geoffgarcia
02-26-2004, 10:40 AM
Chris,
LipoDerm-ULTRA 4 oz Bottle $34.99
Containing Yohimbine Hydrochloride in Avant Labs' hydroalcoholic gel, Lipoderm ULTRA activates targeted fat reduction at the site(s) of application, while avoiding the negative side effects associated with systematic distribution. Expanding upon its predecessor's revolutionary formula, LipoDerm-ULTRA utilizes a number of ancillary fat-fighting ingredients that decrease nutrient uptake and insulin sensitivity in the fat cell, while concurrently increasing leptin expression, leptin sensitivity, and other lipolytic signals such as cAMP and norepinephrine, for maximal fat depletion. In addition, this new formula modestly facilitates increased utilization of fatty acids in muscle while sparing glycogen. Lastly, Lipoderm-ULTRA incorporates a local diuretic that neutralizes water retention, making it easier to evaluate progress during use.
In addition to Yohimbine, each bottle of Lipoderm-ULTRA contains:
Lecithin
Sesamin
Caffeine
Octopamine
Synephrine HCl
ALCAR
Ascorbyl Palmitate
Each 4oz bottle contains 30-60 applications
Update -- I have noticed a few posts by people who have not gotten good results with Lipo-Ultra who got extremely good results with Ab-Solved, so I just wanted to mention that this is pretty much expected, especially if your Ab-Solved results carried over to abdominal SubQ fat -- so, if Ab-Solved is a wonder product for you, you will probably do best to stick with that. The vice versa is also generally going to be true (i.e. if Lipo was great for you, Ab-Solved probably will not be (especially for subQ fat), unless you have become stressed, started using chemicals of abuse, or androgens)
The reason is that cortisol induced fat gains and "regular" fat gains are in opposition, to a great extent -- for example, PPAR-gamma agonism increases peripheral subQ fat, while decreasing VAT; sympathetic nervous system stimulation causes subQ fat loss, but contributes to VAT gains; cortisol, itself, is generally lipolytic, overall, in subQ fat (especially peripheral, and in those relatively thin and unstressed, who do not have strong disposition to male pattern fatness) but obviously quite the opposite in VAT.
Then, there will be also be a group of people who will get decent, but not incredible, results from both. because the "opposing" systems are in relative equilibrium
Well, after a year and a half of waiting, the much anticipated follow-up to the groundbreaking LipoDerm has finally arrived. When you do a bit more than just add caffeine to the original formula, such things can happen. But, good things come to those who wait, and I think you will find it well worth it. So, without further adieu, let’s take a look at the science.
LipoDerm-Ultra and LipoDerm-ODB represent a 5-pronged approach to spot reduction:
“Fed state” signaling – as we have learned, if the cell thinks it is starving, it slows down metabolic processes, including lipolysis, thermogenesis, and fatty acid oxidation, as a protective measure against energy depletion and death.
Lipolysis – no matter how high our energy expenditure is, if we are not mobilizing fatty acids, we certainly are not going to get the kind of spot reduction we are looking for.
Beta oxidation – even if we mobilize our fatty acids from triglyceride stores, via increased lipolysis, if they are not metabolized for energy, they will just be redeposited, eventually.
REDOX – metabolic processes such as lipolysis, thermogenesis/uncoupling, and beta oxidation create free radicals which can damage the cell, thus the cell will shut these processes down as a protective measure, if substrate is not provided to neutralize them. LipoDerm Ultra will facilitate fat burning a plenty, thus oxidation products a plenty. In addition, these same substrates, in more moderate amounts, mediate signal transduction involved in fed state signaling. To put it simply, REDOX modulators make the cell function optimally.
Diuresis – It is not as rewarding to have fat melting away, if the same ingredients are causing the retention of water, in their place -- and losing a week of fat loss, because you have to stop usage a week before your contest or shoot, is particularly troublesome. Not only have we eliminated the unsightly water retention, but we have created a formula to actually improve the situation vs. baseline, via 2 different mechanisms, so you will notice an enhanced appearance in a matter of days.
Several ingredients have activity that crosses over into multiple categories, so in order to avoid this write-up becoming overly cumbersome, we will just address the science of each active, and you should be able to figure out where everything fits, if you even care.
Lecithin (Ultra/ODB)
Well known as an emulsifier, in food preparation, lecithin is also often referred to a s a “superfood”, and for good reason. Though we will not be eating it, it will still impart a number of benefits for our purposes. Emulsion of lipids is necessary for optimal activity of Hormone Sensitive Lipase (HSL), whose activity/translocation is generally considered rate-limiting for lipolysis (, ), on its substrate (). This translocation requires cAMP activation of Protein Kinase A (), and a fluid phospholipid membrane, as facilitated by the unsaturated fatty acids in lecithin phospholipids, is required for optimal activity of Protein Kinase A (Gavriloval 1992).
One also cannot help but speculate that membrane fluidity increase may underlie a big part of leptin sensitivity, because of the well known effects of fish oils on both of those parameters (, ). Lecithin increase adrenergic binding to TG’s (), and adrenergic signaling seems to be the primary determinant of leptin sensitivity, as reflected by the increased beta receptor density in males vs. females, which is concurrent with their increased sensitivity.
Lecithin also shows remarkable similarity with fish oils, in regard to bodyfat accumulation and triglyceride levels, but differs in regard to fatty acid oxidation and lipogenic gene expression (, , , ), arguing against a PPAR-alpha mechanism. This could further support the membrane fluidity angle, or perhaps even be suggestive of PPAR-gamma antagonism (). The latter would be most welcome, as PPAR-gamma, for those unaware, is a major mediator of “thrifty” phenotypes, producing adipocyte differentiation and increased triglyceride storage (, )
Sesamin (Ultra/ODB)
I have been waiting on sesamin to become commercially available for over 2 years, so now that it is, expect to see it in several products, as the data on it is truly remarkable. It is 10-fold MORE potent than fish oils in the modulation of PPAR-alpha inducible fatty acid oxidation genes, such as CPT1, pyruvate-dehydrogenase kinase, and UCP3 (, )
Of even more interest, sesamin inhibits expression of lipogenic enzymes, whose activity have been found to be independent of PPAR-alpha, such as FAS, SREBP-1, ATP-citrate lyase, and Glucose-6-phosphate dehydrogenase (, ). Such anti-lipogenic activity would, however, be expected from antagonism of the dreaded PPAR-gamma (, , )
And, as would be expected from its activity on these enzymes, sesamin provokes a strong increase in beta oxidation of fatty acids and decreases lipogenesis/TG formation. IOW, this is good ****.
Yohimbine Hydrochloride (Ultra/ODB)
Most are probably pretty familiar with yohimbine, from LipoDerm and it’s write-up, but we will reprint that information here, with a bit more science added:
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, amongst 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 primarily 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 alpha2 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 (). The anti-lipolytic effect of alpha2 is stronger in humans than any other species studied (, ). Thus, thermogenesis is basically always turned off.
It is the differences in regional distribution of alpha2 and the beta receptors that is responsible for a large part of the gender differences in body fat storage (). Indeed, regional variations in lipolysis are correlated with alpha2 activity in both men and women (, ).
The results of a study (in humans) on catecholamine-induced lipolysis is particularly telling ():
“Isolated subcutaneous adipocytes were obtained from the abdominal and gluteal regions. The lipolytic effect of noradrenaline was four to fivefold more marked in abdominal adipocytes than in gluteal fat cells. This regional difference was more apparent in females than in males. The beta-adrenergic lipolytic sensitivity was 10-20 times greater in abdominal adipocytes from both sexes than in gluteal adipocytes. Abdominal adipocytes from females showed a 40 times lower alpha 2-adrenergic antilipolytic sensitivity than did gluteal adipocytes, but the adenosine receptor sensitivity was similar in both sites. Beta-receptor affinity for agonists displayed no site or sex variation. Abdominal adipocytes showed a twofold increased beta-adrenoceptor density than did gluteal cells from both sexes. The alpha 2-adrenoceptor density was similar in all regions, but in females the affinity of clonidine (a2 agonist) for these sites was 10-15 times lower in the abdominal fat cells compared with gluteal cells. In conclusion, regional differences in catecholamine-induced lipolysis are regulated at the adrenoceptor level, chiefly because of site variations in beta-adrenoceptor density. Further variations in the affinity properties of alpha 2-adrenergic receptor in females may explain why the regional differences in catecholamine-induced lipolysis are more pronounced in women than in men.”
Males have greater alpha2 density and anti-lipolysis in abdominals vs. women (), which contributes to increased storage in that area, but the main difference is caused by higher lower body alpha2 activity in women, as well as by beta receptors, which are more highly expressed in males (and, don’t worry, we have ingredients to cover this). Cortisol mediates male abdominal fat accumulation as well (for more on this, see my article on the topic),
Females were found to have 73% higher alpha2 binding in lower body adipose than men, which was reflected by increased sensitivity and maximal anti-lipolytic effect (). Females exhibit decreased energy expenditure in gluteal obesity vs. abdominal adipose (), as well as a decreased diet induced thermogenic response (). Obese women have greatly decreased NE spillover per unit fat mass than lean, likely as a result of alpha2 inhibition, which would be expected to result in less lipolysis, which would make them more prone to said obesity. Finally, decreased alpha2 sensitivity has also been found to be predictive of weight loss ().
With exercise or the use of compounds such as the ephedrine/caffeine stack, catecholamine levels can be increased to a point where the alpha2 induced inhibition of lipolysis is partially overcome (). However, even then, the alpha2 receptors ARE still acting to reduce lipolysis.
Yohimbine is a selective alpha2 antagonist () 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. Considering the subject of this article, I obviously believe the solution lies in topical administration, but that has been covered in my original LipoDerm article
Blood Flow
A second, more indirect, mechanism by which Yohimbine can aid lipolysis via the adrenergic system is by increasing peripheral blood flow (, ). 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 (). Alpha2 receptor activation, on the other hand, causes a decrease in blood flow (, ). Thus, antagonism of the alpha2 receptor with yohimbine would be expected to increase blood flow, and thus increase the mobilization and disposal of these fatty acids, further aiding fat loss. And, again, the more we can get in the adipose tissue without it reaching the heart and CNS, the better.
Yohimbine should also block negative feedback on dopamine signaling, which we will cover (, , ), via alpha2 antagonism, which is normally activated by dopamine, via NE (), so this gives us a third mechanism by which yohimbine will help eliminate fat.
Synephrine Hydrochloride (Ultra/ODB)
Synephrine is a selective alpha1 agonist (, ). Alpha1 activation has been found to be directly lipolytic, similar to beta receptor stimulation (, ), as well as to potentiate the activity of beta receptors (, ). This thermogenic effect is enhanced by adenosine antagonism (i.e. caffeine), just as is the case with NE ()
It also potentiates dopamine activity, via increased IP3 release (, , ). Both IP3 and dopamine seems to be involved in leptin sensitivity/signaling (, ), and leptin uptake into the brain, a determinant of leptin sensitivity, is increased with alpha1 agonists ()
Finally, the active ingredient in Preparation-H gel (phenylephrine), well known, anecdotally, for its abilities as a local diuretic, is also an alpha1 agonist, so synephrine would be expected to share its water removal properties.
Caffeine (Ultra/ODB)
Caffeine is a phosphodiesterase inhibitor and adenosine antagonist – both of which are negative feedback signals inhibiting lipolysis. It increases the thermogenic response to norepinephrine (), via elevation of cAMP levels (due to decreased breakdown) and increases in adenyl cyclase, respectively. However, it is controversial whether the phosphodiesterase inhibition takes place at relevant dosages (), so it may only work through adenosine mediated elevations in NE levels ().
Another very desirable effect of caffeine and its adenosine antagonism, is on diuresis (), and uptake of other anti-lipolytic nutrients into the fat cell. Normally, ATP hydrolysis increases the AMP/ATP ratio, indicating a lack of cellular fuel (if more substrate is not taken up), but caffeine blocks AMP binding to the adenosine receptor, tricking the cell into thinking it is fueled, thus making it insensitive to these nutrients.
Octopamine (Ultra/ODB)
Octopamine is a Beta3 agonist, which some may remember from an article in MM2K, back in the day, which touted them as future wonder drugs, because, unlike beta2 receptors, beta3 receptors are quite resistant to downregulation. Unfortunately, humans express far less beta3 receptors than rats and mice, so the profound fat loss did not occur in studies in people.
However, we now actually have some decent data in humans, suggesting beta3 agonists should help with body composition. Beta3 receptors seem to be tied in with AMPK (which modulates some of the nutrient repartitioning effects of exercise and Metformin), as they both selectively promote decreased glucose uptake in adipose () and increase lipolysis (, ), as well as increased glucose uptake and glycogen storage in muscle (, ).
Beta3 activation will not have the profound lipolytic effect seen in rats, but should exert some modest repartitioning.
In addition, octopamine is metabolized to norepinephrine by MAO or the cytochrome-450 system (I cannot locate the reference, sadly, though I did find that octopamine levels decrease in the fetus, when MAO and NE increase () and conversion would only require removal of a hydroxyl group). It also directly stimulates NE release (), as well as competitively inhibiting MAO (highly expressed in adipose) metabolism of NE (, ) -- all of which is most welcome in the days without ephedrine; because we all know NE is quite the fat burner.
However, oxidation of octopamine, via MAO, generates H2O2, which is anti-lipolytic in adipose (, ), thus we have included NAC and ascorbyl palmitate to inhibit H2O2 formation (, , ).
Octopamine has also been found to decrease prolactin, likely via increased DA signaling (). Prolactin has also been found to increases PPAR-gamma expression, which could account for some of the effect of dopamine on leptin sensitivity (), so we have one more positive for octopamine
Tyramine (ODB)
Tyramine seems to be pretty worthless, per se, in humans, however, it is converted to dopamine via CYP-2D6 (). It also decreases prolactin, likely via increased DA signaling (). Dopamine seems to increase leptin sensitivity, as mentioned (), likely via its direct activation of beta3 receptors (, ) and AMPK, as well as possibly through D1 receptors (, ), via its stimulation of cAMP (, )
Dopamine also potentiates beta receptor induced lipolysis (), perhaps via increased NE release () in addition to being lipolytic and thermogenic on its own (, , ). It’s stimulation of cAMP is potentiated by phosphodiesterase inhibitors (), just as with NE.
As with octopamine, tyramine exerts insulin like effect on adipose, via interaction with MAO and subsequent generation of H2O2, but we have taken care of this with NAC and AP. Interestingly, low level of H2O2, via tyramine, as we would expect in conjuction with anti-oxidants, actually increased forskolin induced cAMP and potentiated beta adrenergic stimulation of lipolysis ()
Finally, competitive inhibition of MAO (, , ) would increase NE, as MAO quite high in adipose and muscle (, ). Like octopamine, it also directly increases NE release (, ). Octopamine and tyramine will also interfere with MAO’s metabolism of each other, in addition to NE ()
NAC (ODB)
We have mostly covered this – NAC scavenging of H2O2 from octopamine and tyramine, will prevent inhibition of lipolysis, and thiols’ modulation of REDOX is involved in signal transduction and fed state signaling. Oxidative stress has been found to activate adenosine (), which is likely a major mechanism of the brake on cellular metabolism produced by large amounts of free radicals.
Acorbyl Palmitate (Ultra/ODB)
Like NAC, the ascorbate part of AP (ascorbate = vitamin C) will increase scavenging of H2O2 and other oxidation products, to keep cellular metabolism optimized Ascorbate should also inhibit uptake of glucose into adipocytes (which would blunt lipolysis) via competition for the sodium dependent glucose transporter (), as well as independently of it, as well (). It has also been found to increase lipolysis in adipocytes as well decrease glycerophosphate dehydrogenase, a marker of adipocyte differentiation ().
In addition, palmitate strongly potentiates hexosamine flux, a major nutrient signal of leptin expression (, )
Acetyl-l-carnitine (Ultra/ODB)
ALCAR Improves mitochondrial bioenergetics, for better beta oxidation of fatty acids (, , ). This is potentiated by R-ALA via peroxide scavenging () – NAC should share this synergistic effect, but without the unwanted anti-lipolysis that R-ALA would provide. It also seems to be associated with AMPK/beta 3 (), which might account for its increasing of leptin sensitivity ()
Green Tea (ODB)
Green tea polyphenols, especially ECGC, have a number of nice effects. It inhibits COMT, which breaks down NE and dopamine (), which could account for its potentiatiation of NE induced thermogenesis (, ), as well energy expenditure and fatty acid oxidation (10584049). It also inhibits FAS, thus triglyceride synthesis (), as well as glucose uptake (, ).
Summary
To summarize, LipoDerm-Ultra encourages Fed state signaling, stimulates lipolysis and increases Beta oxidation. In addition, it targets the REDOX system to prevent free radical-related slowdown of these processes, ensuring fat loss continues at accelerated rates. Lastly, via the judicious use of diuretics, Lipoderm-Ultra’s effects will be rapidly apparent, allowing users to see precipitous changes in appearance within a matter of days.
These ingredients formulate a revolutionary synergistic blend, designed specifically to target localized spot reduction from a number of angles. Utilizing the percutaneous delivery system and penetration enhancers that made Lipoderm-Y the most innovative supplement ever released, Lipoderm-Ultra expands upon that technology, coupling a potent delivery system with the most effective fat-fighting ingredients ever assembled in one topical product. The result: maximal fat loss in minimal time.
http://www.1fast400.com/?products_id=875 = 34.99
http://www.bodybuilding.com/store/al/lipoultra.html = 38.55
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Q&A I had w/ Bradley via private message a month or two back
Lipoderm vs. Ab-Solve
Q. I'm in fairly good shape, am 27 and 5'10 at 188 at around 8-10% bf. My stomach tends to hold a bit more stubborn fat than other parts of my body and I'm wondering if either of these products, or both would be good for me?!
A. Ab-Solved will be useful in reducing visceral fat, which is the fat that surrounds your organ (appears to be under the muscle), where as Lipoderm will be useful in reducing subcutaneous bf, i.e. stubborn bf (love handles, lower abs, lower back, etc.).
Q. Are they short term or long term gains?
A. The products will have long term effects, assuming that you do not gain any fat after you discontinue use. Obviously if you switch to a hypercaloric diet you will increase the probability of gaining fat back in those particular areas.
Q. Do they have to be used in conjunction with a special diet?
I'm currently on a bulk trying to get up to 200 by January at which time I'm going to cut.
A. These products are best used in conjuntion with a hypocaloric diet, especially Lipoderm. Lipoderm will only work if you are in a calorie deficit, where as Ab-Solved "could" help with reducing visceral fat, even if eating above maintenance. Needless to say, I would recommend that you eat below maintenance if you do decide to use either of these products.
geoffgarcia
02-26-2004, 02:34 PM
Lets not jump the gun on this one and rule out taking both...
Chris, what do you think is "above the limit" on these supps?
Thermocin has:
Guarana Extract (22% caffeine) 1000 mg *
Citrus Aurantium Extract (4% synephrine) 225 mg *
Sida Cordifolia 100 mg *
White Willow Bark Extract (15% salacin) 100 mg *
Zingaber Root 60 mg *
Hydroxycitric Acid (50% HCA) 50 mg *
Proprietry Blend 250 mg * L-Tyrosine, Acetyl-L-Carnitine (ALC), Fisitin, Magnesium Phosphate, 2 Dimethylaminoethanol
I just emailed Avant for the ingredients of their ab-solve and lipoderm products along with the gist of this thread and the ingredients of the Thermocin to see what their reaction is.
In the meantime, here is more interesting reading:
Kick it Up a Notch
by Spook
How to Enhance Your Lipoderm for Greater Fat Loss
Lipoderm-Ultra and Lipoderm-ODB have finally been made available for public consumption. Feedback is starting to mount and both products seem to be a significant improvement over the original version. Truly, Par Deus deserves a hardy pat on the back as he did a marvelous job; these are two killer products in their own right. However, I would like to take some time in this issue of Mind and Muscle to discuss how we can improve these products even further.
There is one very intriguing way in which we can enhance Lipoderm’s efficacy. Namely, I want to talk about reducing adipose tissue insulin sensitivity. I would like to make real Lyle McDonald’s ultimate dream of insulin resistant fat tissue that does not negatively affect muscle tissue. Theoretically, this should be possible via Lipoderm’s localized delivery vehicle. Often in bodybuilding literature we discuss things that improve one’s insulin sensitivity. However, it is pretty rare that we converse on how we might induce insulin insensitivity. The problem is even more complicated if we want to keep the effect as localized as is physically possible.
What I would like to present to you is a theory on how we might accomplish this task. I believe I have an excellent solution, however to my knowledge I am currently the only one who has tested my theory. Because of this, my results may not be typical nor what is normal. So, take the following information with a grain of salt. Though, I suggest you try my approach, as my results may very well be what are typical. Those of you who do try my concoction, please take the time to post your results—good or bad—on the Avant Labs forum so that everyone can benefit from your experience. So, without further adieu let’s get to the meat of this discussion….
There is indeed a way to induce localized insulin resistance. The key compound involved is Calcitonin Gene Related Peptide or CGRP for short. CGRP is an interesting little molecule that is released from the sympathetic nervous system. It tends to cause calcium depletion from cells. Interestingly, one of CGRP’s side effects when released in large amounts happens to be insulin resistance. In fact, it has been proposed that CGRP is one of the prime factors responsible for inducing the small amounts of insulin resistance seen in smokers. People who have smoked for several years generally exhibit a very mild insulin insensitivity that resembles a pre-diabetic state, though it seldom develops into real diabetes unless one is genetically prone. This mild insulin resistance generally disappears if the subject quits smoking. It just so happens that nicotine causes a large release of CGRP through interaction with the nerves that compose the sympathetic nervous system. So, nicotine is one way of eliciting localized insulin resistance. I will talk more about that later. Instead I would like to move on to the compound that I think holds more promise: namely, Capsaicin.
Capsaicin is the stuff in peppers that gives them their hot taste. Of interest here is that, when nerves are exposed to capsaicin, they release a very large amount of CGRP. Of course, too much CGRP and you can actually damage the nerve permanently. Curiously, by permanently damaging capsaicin-sensitive nerves, rats and mice actually get leaner. For example, in one study researchers took mice and desensitized them to capsaicin by giving them a very large dose of the compound at the age of 1.5 months. They then compared those mice with matched controls at one year of age. What they found was that that the desensitized mice had 9% less epididymal and 30 % less retroperitoneal fat than the controls. This was due to a reduction in the number of fat cells. The authors proposed that by desensitizing the capsaicin-sensitive neurons they attenuated the normal age-associated increase in CGRP activity and thus promoted whole body insulin insensitivity.
Now it’s entirely questionable if humans would have a similar reaction, as rats and mice use their capsaicin-sensitive neurons to regulate thermogenesis in their brown fat tissue. So, we could be witnessing some kind of interaction with the brown fat thermogenesis system, which in turn causes this leanness. Now, much can be said about capsaicin as a fat loss aid at least in rats. But we are kind of getting off track.
What we really want to do for our purposes is provide a small dose of capsaicin to the nerve tissue that surrounds our subcutaneous adipose tissue. This way CGRP is released in this region resulting in localized insulin resistance, which should enhance fat loss from the targeted area. Furthermore CGRP is one of the most potent—if not the most potent –vasodilator naturally produced by the human body. So, it should substantially increase blood flow to the area, allowing for removal of the fatty acids that are released by Lipoderm’s lipolytic ingredients.
Now back to nicotine. Not only does nicotine also cause the release of CGRP, it does so synergistically with capsaicin. In fact it seems that nicotine may sensitize the vanilloid receptors that capsaicin binds to (Yes that’s vanilloid as in vanilla; capsaicin and vanilla are very close cousins at the molecular level). Nicotine is of course mildly lipolytic in its own right, which is an added benefit. In short I propose the addition of nicotine and capsaicin to the Lipoderm formula of your choice for enhanced fat reduction.
You may be wondering why this was not included in the formula if it’s so potent. Well there is one downside and let me tell you it’s a big one: that downside is pain. I have tried this concoction and I will say it is not even remotely pleasant. It induces a severe burning sensation that subsides into a mild burning/numbness that can be felt fairly deeply in the tissue. However, if you are willing to put up with the pain you will be rewarded with accelerated fat loss. Personally I tried this with the original Lipoderm formula and felt the results were at least an order of magnitude better than what I experienced with Lipoderm alone. That said, many people have complained about how Lipoderm-Y feels on their skin. If you were one of those individuals then you do not want to try this concoction. If however you are feeling brave, then I highly recommend you give it a shot. For me, the results were worth the pain. The addition of capsaicin and nicotine allowed me to burn some very stubborn fat right below my navel that I had never previously succeeded in dieting away.
I will leave it to the reader to figure out how to obtain nicotine or capsaicin. I will however mention that capsaicin is used in many over-the-counter arthritis creams. There is one arthritis medication in particular that is a liquid and not a cream that contains little more than alcohol, menthol, and capsaicin. This is a perfect choice as menthol is one of the penetration enhancers used in the original Lipoderm formula. Nicotine is available in patches or crushable lozenges these days so it should not be too hard to come up with a way to add that as well.
Well I hope the more adventurous of you out there give this a try. Should you do so, please do give your feedback in the Avant Labs forums, as I would really enjoy hearing about your successes or failures. Just remember to avoid applying this on any sensitive area during your first treatment. As always, I will be available in the Avant Labs forums to answer any questions you might have.
http://www.avantlabs.com/page.php?pageID=175&issueID=16
The thread where this experimentation is discussed:
http://forum.avantlabs.com/?act=ST&f=2&t=6647&hl=ingredients,and,lipoderm&st=0
WOW!!! you guys have to read that thread! its hilarious!!!!
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