be a substrate for the enzyme and hormones can be converted to estrogen. The testosterone is converted to estrogen androstenedione is converted to estrone. You can not convert all of them to 5α hormones estrogen, estrone and can be converted to estrogen via the enzyme 17β-HSD itself mentioned above. [6] [5]
In a sense, androstenedione and testosterone hormones are bidirectional and can become more effective androgen (via 5α reductase) or estrogen more effectively (through hormones). Androstenedione make up this multi-track start, but DHEA formation of the grouping to be derived from androstenedione
DHEA independent paths completely classical steroid mentioned above, can be converted into biologically active DHEA derivatives. Another possible to show the process of metabolism of DHEA road.
DHEA can become 7α-hydroxyDHEA through enzyme oxysterol 7α hydroxylase (CYP3A4 / 5 also been implicated [11]), and can convert this molecule to beta (7β-hydroxyDHEA) was formed through the 11β-HSD 1. Type [6] [12] This is the same path enzymatic that can take androstenedione, then isomerization epiandrosterone create 7α and 7 β-hydroxyepiandrosterone hydroxyepiandrosterone. Conversion of DHEA in 7α and metabolism of oxygen 7β mentioned above is not limited to steroid origin tissues (testes and ovaries) and adrenal glands and can occur in the brain, spleen, thymus, and the skin around the anus, abdominal skin, intestines, colon, coecum and muscle tissue. [13] [14] both 7α and 7 β hydroxyDHEA can be converted to more oxo DHEA 7, which is known as 7-Quito (trade name) through the same enzymes times 11β-HSD. [15] [16]
In short, DHEA can be metabolized by CYP7B1 derivatives and this is irreversible. 7α and 7β can compare the secret to and from each other, using a 7-of polyolefins (also known as 7-Quito) feedstock.
These compounds of DHEA are more involved with inflammation and immunological aspects of supplements DHEA, and some neurological aspects.
DHEA can be an active metabolic products of vital independent classical steroid synthesis rather than through androstenedione
2.2. Secretion
Androgens tend to glucuronide androstenedione be converted to derivatives water-soluble testosterone and DHT, and then excreted in the urine. [17] This is not the only metabolite urine, like most of the steroid molecules can be excreted in the urine and DHEA.
2.3. Mechanisms of action
DHEA as well as a gathering of steroid hormones (practiced metabolic effects indirectly through other hormones), DHEA may also have direct action. [6] It was found that, in itself enable the addition membrane protein G cytosolic [18] [19] that, when incubated with endothelial cells, can increase the boat and NO levels [20] through the PI3K / AKT. [19] This effect was seen (the boat and NO to high) in men after supplementation DHEA 50 mg per day, and can be a mechanism for the effects of heart disease. [21] When coincubated with androgenic, estrogenic and liabilities progesteronic (to see if the effects indirectly through these hormones) did not prevent the anti-effects, suggesting that DHEA is an agonist / activated directly in spite of metabolites DHEA (7α- hydroxy, -7β hydroxy 0.7 oxo) it has not been disposed of. [18] [19]
This receiver has a good affinity for 48.7 DHEA evening and saturated within 1-10uM. [20]
G Dynamic same receptors can be phosphorylated ERK 1/2 [22], has been implicated in the stability of the Bcl-2 [19] and phosphorylation of ERK1 / 2 led to an increase of blood vessels, and this was observed with DHEA DHEA and incubated bound to albumin. [22]
In immune cells, as has been proved DHEA-S (sulfated version) for the generation of ultra-dose dependent increase in human neutrophils and directly through the activation of PKC. [23] has also been known as DHEA metabolism 7β-hydroxy-DHEA has shown to possess anti-inflammatory effects in relieving the laboratory of pro-inflammatory response to TNF-α and modify the synthesis of prostaglandins [12] and relieve inflammation later. [24]
DHEA also practiced androgenic and estrogenic activity directly, without metabolism in androgen or estrogen. However, their work on these receptors are weak with respect to androgen and estrogen. [25] and metallization of DHEA can also modulate these effects. [26] [6]
2.4. Drain adrenal fatigue
Self levels of DHEA and DHEAS and sulfur associated DHEA, seems to be a significant reduction in cases of "fatigue," the adrenal gland.
Bio X4 Depending on age
DHEA and DHEAS cojugate them seem to be related to age, and a reduction in both men and women during the aging process. [27] [4] DHEA levels are relatively high after birth, fast and low until adulthood where what appears to supraphysiological levels again, and remained stable until about 25-35 years of age, and a steady decline thereforth. At the age of 70, DHEA levels are about 20% of the average 25-year-old. [28] [27]
A generalization of 4.1umol / L, or 1500ng / ml level, is usually seen closer to the lower range of average concentrations of DHEA for young people (15-39) men. [4] Several studies indicate "a lack of DHEA" in older men used to define the lack of this level.
DHEA supplementation does not appear in the level at which restores DHEA serum levels (50-100 mg daily) to face the common "side" of aging such as loss of libido, bone metabolism, for most part DHEA levels and symptoms we call "aging" effects are not relevant. [29] and low trading of DHEA with aging, unlike the low levels of L- carnitine or creatine is seen in some of the mobility of the population, it does not seem to be an indication of the state of DHEA deficiency that needs to be corrected. [30]
3. Pharmacy
3.1. Bioavailability topical administration
DHEA is sold usually Kkarim for application on the skin. For most purposes, because the products are intended to help the quality of the skin topical administration still still affects the blood and body.
In 36 healthy elderly (60-70yrs), 4 grams of cream DHEA (10%) or gel (10%) applied to the area 30x30cm compared with oral administration of 100 mg DHEA. The oral administration Cmax for 15.6 +/- 2.5 ng / mL (from baseline of 2.3 +/- 0.3) in TMAX than one hour, measuring 5.7 + / - 0.5 ng / ml in 6 hours and hit the baseline in 24 hours. The application of gel or cream was 8.2 +/- 2.0nmol / L +/- levels of 8.0 1.2nmol / liter in 12 hours, and gradually increase to 24 hours when the study stopped (above baseline) values; it seemed serum crossing in 18 hours. [31] It is interesting, did not notice any differences in circulating DHEA, testosterone or estrogen between cream or gel, cream, however, constitute the highest concentration as a result of androstenedione in 24 hours, and topical androgen metabolism public administration preferred to oral administration. [31] more than 14 days of submission of the application, cream seemed to increase the gel better and there was no effect observed in DHEA-S with hormones topical application. [31]
And topical administration also shows greater blood levels of hormones during the days; although suggestive to enhance the effect, and this may be due to the effects of DHEA applied topically lasted more than 24 hours. [31] During the period of 12 months, the daily application in the blood appear similar to when measured after 28 days. [32]
Despite the marked differences in the kinetics, and the availability of public biological topical and oral administration to reach the serum is not comparable with the presence of slight differences in the American University in Cairo, but that does not seem DHEAS greatly enriched with topical application. It is to some extent simply the minimum. [31] [32]
May be caused by high levels of androgens noted with topical administration to undergo the process of enzymatic digestion of androgens by UDP-glucuronosyltransferase [33] [34] Enzymes, which are more prevalent in the digestive tract and liver. [35] When measured in the blood, the most common androgen is actually ADT-G (androstenedione glucuronide) metabolite consisting of up to 90% of all androgen after the application or post-menopausal women break, and reaches 70% of the controls. [32] [36] ADT-G is important to note that there are women in most androgen synthesis of women DHEA in peripheral tissues, and can be more reliable than the effects of the male testosterone circulating that indication. [17]
Topical administration appears to have a similar overall bioavailability (percentage reached the bloodstream) compared to oral ingestion. It seems topical androgen like testosterone influence on the oral ingestion, and although there are no differences in the short-term DHEA cream seems better than gel DHEA
3.2. Oral administration
TMAX DHEA complementary, orally, fluctuates wildly. According to several large boluses acute studies on TMAX about 1-3 hours, [31] [37] but has been reported to TMAX values of 7.12 for in some cases. [37]
Youth (18-42), supplements DHEA 50 mg it is not enough to make a huge difference circulating DHEAS to DHEA levels while 200 mg / seem to be able to. [37] In this same population group, testosterone plasma and DHT of DHEA did not increase significantly, while ADT-G serum rose (androgen metabolism) dose-dependent rate of AUC 24 hours of 198ng / h / ml to 603 (after giving 200 mg). [37]
3.3. Metabolism and metabolism
A metabolite of DHEA practiced anti-inflammatory properties of large non-β-AET, also known as androstene -3 β, 7β, 17β-triol. [38]
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