xtreme syntenhance

czy ktoś może mi coś o tym napisać. czy jest to dobry środek czy lipa. czy może być brany sam czy coś dołozyć. dziędki za odpowiedzi

A co to jest?

Pierwsze słysze

pewnie jakiś stack ph

nowy ph wchłaniany przez skóre. właśnie zamówiłem i podobno jest ok.

podaj skład

nie wiem czy doczytales ale to nie jest zwykly transdermal, a rozni sie tym, ze dziala lokalnie (wsmarujesz w lape - dziala na lape itp)

om
po ile to idzie dostac ? czy to działa ? ile tego cza na cykl ?

a co ja jestem informacja?
jako jedyny PH bym tego nie bral, poprostu mniejsze dawki ogolne i uzupelnienie slabszych partki lokalnie.

Par Deus Presents: The Science of……

SYTENHANCE

Yes, I said “Sytenhance”

No, it was not a typo.

Sytenhance is indeed a reality.

From the scientific mind that brought you ONE+, LipoDerm-Y, Ab-Solved, and LeptiGen, and from the company that brought you ICE, Vendetta, and Relentless, comes perhaps the most intriguing formula to hit the market to date.

This is THE REAL Sytenhance formula, designed by Par Deus, which Avant Labs was going to release early this year.

For those unaware, Sytenhance is a locally acting androgen, in a topical gel.

Basically, as the name implies, it is like Synthol, except that it actually promotes real increases in contractile protein synthesis and glycogen storage and muscle strength -- and, it does not make the muscle or muscle groups it is applied to look retarded :)

So, without further adieu, let’s talk about how we have made localized muscle growth a reality.


Actives – 1-test and 4-AD

1-testosterone is without a doubt the most powerful muscle building substance in the history of bodybuilding supplementation. With its discovery, the gap between legal supplements and "real gear" was closed overnight -- in fact, unless the term "real gear" necessitates that a product be illegal or injecting into one's ass, 1-test is "real gear". It is a legal anabolic steroid, found to be 700+% more myotrophic than testosterone in the classic rat levator ani assay, used to determine the anabolic potency of pretty much every androgen ever created. You get enough in the muscle cell, and you will grow.

4-AD, to its credit, has been found to be 80-90% as anabolic and 120% as androgenic vs. testosterone, when injected into rats. How much of this is from the inherent activity at the AR one would expect from a 17beta-diol and how much is from its conversion to testosterone is anyone’s guess, but it is also pretty much irrelevant. It will also provide some estrogen, which will potentiate androgen action via upregulation of the receptor, as well as promote glycogen storage.


Androgen Signaling

Androgens exert much of their effects locally, at the cell level, be it in muscle, fat, the brain, liver, etc. They are taken up by the cells in those tissues, they bind to the AR in those cells, and subsequently cause direct activation transcription, thus protein synthesis, glycogen storage, etc., within those cells (12956285).

IOW, high androgen concentrations (and binding), in a cell in the muscle, does not cause promote signal transduction in the hypothalamus and vice versa.

That is pretty straightforward and basic, but it tells us that if we could get high concentrations in one tissue over the other, we could achieve a stronger effect in that tissue over the other (all else being equal).

This is a very good thing, in regard to Sytenhance, for a number of reasons. First, as you probably know, the negative feedback inhibition on the HPTA (which shuts down natural testosterone production), which normally occurs with androgen administration, is primarily manifested in the hypothalamus, via the androgen itself, and through estrogen, if using an aromatizing steroid. Androgens are also directly suppressive to steroidogenesis at the testicular level.

Thus, if we localize delivery of our androgen to peripheral tissues such as muscle and adipose, that negative feedback signal will not be sent in the hypothalamus and testes. IOW, we get the increased protein synthesis and faster recovery/repair from workouts – i.e. greater muscle growth -- increased glycogen storage (for those hurts so good pumps), and the increased strength that come with larger muscle cross sectional area and androgen facilitation of neural firing – and, we get it all, while still keeping our balls at an aesthetically acceptable size and still producing testosterone.

It will also avoid increases in irritability and the manifestations of “roid rage” episodes, if you are among those who are prone, as well as limiting the likelihood of addiction and post-cycle depression.

A couple other well-known side effects of androgen use are acne and hair loss – again, it will eliminate these, other than in the area of application, in regard to acne.

And, not only will it prove advantageous on all of these levels, during the cycle, it will allow for much longer cycles, without fear of permanent damage to the HPTA. Cholesterol uptake and steroidogenesis occurs locally, in a multitude of tissues, including muscle, in addition to the testis, so I would not advise a permanent cycle, as androgens downregulate this process, via HDL depletion (10706582, 11387942) (estrogens upregulate it, via the HDL-R (12021179), so the 4-AD should mitigate it some), but 16-24 week cycles probably would not be unreasonable or irresponsible.

Androgens are metabolized locally, in basically all tissues (intestines, liver, testes, blood, brain, muscle, etc.) -- both Phase I and Phase II metabolism takes place (12406645, 5547266, 7011411), so with oral use, your active basically has to run the gauntlet, rendering most of it inactive, before it ever reaches the muscle fiber and starts producing muscle growth. With topical delivery, we just have to make it through the skin, which has relatively low concentrations of metabolizing enzymes, thus we get more where we want it, in addition to much less, where we do not.

The delivered active will not stick around in the muscle, forever, even with the proper carrier, but this local metabolism means by the time the steroids are finally taken up by the blood, and delivered systemically, most of it has been metabolized to inactive compounds, which would be excreted, thus it would not activate negative feedback in the hypothalamus and testes.


Androgens and SubQ adipose

As a bit of an aside, androgen are also quite ant-lipogenic in adipose, downregulating LPL and inhibiting preadipocyte differentiation, as well as upregulating beta receptor expression and HSL/PKA, for increased lipolysis (10997611, 8384992), as well as decreasing triglyceride uptake (8697064), so one might see some localized fat loss as well.

As to getting higher concentrations in one tissue versus the other, that is all about delivery.



Percutaneous Delivery

Though the terms are often used interchangeably in the literature, there are two distinct forms of drug delivery through the skin. The first, and most common, is "Transdermal Delivery" -- this involves a drug bypassing the skin barrier in order to be taken up into the bloodstream and distributed systemically (9363373).

The second is "Percutaneous Delivery" (9363373)-- with this method, one bypasses the skin barrier, but with the purpose of delivering the drug to specific local target tissue, while AVOIDING uptake into the blood and subsequent systemic delivery. So, how do we do this?

So, how do we do this?? You first need to know a bit about the structure of the skin barrier, as unfortunately, it is easier said the done -- the skin is “designed” specifically to prevent these type of things and does so in a rather ingenious way. Basically, the skin is made up of both lipid and aqueous layers, with the former preventing the diffusion of hydrophilic subsyances and the latter blocking lipophillic ones. Our active is lipophillic, so that is the aspect we will address.

The first barrier for entry into the skin is the stratum corneum (SC), with transport occurring primarily through the intracellular regions (9363373). These regions are made up highly ordered lipid bilayers, composed of various (non-polar) lipids -- ceramides, cholesterol, fatty acids, and triglycerides (8818988) -- stacked on top of each other, each bilayer separated from the others by a very thin water sheet associated with the lipid's polar head (9297687).

Diffusion through this area is hindered by hydrogen bonding, making polar (hydrophilic) substances particularly resistant to penetration. Conversely, it offers relatively little resistance to fairly non-polar (lipophilic) compounds (2886623). It has been suggested that a partition coefficient (Log P) of around 3 is ideal for penetration of skin (4550859). That is right about what androgens are, thus the SC is not our concern.

Below the SC is the viable epidermis and the dermis. Because of its aqueous, hydrophilic nature, this region provides substantial resistance to the diffusion of lipophilic compounds (28395, 5046096) and is perhaps even the rate-limiting step in their transport (7494819, 8008702). Nestled nicely in this hydrophilic region is what is known as the dermal miscovasculature.

Typically, drugs that penetrate the skin barrier and traverse the epidermis and dermis are rapidly taken up by the dermal microvasculature, where they are delivered systemically (just like with orals) -- this is well characterized in the literature (9363373, 8301551, 9120805) -- with direct tissue penetration being limited to 1-4 mm, which obviously is not exactly deep into the muscle tissue.

With hydrophilics, this is due to their preference for diffusion into the hydrophilic plasma over the lipophillic adipose tissue. With our lipophillic androgen, this is due to the androgen getting stuck in the dermis, where the vasculature can take it up at its leisure (the phosholipid membranes of the vasculature are quite inviting to the androgen), thus it never makes it to deeper tissues.


Targeted Delivery

So, how do we traverse the SC, but also avoid getting stuck in the dermis? The answer is to place your active in an amphiphillic carrier, which will be equally at home diffusing through the lipid layers of the SC and the aqueous layers of the dermis. This will allow the active to be sped past the dermal miscrovasculature, into deeper tissues, such as our target, the muscle.

This has been done successfully in the literature with antibiotics, anti-fungals, and NSAIDS. And, this is exactly what we have done with Sytenhance.

While we have made it clear that it is quite possible to achieve targeted delivery, if we cannot get adequate amounts of our substance past the skin barrier, it is a mute point.


Penetration Enhancement

I have previously written in great depth about penetration enhancement from a qualitative perspective, in regard to our now defunct transdermals. Sytenhance is not a transdermal supplement, as it is delivered locally, making it a cosmetic, but the penetration enhancement complex is the same, so the expected efficacy should be about the same.

If you have not read the article “Battle of the Transdermal Prohormones”, you should do so now, and if it has been awhile, you should read it again, as it will help in understanding what is to follow (which also is based on an article for our defunct transdermals, so you will note the mention of “ONE+”).

The multiple components used in the formulation, however, make it difficult to quantify precisely -- i.e. give a % absorption -- so, I have previously given an estimate based on feedback in comparison to other products, but such data is obviously not obtained under experimental conditions, and the bioavailability of the other products are estimates as well, so an exact number is certainly not possible through that method, thus I have been a bit conservative in said estimate.

Today, I am going to look more closely at the data, from a quantitative perspective, and analyze that, along with the afore mentioned feedback comparisons, in order to hopefully justify a more brash estimate.

Each ingredient in our formulation addresses a different mechanism -- with the possible exception of octyl salicylate, whose mechanism has not been explored, but which had data far too good to leave out -- and, there is nothing in the literature showing multiple compounds to hinder absorption, assuming the compounds are efficacious individually, but there is a great deal of data showing multiple compounds to synergistically improve uptake (1,2). Thus, I think we can get a decent idea of the whole looking at the individual parts. So, here goes.

Androgens dissolved in a volatile solvent (ethanol, acetone, isopropanol) at relevant concentrations should get about a 5% absorption rate over 24 hours (3), so that is our starting point. I am well aware that another company claimed that their androgen in isopropyl alcohol concoction gets about 50% delivery or something, but that is just as absurd as their oral that they claim gets close to 100% (which they also claim to somehow have improved by 30%) – but, that is nonsense, to put it nicely.

The first ingredient we will look at is octyl salycilate (4). This was found to result in a SIX FOLD higher flux for testosterone than an ethanol only vehicle. Can we thus claim 30% based on that?? Let's look at the study more closely. The study utilized a topical spray, using finite dosing techinique, thus simulating real world usage. The concentration of the vehicle was 5uL/cm2. A normal application area for a 200 lb person is about 2000 cm2, which equates to a total a 10ml -- a dose of ONE+ is about 8ml, so we are quite close here. The concentration of testosterone was 120mg/ml, which is higher than the 50mg/ml we use -- increasing the concentration would increase the total flux, but would decrease the efficiency, because it would overwhelm the rate-limiting step.

Total flux in 24 hours was found to be 107ug/cm2, which would equate to 214mg of androgen delivered. This is 18% of a 1200mg dose. Using the same method, the volatile solvent only vehicle achieved a mere 3%, compared to 5%, at lower drug concentrations, which would bring the 18% number to 30%. However, the octyl salicylate may have had a greater effect at greater drug concentrations, so we will go half-way in between. This takes our estimated bioavailability to 24%

There are a couple of other variables that must be considered. First, the study used snake skin, not human skin, but the water permeability coefficient was within the acceptance range for human skin, and snake skin is considered as providing a good model (5). Second, the skin used was not viable, thus cutaneous metabolism did not occur, while it would in humans. However, such reactions favor the formation of more potent androgens (androstenediol to testosterone and testosterone to DHT -- and 5-alpha reductase, does not affect the already reduced 1-test, anyway). In addition, such metabolism has been estimated at only 1-2% for non-scrotal skin (6), so this is a non-issue.

Finally, the dose was studied over 24 hours, when real world usage is every 12. The effeciency of the second dose would not be as high, due to saturation of the stratum corneum and epidermis, which would lower its diffussion gradient. However, it would increase the efficiency of the first dose, since it would increase its diffussion gradient -- so, they would cancel out to some extent. We will estimate that we lose 25% efficiency from this, thus we are left at 18%.

Next we will look at d-limonene. In a study using butylparaben (7), which has a partition coefficient almost identical to testosterone (LogP 3.5 vs. LogP 3.3), thus providing an excellent model, d-limonene was found to increase the amount of drug reaching the receptor by 20%, using a concentration similar to that in our formulation. Guinea pig skin was used in this study, and while the permeation of drugs through human skin is lower overall, the mechanisms are the same, thus the enhancement ratio would be expected to hold. Thus, we have taken our bioavailability to about 22%.

Next are our fatty acids, oleic and linoleic. In human skin, saturating amounts of linoleic acid were found to increase flux of testosterone by 15-fold vs. 50% ethanol/50% saline (E/S) (8). This is one that needs to be examined more closely. First, it did not use finite dosing model, thus lipid extraction could occur, which is not likely with a thin layer.

We will look at the ethanol vs. real world for a comparison to get an idea of how much lipid extraction was a contributor. The flux in this study was 8ug/cm2 vs. 16ug/cm2 in the octyl salicilate study we looked at earlier. However, concentration in this study was 6.4mg/ml vs. 120mg/ml in that study, and flux is proportional to concentration, so that must be taken into account, leaving us with 9.4 fold greater flux in this study.

But, as we have mentioned, efficiency decreases as concentration increases, -- 6.4mg/ml is likely to result in concentrations well below the capacity of the rate limiting step, so we will just use our 40% figure from the octyl salicylate study. Thus, 9.4 goes to 6.8. It is unlikely that the oleic acid would have caused lipid extraction above and beyond what ethanol did, as it apparently caused a great deal. Thus, we are left with a 2.2 fold enhancement from the fatty acids.

The concentration of linoleic acid used is not given, but given its likely solubility in the solution and the solubility increase it provided for the drug, it is likely quite similar to the amount of the combination of linoleic and oleic acid in our formulation. Because of the presence of 2 double bonds rather than 1, linoleic acid might be superior to oleic acid in disrupting the lipid bilayer of the stratum corneum (9). However, it has also been shown that a combination of fatty acids are superior to the individual constituents (10), so the two factors probably cancel out to some extent. We will consider the oleic acid as being half as effective, thus 2.2 becomes 1.6. Thus, 22% goes to our final of 35%.

This is all assuming ideal conditions -- clean, well scrubbed, hairless skin and a fairly large area of application -- on the order of 2000 cm2 (which would be the abdomen, chest, and lower back for a 6' 200 pound person).


Editors Note: Sytenhance will utilize a smaller surface are than is used with transdermal administration, but it will be a smaller dosage, as well, so the concentration to surface are will remain about the same, so the efficacy numbers should as well.

It should, of course, be noted, that while I am quite confident in my ability to speculate/extrapolate based on a great deal of indirect data, and my previous attempts have been quite fruitful (see the feedback on all of the other products I designed :), there really is a TON of speculation going on here, so there is room for error. However, we do have a bit more evidence in the form of real world feedback comparisons:


Real World Feedback

Oral 4-AD, even at doses of 3 grams/day does not equal the gains seen on full dosing of 4-ADerm (667mg/day), in addition oral usage should decrease SHBG by 50% or so (13) -- thus, given 5% bioavailability for high dose oral, we have 22.5+% mutliplied by 1.5 (for increased free androgen ratio with orals), giving us at least 34%.

Oral 1-Test requires 400-600 mg for results comparable to 200mg of ONE -- given 15% oral (see below), that is 30-45% for ONE.

Given that not everyone applies the product ideally in the real world, the slightly lower figures provide good support for the estimates based on the studies with ideal conditions.

The only way to be 100% confident in any number will be to have a study done on our actual product, and this is something that we certainly plan to do in the, hopefully, not too distant future. But, until then, I do offer 30-40% with confidence.

Supplement Facts
Serving Size: 1 Pump (1.75-3.5ml)
Servings Per Container: 35
Amount Per Serving:
4-Androstenediol / 1-Testosterone Complex: 170mg




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