Since apparently the silly-effectiveness of ‘Spooky-Lipoderm’ still isn’t quite enough for some folks, here’s another transdermal spot-reduction potentiator you can toss in your Lipoderm-ULTRA to help improve the local lipolysis: Clenbuterol HCl.
Highly hydrophilic, the HCl salt of clenbuterol makes it an ideal target for Lipoderm-ULTRA’s amphiphillic carrier, which can support both hydrophillic and lipophillic actives. The logP of free-base clenbuterol is actually somewhat higher (~2.0), and could be used in Ab-Solved if you can still find it anywhere, or in our upcoming Matrix-ABSTM Gel #3, to be released later this summer. And of course there’s always delightful DMSO for those who don’t mind the soul-grating stench and occasional dermal chemical burn.
For homebrewing, you want to add about 5,000 micrograms of clenbuterol (ideally in bulk powder form) to your transdermal carrier of choice, and shake well to disperse it (heating ought not to be necessary).
Now, because we’re not taking it systemically, we’re introducing the drug in a much more benign way. This has both upsides and downsides. On one hand, this allows us to avoid the clen’s side effect profile almost entirely. Unfortunately, this also means we get no interaction in skeletal muscle, and, subsequently, no cash-money repartitioning. It should still markedly increase adrenergic stimulation and accelerate lipolysis in the application area(s), and the majority of user feedback has noted that spot reduction with Lipo-Clen or Clen-Derm or Lcilpeondbeurtmerol or whatever the hell you want to call it is superior to stand-alone Lipoderm-ULTRA. The combination still may not be able to convert your midsection from Buick to boney overnight, but we’re definitely making it pretty difficult of late to keep those last elusive little abdominal muscles submerged in SAT for much longer. Throw in some capsaicin cream and a good diet and exercise plan, and be prepared to smile like you mean it by the end of your cut.
Clen, if it Doesn’t Kill You, it Just Might Save Your Life?
Recently, researchers have been looking more into the neurological effects of clenbuterol, and coming up with some interesting findings. One in particular involves nerve growth factor (NGF), a naturally occurring protein in the body which stimulates the growth of sympathetic and certain sensory nerves. Last year, in a groundbreaking study, Zhou et al. demonstrated that the NGF beta chain (NGFB), one of the three polypeptide chains that comprise the NGF protein, stimulates a molecular pathway directly responsible for nerve growth and axon creation (1). Axons, for those in need of a refresher, are the tendril/process that connect nerve cells and relay nervous signals throughout the body. In their study, Dr. Zhou and his colleagues found that NGF signals via PI3K and GSK-3beta to stimulate axon synthesis downstream from microtubules.
Now, in most parts of the body, if nerve cells are damaged they can be repaired. However, there’s one very prominent area of the body where axon disruption gets extremely ugly and very serious: the spinal cord. But, thanks to the recent look at NGF and clenbuterol, researchers are beginning to think that clenbuterol may have merit in illuminating (if not providing) a potential treatment for spinal paralysis through axon growth and regeneration. After all, studies have demonstrated that cells treated with clenbuterol display increases in nerve growth factor mRNA and protein levels that are roughly 200-300% higher than control cells (2,3). And, according to Dr. Joseph Etlinger of the New York Medical College, one of the nation’s leading researchers on the drug, “our results with clenbuterol so far are as effective as any drug given for human spinal cord injuries to date, and that includes steroids and free radical scavengers.” Clinical human research trials backed by MotoGen and the N.I.H. are pending, but auspices (re: ‘this shit’) actually looks rather promising.
Additionally, this same property of clenbuterol also lends it a confirmed neuroprotective quality after it was recently demonstrated that clenbuterol could protect cerebral tissue against hypoxic (ischemic) damage. Cerebral ischemia, more commonly known as a stroke, is a decrease in cerebral blood flow that shunts cerebral oxygenation and the brain’s aerobic metabolism, causing brain damage and neuronal apoptosis (cell death). Clenbuterol, by altering the expression of apoptotic proteins and inducing neurotrophic growth factors like NGF, bFGF, and TGF-ß1, seems to be potently cerebroprotective against hypoxic damage (3,4,5).
Culmsee et al. have also shown it to be synergistically neuroprotective when combined with an NMDA (N-methyl-D-aspartate) antagonist to prevent excitotoxic overactivation of glutamate receptors, disruptions in cellular calcium homeostasis, and increases in cerebral ROS/free-radical buildup (6). It even protects retinal cells from UV-damage (7). The irony, right? Looks like the same drug that may very well cause ischemic damage in cardiac cells (if you’ll remember from Part I) prevents the exact same process from happening in the brain. Pharmacology has kind of a sick sense of humor, doesn’t it?
Still, clenbuterol has been receiving more and more attention from the scientific community of late thanks to its diverse and intriguing activity profile in the human body. We can only hope that in the future this will lead to more elucidation of how clenbuterol might hurt or help us in our search for health, longevity, and the mythical munificence of El Dorado. And by ‘El Dorado’ I mean hookers. And by ‘hookers’ I mean happiness. I swear. Cheers all.
1. Zhou FQ, Zhou J, Dedhar S, Wu YH, Snider WD. NGF-induced axon growth is mediated by localized inactivation of GSK-3beta and functions of the microtubule plus end binding protein APC. Neuron. 2004 Jun 24;42(6):897-912.
2. Culmsee C, Semkova I, Krieglstein J. NGF mediates the neuroprotective effect of the beta2-adrenoceptor agonist clenbuterol in vitro and in vivo: evidence from an NGF-antisense study. Neurochem Int. 1999 Jul;35(1):47-57.
3. Semkova I, Schilling M, Henrich-Noack P, Rami A, Krieglstein J. Clenbuterol protects mouse cerebral cortex and rat hippocampus from ischemic damage and attenuates glutamate neurotoxicity in cultured hippocampal neurons by induction of NGF. Brain Res. 1996 Apr 22;717(1-2):44-54.
4. Zhu Y, Prehn JH, Culmsee C, Krieglstein J. The beta2-adrenoceptor agonist clenbuterol modulates Bcl-2, Bcl-xl and Bax protein expression following transient forebrain ischemia. Neuroscience. 1999;90(4):1255-63.
5. Zhu Y, Culmsee C, Semkova I, Krieglstein J. Stimulation of ß2-adrenoceptors inhibits apoptosis in rat brain after transient forebrain ischemia. J Cereb Blood Flow Metab. 1998; 18: 1032–1039.
6. Carsten Culmsee, PhD; Vera Junker, MD; Wolfram Kremers, PharmD; Serge Thal, MD; Nikolaus Plesnila, MD; Josef Krieglstein, MD, PhD. Combination Therapy in Ischemic Stroke: Synergistic Neuroprotective Effects of Memantine and Clenbuterol. Stroke. 2004;35:1197.
7. Von Deutsch et al. Clenbuterol’s neuroprotective effect on UV-C exposed human retinal cells. SGSB 2003 Annual Meeting Abstracts.