Anabolic steroids, bodybuilding discussion forums. - Steroidology

 

(Forum for members to discuss the use of anabolic steroids)

Results 1 to 18 of 18
  1. #1
    I am banned! Drveejay11's Avatar
    Join Date
    Jan 2003
    Posts
    4,857
    Rep Power
    0
    Thumbs up The SCIENCE of Topical Fat Loss
    Written by Par Deus

    Introduction

    I have previously stated that I believe transdermal prohormones to be the most effective supplements ever to hit the market. That statement must now be amended. Transdermal prohormones are indeed the most effective MUSCLE BUILDING supplements ever to hit the market. But, topical fat loss products have the potential to be an even bigger overall breakthrough in the never ending quest to improve body composition.

    There are four areas that need to be addressed in regards to topical fat loss products and so called "spot reducers" in general.

    First, one needs to distinguish between the products that are merely diuretics and those that the manufacturer (assuming they have a brain) actually thinks might significantly reduce body fat.

    Second, we have to have an understanding of the andrenergic system, which is primarily what these products attempt to manipulate in order to aid lipolysis.

    Third, we must have an understanding of transdermal/percutaneous delivery, in order to understand why a topical formulation could present advantages vs. orals, as well as to understand why nearly every product on the market fails miserably. Within this category there are two issues -- getting adequate amounts past the skin barrier and localizing its distribution to adipose tissue.

    And, finally, there is the issue of Yohimbine HCl vs. yohimbe.

    After reading this, you should have an understanding of why true "spot reduction" is physiologically quite possible, as well as enough information to make an informed decision as to which products can and cannot accomplish it.


    Fat Loss Agents vs. Diuretics

    Assuming we are not preparing for a photoshoot or competition, a product that merely acts as a diuretic rather than significantly aiding actual lipolysis is not what we want. "Cutting Gel" and "Dermalin-APg" belong in this category -- their active ingredient is aminophylline:

    Aminophylline is a xanthine derivative, similar to caffeine, which, as we know, is not a particularly potent fat burner on its own. In rat studies, it has shown good thermogenic properties due to blockade of adenosine receptors (which provide one of the negative feedback mechanisms for catecholamine induced thermogenesis) and inhibition of phosphodiesterase (which degrade cyclic AMP) -- but this is at extremely high doses, which would kill a human, so it is not applicable (1,2). At therapeutic doses, only adenosine blockade occurs, which will act to increase norepinephrine levels (3)-- but as you will see, norepinephrine stimulates alpha 2 receptors (bad) in addition to beta 2 receptors (good) -- and in stubborn fat, alpha 2's outnumber beta 2's (4).

    Like caffeine, aminophylline IS a good diuretic (5), which would account for the girth loss in the studies they reference, which did not measure actual fat loss (6,7). One study did look at fat depth after use of an aminophylline cream, and no difference was found vs. control (8). As a local diuretic, it is likely effective, but as a true fat loss agent, it quite likely is not. Such products WILL make you look more cut while you are taking them, but the true test of their efficacy is a week or two after you have stopped.

    Products such as Avant Lab's LipoDerm-Y, Impact's DermaLean, SAN's LipoBurn, and Yohimburn -- basically any of the products with yohimbine and a handful of other ingredients -- fall into the latter category. They are intended to manipulate the adrenergic system, thus such products could cause true localized fat loss if formulated properly (and since yohimbine tends to make you HOLD water, their true test is also a week or two after you have stopped).


    THE ADRENERGIC SYSTEM

    Introduction

    One of the major contributors to body weight homeostasis in the human body is the adrenergic system. There are two types of adrenergic receptors, alpha and beta, as well as subtypes of each -- and depending on which are activated, lipolysis (breakdown of fat) can be either stimulated or inhibited.

    The most well-known adrenoreceptors to bodybuilders are the beta receptors. These can be divided into subtypes 1, 2, and 3 -- and it is through these receptors that drugs such as the ephedrine/caffeine stack and Clenbuterol exert their effects. While Clenbuterol acts directly on beta 2 receptors, ephedrine exerts its effects indirectly by stimulating the release of norepinephrine (NE), the body's primary endogenous thermogenic hormone. Unlike Clenbuterol, NE is not selective in its binding. In addition to binding to the beta 2 receptor, it also binds to both alpha receptors, as well as the beta 1 and 3 receptors. It is in regards to its binding to the alpha 2 receptor that yohimbine comes into play.

    Norepinephrine and Yohimbine

    Activation of the alpha 2 receptor inhibits the release of NE. Thus, by binding to this receptor, NE functions as its own negative feedback signal. In other words, it shuts off its own release. Obviously, this is not a good thing for fat loss. This is particularly true at rest (which, unless you are a marathon runner is 95% of your day) -- this is because alpha 2 receptors are activated at lower catecholamine levels than are the beta receptors (9). Thus, thermogenesis is basically always turned off, particularly in areas with high alpha 2 densities.

    There are regional differences in the distribution of alpha 2 and the beta receptors as well as gender differences -- this is what is responsible for the observed variations in bodyfat storage patterns(4). Basically, females tend to have a large number of alpha 2 receptors and few beta receptors in the gluteofemoral area (hips, thighs, and butt), while men have the same problem in the midsection. With exercise or the use of compounds such as the ephedrine/caffeine stack, catecholamine levels can be increased to a point where the alpha 2 induced inhibition of lipolysis is partially overcome (9). However, even then, the alpha 2 receptors ARE still acting to reduce lipolysis.

    Yohimbine is a selective alpha 2 antagonist (10) and can thus short circuit this feedback loop, maximizing NE levels, thus maximizing fat loss, particularly in these problem areas -- and even more so if we can achieve high levels of yohimbine and NE in the adipose tissue. Unfortunately, to do so with orals, or any other method that results in high blood levels, means that we will also have high levels in the heart and CNS -- thus, we will also have unpleasant and dangerous side effects such as tachycardia, high blood pressure, and anxiety. Considering the subject of this article, I obviously believe the solution lies in transdermal administration -- but more on that in a bit.

    Blood Flow

    A second, more indirect, mechanism by which Yohimbine can aid lipolysis via the adrenergic system is by increasing peripheral blood flow (11, 12). Adipose tissue is known to have rather poor vascularity. When triglycerides are broken down into free fatty acids and glycerol during lipolysis, they must also be transported away from the fat cell or they risk being reincorporated into adipose tissue. Beta receptor activation causes vasodilation, thus increasing blood flow, however, it does not increase enough to remove all of the free fatty acids released during lipolysis (13). Alpha 1 and 2 receptor activation, on the other hand, causes a decrease in blood flow (4, 14). Thus, antagonism of the alpha 2 receptor with yohimbine would be expected to increase blood flow, and thus increase the mobilization and disposal of these FFA's, further aiding fat loss. And, again, the more we can get in the adipose tissue without it reaching the heart and CNS, the better.


    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 (15). This basically does the same thing as oral delivery, but it is inherently time released and avoids first pass metabolism in the liver which can limit bioavailability and cause hepatotoxicity, so it is advantageous for delivering many drugs.

    The second is "Percutaneous Delivery" (15)-- with this method, one bypasses the skin barrier, but with the purpose of delivering the drug to specific target tissues in the body, while AVOIDING uptake into the blood and subsequent systemic delivery. In the pharmaceutical realm, this has been pursued primarily for antibiotics and NSAIDS -- the former, to avoid destruction of systemic microflora (so-called "good bacteria"), and the latter to avoid hepatic recirculation, which is responsible for gastrointestinal problems.

    Unfortunately, those who have developed most of the topical fat loss products thus far either do not know about or understand this difference, or they do not understand its PARAMOUNT importance in regards to adrenergic modulators such as yohimbine. With prohormones, systemic uptake and distribution is our goal -- they have poor oral bioavailability, so we are just trying to avoid the liver in order to get significant amounts in the bloodstream. However, with yohimbine and other adrenergic agents, oral bioavailabilty is not the issue -- at about 22%, it is more than adequate (16). We can readily achieve adequate blood levels with oral usage.

    The issue with adrenergic modulators is that as we increase dosages (and thus blood levels) in order to increase distribution to adipose tissue to aid fat burning, we also increase distribution to the heart and CNS where we create numerous unwanted side effects such as rapid heart rate, high blood pressure, and overstimulation -- which become particularly noticeable with exercise. In addition, yohimbine is used clinically to produce anxiety (17). Ideally, we want our drug to reach fat cells in high concentrations, without the dangerous side effects of high levels in the heart and central nervous system, and this WILL NOT happen with typical transdermal delivery.

    So, how do we do this?? Unfortunately, it is easier said the done. 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 very well characterized in the literature (15,18,19) -- with direct tissue penetration being limited to 1-4 mm, which obviously is not exactly deep into the adipose tissue.

    Let me repeat, if nothing is done to bypass the dermal microvasculature, our drug enters systemic circulation before it ever reaches the adipose tissue.

    And, considering that these substances have good oral bioavailability, if the dermal microvasculature is not taken into account, we end up with a product that not only does not localize delivery, it does not even deliver it systemically as efficiently as an oral would do. Considering these products cost far more than there oral counterparts, and could also be thought of as inconvenient in that you have to rub them on your body, wait for them to dry, etc., any supplement developer who does not take dermal uptake into account has obviously missed the boat quite badly. And, guess what... There is only one product that does. And guess what else -- it will likely stay that way because a use patent has been filed on the one carrier that has been shown in the literature to effectively accomplish this.


    Targeted Delivery

    Let's now take a look at the literature that supports the idea of tissue specific delivery of therapeutic substances. As mentioned previously, when it comes to targeted delivery, the pharmaceutical realm, and thus the literature, has primarily concerned itself with antibiotics/anti-fungals and NSAIDS. We will look at the three most important ones.

    The first study (19b) involved the NSAID indomethacin as the drug to be delivered. The drug was given orally (O) , topically without the "special delivery solvent" (WO), and with the "special delivery solvent" (W). The topicals were applied to the shoulder. For the first two hours after administration, concentrations of the drug in the deltoid (which is obviously even deeper than adipose tissue) were 5 times higher in W than in either O or WO. After 4 hours, it was 3 times as high, and by 8 hours it was still twice as high. Obviously, the formulation containing the "special delivery solvent" was vastly superior at delivering the drug to the target tissue. But what about delivery to unwanted tissues? If it was just a case of the "special delivery solvent" allowing more drug to cross the skin, this would not be a big deal -- we could just use more. What we also need is for a minimal amount of the drug to be delivered systemically, and once again, the "special delivery solvent" was shown to be superior. Maximal blood levels of all three compounds occurred at the 2 hour mark. W displayed levels about 1/3 that of O and 1/2 that of WO.

    If the significance of this is not clear, it basically means that localized delivery (what we want) per unit systemic delivery (what we don't want) for W was 15 times that of O and 10 times that of WO -- and this was to the muscle. Considering the adipose tissue is closer to the skin (which had levels 10 times as high as the muscle) and that the joint capsule (which is below the muscle) had levels 1/3 that of the muscle while with WO there were equal levels at the muscle and joint, the ratio of delivery to adipose tissue vs. systemic delivery for W is likely quite a bit higher -- somewhere between 10 and 100 to 1.

    The second study (19c) utilized the antibiotic erythromycin as the delivery drug. Formulations for W and WO were identical to the above study. Oral administration was not tested. Exact counts of the concentration in muscle tissue was not reported, but the authors stated that after 4 hours, there was a major increase in the muscle mass below the site of application. Kidney and liver levels (indicative of systemic distribution) were significantly lower for W than WO -- about 1/2 for the former and 1/4 for the latter over 24 hours.

    The third study (19d) we will look at utilized the antifungal griseofulvin as the delivery drug and compared W with oral intake. The formulation for W was the same as the previous two studies. The accumulation of the active compound in the area of application for W was several HUNDREDFOLD greater than that which accumulated in the organs, and brain levels were non-detectable, which is extremely important considering we are trying to avoid excessive CNS stimulation -- and all of this was a full four days after application. Compare this to oral delivery which showed concentrations that were approximately identical in all areas (which would be expected if systemic uptake occurred).


    Penetration Enhancement

    I think it should be clear from the previous studies that it IS possible to achieve targeted delivery if the proper carrier is employed. However, if we cannot get adequate amounts of our substance past the skin barrier, it is a mute point. And, considering one of the skin's primary purposes is as a water barrier (20), hydrophilic substances such as yohimbine do not readily pass through (21, 22,23). Thus, we need to turn to the topic of penetration enhancement (for a more thorough presentation, see my previous article Transdermal Delivery.

    Yohimbine HCl, with a LogP of about .75 (24), is fairly polar/hydrophilic, thus penetration enhancers should be chosen accordingly -- namely we want those which affect the polar route. This rules out many commonly employed penetration enhancers -- a fact many companies do not seem to be aware of. Since there is very little direct data on penetration enhancement with Yohimbine HCl, we will look at data when substances with similar physical properties were used.

    One promising chemical in this area is the monoterpene, l-menthol. Polar molecules undergo significant hydrogen bonding in the stratum corneum, which is the primary reason for their poor passage through the skin barrier (23). Because of the presence of a hydroxyl (OH) group, l-menthol would be expected to bond to these hydrogens (25), leaving our drug free to more easily traverse the skin barrier. And, indeed the data has supported this. It increased the permeability coefficient of mannitol 100 fold vs. control (26). In a study using Propranolol HCl which has a partition coefficient almost identical to yohimbine (Log P .74 vs. .75), it increased flux 1000 fold vs. control and also displayed the shortest lag time of all terpenes tested (25). This is in contrast to fellow monoterpene d-limonene (almost identical, structurally, to l-menthol, with the exception of lacking the afore mentioned hydroxyl group) which has been shown to be much less effective for polar compounds (25, 27).

    A second chemical is laurocapram. It too has been shown to be quite successful with polar drugs (23,28,29), likely due to its increasing the water content of the lipid phase of the stratum corneum. In one study, it enhanced the flux of mannitol in a propylene glycol vehicle by over 350 fold (23). In another, it enhance 5-fluorouracil delivery by 100 fold (29). Unfortunately, it displays a significant lag time -- meaning it can take as much as 10 hours before it starts to work (30, 31, 32). Consider most of us shower daily, this is not acceptable.

    That brings us to n-methyl-2-pyrrolidinone (NMP). In combination with laurocapram, in a study using morphine hydrochloride, which has physical properties similar to Yohimbine Hydrochloride -- both polar molecules, molecular weight of 322 vs. 390 -- and is thus quite applicable, NMP was shown to significantly reduce the lag time (down to as low as 2 hours) as well as increase the rate of penetration for the drug as indicated by blood levels that were several THOUSANDFOLD higher than controls (32). In addition, it has been shown in several other studies to enhance penetration of polar molecules on its own, including a 256 fold increase with mannitol (23).

    Another good candidate is glycerol, which provides dual functions. First, it helps to counter any skin irritation that might be caused by the alcohol carriers. This is due to its increasing the water content of the skin, and as alluded to in regards to laurocapram, this increase in water content has the added bonus of increasing penetration for polar molecules such as yohimbine (33, 34).

    Other substances that are likely to be effective include various other pyrrolidones and derivatives (23, 35, 36), terpenes with hydroxyl groups, such as geraniol, 1,8 cineole, nerolidol (37, 38, 39) and Azone derivatives (40, 41).


    Yohimbine vs. Yohimbe

    Quite a bit of confusion seems to exist about the difference between Yohimbine and yohimbe. Yohimbine is the principal alkaloid from the herb P. yohimbe. However, there are 31 other yohimbane alkaloids that can be present in herbal yohimbe preparations. Some of these have different and unknown selectivities and potencies (and thus, effects) at the adrenergic receptors (42, 43) -- in addition, these preparations vary greatly from brand to brand and even from batch to batch, as no standardization for extraction exists. In fact, a recent investigation found that most over the counter preparations have little to no actual yohimbine (44). And, even in the more potent preparations, most people find a higher degree of undesirable effects with the herb vs. pure Yohimbine (due to the afore mentioned 31 other yohimbane alkaloids that can be present). So, make sure and go a product that contains pure, pharmaceutical grade Yohimbine HCl, which will avoid the added side effects from other alkaloids - thus, allowing safer, more reliable dosing.


    Dosing

    Because some people are unusually sensitive to yohimbine, I would recommend that one start with a small dose -- 25-50 mg and then increase the dosage by 25-50mg each day until side effects become unacceptable. Dividing it into two doses would be ideal, but probably not necessary. Assuming the product is formulated properly, and delivery is localized to the adipose tissue, most people will be able to safely use very high doses -- 300+ mg/day.

    Another thing to be considered when using yohimbine is that insulin blunts its lipolytic effects. Because yohimbine is not reaching the pancreas in significant amounts as it would with oral administration, insulin levels will not be as high for a given amount of carbohydrates, but they will still be elevated. Thus, it should ideally be used on a low-carb/ketogenic diet, or at the very least, one should do moderate aerobic activity for an extended period first thing in the morning on an empty stomach.


    CONCLUSION

    I think it should now be exceedingly clear that true "spot reduction" of bodyfat is indeed possible -- but it should also be clear that not all topical fat loss products are created equal. And, you should now be equipped to make an informed decision on which one to use.

    To sum up:

    The formulation should contain active ingredients that are significantly lipolytic rather than mere diuretics -- this rules out the aminophylline only products.

    The formulation should use yohimbine hydrochloride rather than the yohimbe herb. Make sure the ingredients state "yohimbine HYDROCHLORIDE or HCl" not just "yohimbine".

    The formulation must not only include penetration enhancers, but they must be appropriate for polar a molecule. Ask the company what penetration enhancers are employed, and ask them to provide references where they were shown to be effective with polar/hydrophilic compounds.

    And finally, and most importantly, the formulation MUST avoid uptake by the dermal microvasculature, or it will merely be an expensive, inefficient version of a pill. Let me repeat: "The formulation MUST avoid uptake by the dermal microvasculature, or it will merely be an expensive, inefficient version of a pill." Say it with me this time: "The formulation MUST avoid uptake by the dermal microvasculature, or it will merely be an expensive, inefficient version of a pill." Ask the company what they have done with their formulation to account for this uptake, and ask them to provide references.

  2. #2
    A Legend bleachcola's Avatar
    Join Date
    Jan 2004
    Location
    Middle Tennessee
    Posts
    31,641
    Rep Power
    17
    Excellent post. And good timing with spring break right around the corner.

  3. #3
    I am banned! Drveejay11's Avatar
    Join Date
    Jan 2003
    Posts
    4,857
    Rep Power
    0
    Originally posted by bleachcola
    Excellent post. And good timing with spring break right around the corner.
    I hear ya----I need it too! Winter killed me this year!

  4. #4
    tee
    tee is offline
    old...old man tee's Avatar
    Join Date
    Jun 2003
    Posts
    1,943
    Rep Power
    12
    Just hang out with fat friends so you'll look good! Thanks for the informational post Doc!

  5. #5
    Novice
    Join Date
    Oct 2003
    Posts
    52
    Rep Power
    12
    still skeptical of topical fat burner...are there any products that you would reccomend ???

    has anyone had good experiences with any particular brands??

  6. #6
    Junior Bodybuilder
    Join Date
    Jan 2004
    Posts
    156
    Rep Power
    11
    I really liked the way that Avant's Absolved and Lipoderm-Y worked.

  7. #7
    Suspended
    Join Date
    Sep 2003
    Posts
    332
    Rep Power
    12
    Yeah i too am skeptical. The only non-oral fat burner I can imagine working would be one that is injected directly into the fat of the problem area.

  8. #8
    Junior Bodybuilder
    Join Date
    Dec 2003
    Posts
    293
    Rep Power
    11
    Awesome information Dr. Vee..... I'm going to be e-mailing you a few questions, maybe a million, as my show approaches. You guys keep feaking me out with all this information.
    EZ & friends, skeptical or not, don't make decisions based on assumptions. You'll miss out, I remember when GHB was at GNC. No one was interested in it. Over a month ago I was told that PGH was bull shit. Try things. I've noticed that sometimes you have to read between the lines. Maybe the topical fat loss may not work, but maybe it will.
    Its like universal kits PGH. It's for injection. Right into the stomach. Yet all the experts, "except the mods", misinformed about that for weeks. Everyone thought it was another oral GH product. Well, it is, technically. No what I mean? Just try new things.... you may be right, but too often we miss out. Ther are a lot of guys trying to help bodybuilders not break the law. Like this board. Good luck.

  9. #9
    Suspended
    Join Date
    Sep 2003
    Posts
    332
    Rep Power
    12
    On the P-GH(I really should put up a seperate post about this).

    That shit is a trip! When I go to sleep I have hardons all through the night. I had 2 wet dreams last night and woke up and took all that dream shit out on my wife.
    I'm off everything and it could be my hpta is hitting back full swing but it runs parallel with the P-GH. It has also greatly helped my sleep.
    In a few days I'm getting bloodwork done again and will see what has changed in the hormone department.
    I definately have an increased libido that's been pretty raging lately.
    I don't know if that's the P-GH but it's weird..For you guys who have been crashed out; you know the feeling of not thinking about ass...then you conciously DON'T THINK about it...one day you're just aware you been noticing chicks quite abit more and daydreaming of screwing....next thing you know you're spending a little too much time at the XXX section of this board....been asking the wife to get off work early.....sticking your finger in her but while she's sleeping....hell the damn avatars even got ya stopping on threads longer....THEN IT HITS you I must have my hpta back and damned if the old nuts aren't swole up nice and plump.

    Well all this shit happened to me 2 days after the p-gh and last night was the most intense.
    Anyhow I know about trying shit.....See I got the opposite problem i'm always labratting it! I was the fucking kid who bought the x-ray glasses outta the back of the comic book(and had my own sea monkeys breedin! I figured the first pair of specs must've been defective...

  10. #10
    Junior Bodybuilder
    Join Date
    Dec 2003
    Posts
    293
    Rep Power
    11
    bump

  11. #11
    Junior Bodybuilder quesudo's Avatar
    Join Date
    Jun 2004
    Location
    Wellington, FL
    Posts
    150
    Rep Power
    11
    Thanks a lot for the information Dr. you sold me...

  12. #12
    Junior Bodybuilder jrwinny32's Avatar
    Join Date
    Mar 2004
    Location
    NEW YORK CITY
    Posts
    276
    Rep Power
    11
    Quote Originally Posted by crazyscrot
    still skeptical of topical fat burner...are there any products that you would reccomend ???

    has anyone had good experiences with any particular brands??
    I know this thread is old but I recently purchased Skulpt by Ergopharm and Im seeing good results.

  13. #13
    Gettin Swole Swoleburn's Avatar
    Join Date
    May 2003
    Location
    Nunya Biznis
    Posts
    950
    Rep Power
    12
    Is there a Specific product or company that you suggest. And where in the hell can I get it???????????????? LOL

  14. #14
    vikram845
    Guest
    best whey protein .. PH5(Pharma whey) or UBS - wHEY PROTEIN any suggestions ?

  15. #15
    Novice
    Join Date
    Feb 2013
    Posts
    105
    Rep Power
    2
    nice post

  16. #16
    Novice
    Join Date
    Jan 2013
    Location
    Oregon
    Posts
    71
    Rep Power
    2
    Dunno but is there an injectable that actually destroys the fat cell?

    I know a company in England is working on one using dead fat cells to trigger an immune response. Expect FDA trial in the next year I've heard.

    It's called "biological liposuction".

    In the meantime, for those who pin... does anything work?

    Peace!

  17. #17
    Amateur Bodybuilder MattyIce's Avatar
    Join Date
    Oct 2012
    Location
    South
    Posts
    739
    Rep Power
    3
    Quote Originally Posted by AudioMaker View Post
    Dunno but is there an injectable that actually destroys the fat cell?

    I know a company in England is working on one using dead fat cells to trigger an immune response. Expect FDA trial in the next year I've heard.

    It's called "biological liposuction".

    In the meantime, for those who pin... does anything work?

    Peace!
    Mesotherapy - Wikipedia, the free encyclopedia

    I dated a broad who used Meso for like 9mo's or so... the shit actually works. lol

  18. #18
    Novice
    Join Date
    Jan 2013
    Location
    Oregon
    Posts
    71
    Rep Power
    2
    It makes complete sense that it works.

    It's a little surprising that the UGL's haven't picked up the formulas.

    Could be kind of a game changer, or at least an interesting stack addition.

    By the way... my mistake on the company getting "biological liposuction" read for trials. They're in Scotland, not England.


    Cheers!

Thread Information
Users Browsing this Thread

There are currently 1 users browsing this thread. (0 members and 1 guests)

Similar Threads
  1. By house1 in forum Supplement Forum
    Replies: 10
    Last Post: 03-13-2013, 01:43 AM
  2. By adidamps2 in forum Diet Forum
    Replies: 4
    Last Post: 03-25-2007, 06:18 AM
  3. By Bullfx in forum Anabolic Steroid Forum
    Replies: 11
    Last Post: 02-17-2004, 02:58 PM
  4. By RoadHouse in forum Supplement Forum
    Replies: 17
    Last Post: 05-27-2003, 07:14 PM
Tags for this Thread
Bookmarks
Posting Permissions
  • You may not post new threads
  • You may not post replies
  • You may not post attachments
  • You may not edit your posts
  •  
  

3Js Nutrition Network

juicepump











need to build muscle

3Js Nutrition Network



mr supps





health and fitness talk