Enhancing Napalm/Lipo Ultra with nicotine

[Colin]

As nicotine is legally available,unlike clen,I tried this recently with remarkable results.IME it was as effective as using Napalm spiked with clen.

Nicotine extraction - Mind and Muscle Forums


There was a very good discussion on this a while back over on Avantlabs.com/forum but I can't link the thread as the board is currently offline for maintainence.

One must take extensive precautionary measures in extracting nicotine,this is a dangerous process and one small mistake is quite enough to land you in an ER,if you're lucky.

[Colin]

Here's an excerpt from an old article by Par.Note that raspberry ketones and capsaicin are virtually interchangable so the same effects wil be seen with RK as are seen with cap.RK is present in Napalm but is also available cheaply in bulk (and can also be used orally to activate TRPV1,which is a key player in fat loss),2 grams would be a sufficient dosage to add to Lipoderm Ultra.

-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.

[rpen22]

One must take extensive precautionary measures in extracting nicotine,this is a dangerous process and one small mistake is quite enough to land you in an ER,if you're lucky.

It might be a safer idea to utilize nicotine patches as Spook originally did with Spookyderm.

Here's the full article by Spook on this topic from BB.com also.
http://www.bodybuilding.com/fun/par36.htm

[Colin]

Well,as long as one takes care during the extraction process,there are no safety concerns.But you have to be extremely anal retentive in the process of the extraction.

Nicotine patches woudn't cover much space and are intended for systematic delivery anyway,I think Spook was using them like this as he was using nic to mostly help with dieting pangs .Using nic in a topical intended for localized delivery would be much more effective.

[thesinner]

That isopropanol process, hmmm. Are the other alcohol-soluble components really that volatile to leave only the nicotine left at a high purity?

Although I'm not 100% certain what the patches look like, what about trying to dissolve those in alcohol or directly into the carrier? You'll get some miscibility of the non-systematic carrier, but by total percent volume, I wouldn't suppose it would make such a difference.

[Colin]

That isopropanol process, hmmm. Are the other alcohol-soluble components really that volatile to leave only the nicotine left at a high purity?

Although I'm not 100% certain what the patches look like, what about trying to dissolve those in alcohol or directly into the carrier? You'll get some miscibility of the non-systematic carrier, but by total percent volume, I wouldn't suppose it would make such a difference.

I think they're volatile enough and this is something that I would not take my chances with.

As far as the patches,I'd opt for rolling tobacco as outlined in the post below.FWIW,Heavylifter_85 is a high school chemistry teacher (or college,can't remember) and the dude knows his ****.

[quote name='Heavy_Lifter85' date='Feb 15 2008, 04:55 PM' post='458358']
Enjoy:


Place 10 grams of ground rolling tobacco into a beaker. Add 50 mL chloroform and 1 mL NH4OH. Stir occasionally. Allow to sit overnight at room temperature.

Filter liquid through cloth into a flask.

Extract with 3x30 mL water, adjusted to pH = 2 with hydrochloric acid. [The nicotine-HCL salt partitions to the aqueous phase.]

Isolate the aqueous fraction - simply pour or pipette the aqueous layer into another flask.

Adjust the pH of the combined aqueous extracts to 12 with sodium hydroxide. [The nicotine is now present as the free base.]

Extract with 3x30 mL chloroform. [The nicotine is now in the organic phase.]

Isolate the organic phase – either decant the aqueous layer to leave the organic one behind, or remove organic layer via pipette.

Evaporate the chloroform (boiling point 61-61 C) to concentrate the nicotine.

-------------------------------------------------------------------------------------------

Notes:

To perform the first extraction, add one 30 mL volume of water to the chloroform and tightly seal the flask. Repeatedly invert or vigorously shake the flask for 30 seconds, making sure to hold the seal in place (contents are under pressure). Allow layer to separate, carefully open flask. Pour off or remove via pipette the top layer. Repeat for the second and third volumes of water.

The second extraction is performed in the same manner, although the roles of chloroform and water are reversed.

Chloroform – organic phase – non-polar

Acidic/basic water – aqueous phase – polar

Chloroform has a density of roughly 1.5, while water has a density of 1.00. Thus, the aqueous fraction sits above the organic one.

Dichloromethane can be used instead of chloroform.

Nicotine is volatile and susceptible to oxidation. Store in a covered vessel at low temperature. Minimize air space above nicotine by using smallest possible vessel.

Nicotine passes easily through the skin without aid of a carrier. The LD50 of nicotine is 0.5-1.0 mg/kg.
[/quote]

[Colin]

Here are some nice nicotine abstracts,not as relevant here with a localized carrier as systematic usage but still good reads.


Nicotine self-administration acutely activates brain reward systems and induces a long-lasting increase in reward sensitivity.
Kenny PJ, Markou A.

Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA 92037, USA.

Nicotine is a major component of tobacco smoke contributing to the initiation and persistence of the harmful tobacco habit in human smokers. The reinforcing effects of nicotine likely arise through its ability to stimulate brain circuitry mediating the detection and experiencing of natural rewards. Nevertheless, remarkably little is known concerning the acute or long-lasting actions of nicotine on brain reward systems in vivo. Here, we investigated the effects of intravenously self-administered nicotine (0.03 mg/kg/infusion, free base) on the sensitivity of brain reward systems, reflected in alterations of intracranial self-stimulation (ICSS) thresholds in rats. Rats self-administered nicotine during 1 or 12 h daily sessions, with reward thresholds assessed 1 h before and 15 min after each self-administration session. Control rats remained nicotine naïve throughout. Nicotine self-administration increased the sensitivity of brain reward systems, detected by post-nicotine lowering of reward thresholds in 1 and 12 h rats. This nicotine-enhanced sensitivity of reward systems was reversed by the high-affinity nicotinic receptor antagonist dihydro-beta-erythroidine (DHbetaE; 3 mg/kg). Surprisingly, nicotine-induced excitation of reward systems persisted for at least 36 days after nicotine self-administration had ceased. Overall, these data demonstrate that rats can voluntarily consume quantities of nicotine sufficient to increase the sensitivity of brain reward systems, an action likely crucial in establishing and maintaining the nicotine habit. Moreover, self-administered nicotine resets the sensitivity of reward systems to a new increased level, thereby imprinting an indelible 'memory' of its effects in reward systems, an action that so far appears unique to nicotine among drugs of abuse.

Free fulltext: http://www.nature.com/pdffinder/10.1038/sj.npp.1300905

Nicotine blocks stress-induced decrease in BDNF:

QUOTE
http://cat.inist.fr/?aModele=afficheN&cpsidt=17912073
Titre du document / Document title
Chronic psychosocial stress-induced impairment of hippocampal LTP : Possible role of BDNF
Auteur(s) / Author(s)
ALEISA A. M. ; ALZOUBI K. H. ; GERGES N. Z. ; ALKADHI K. A. ;
Résumé / Abstract
Electrophysiological recording reveals that chronic nicotine treatment prevents stress-induced impairment of long-term potentiation (LTP) in the CA1 region of the hippocampus of anesthetized rats. We investigated the molecular mechanism of this action of nicotine in the CA1 region. Immunoblot analysis showed that chronic nicotine treatment (1 mg/kg, 2 times/day) normalized the stress-induced decrease in the basal levels of BDNF, CaMKII (total and phosphorylated; P-CaMKII), and calmodulin. Additionally, nicotine reversed the stress-induced increase in calcineurin basal levels. Chronic nicotine treatment also markedly increased the basal levels of BDNF in naive rats. Furthermore, high-frequency stimulation (HFS), which increased the levels of P-CaMKII in control as well as nicotine-treated stressed rats, failed to increase P-CaMKII levels in untreated stressed rats. Compared to unstimulated control, the levels of both total CaMKII and calcineurin were increased after HFS in all groups including the stressed, but no changes were detected after HFS in the levels of BDNF and calmodulin. These results indicate that normalization by nicotine of the stress-induced changes in the levels of signaling molecules including BDNF may contribute to the recovery of LTP.
Revue / Journal Title
Neurobiology of disease ISSN 0969-9961
Source / Source
2006, vol. 22, no3, pp. 453-462 [10 page(s) (article)]
Langue / Language
Anglais
Editeur / Publisher
Elsevier, Amsterdam, PAYS-BAS (1994) (Revue)
Mots-clés d'auteur / Author Keywords
Anesthetized rat ; CA1 region ; Calcineurin ; CaMKII ; fEPSP ; Population spike ;
Localisation / Location
INIST-CNRS, Cote INIST : 26483, 35400013887881.0010


Nicotine increases BDNF release:

QUOTE
http://www.sciencedirect.com/science...9ad38690a71c7b

Nicotine regulates SH-SY5Y neuroblastoma cell proliferation through the release of brain-derived neurotrophic factor

Florence Serresa, b, Corresponding Author Contact Information, E-mail The Corresponding Author and Stephen L. Carneyb, 1

aUniversity Department of Pharmacology Oxford University Mansfield Road, Oxford OX1 3QT, UK

bLilly Research Centre Ltd, Sunninghill Road, Surrey GU20 6PH, UK

Accepted 8 May 2006.
Available online 21 June 2006.

References and further reading may be available for this article. To view references and further reading you must purchase this article.

Abstract

Nicotine has been shown to produce some beneficial effects in neurodegenerative disorders, and several studies have suggested that these effects may be mediated in part through the action of the neurotrophic factor BDNF. To further elucidate the interaction between nicotine and BDNF, we examined the effect of nicotine on the proliferation of the neuroblastoma cell line SH-SY5Y, which, following differentiation with retinoic acid, expresses both nicotinic receptors and the receptor for BDNF, TrkB. Both nicotine and the nicotinic alpha-7 selective agonist AR-17779 significantly increased cell proliferation albeit with bell-shaped dose–response kinetics. The blockade of this effect with either the alpha-7 nicotinic antagonist methyllycaconitine or the non-selective nicotinic antagonist mecamylamine indicated that the effect was mediated by nicotinic receptors. Prior addition of neutralising BDNF antibodies or of the tyrosine kinase inhibitor K252A (200 nM) completely blocked nicotine-induced proliferation, suggesting the involvement of TrkB signalling in the mediation of the effect. Nicotine also enhanced both the secretion of BDNF from the SH-SY5Y and cell surface density of TrkB receptors. These effects were abolished by pretreatment with MLA. These data indicate that activation of nicotinic receptors has effects upon the BDNF–TrkB pathway, inducing cell proliferation by promoting the release of BDNF, which in turn activates TrkB receptors.

Keywords: Nicotine; BDNF; TrkB; Growth factor; Methyllycaconitine; Mecamylamine


Chronic nicotine increases (and acute nicotine decreases) hippocampal BDNF:

QUOTE
Acute nicotine decreases, and chronic nicotine increases the expression of brain-derived neurotrophic factor mRNA in rat hippocampus1

Paul J. Kenny2, , a, Sandra E. Filea and Marcus RattrayCorresponding Author Contact Information, E-mail The Corresponding Author, b

a Psychopharmacology Research Unit, Centre for Neuroscience Research, GKT School of Biomedical Sciences, King’s College London, Hodgkin Building, Guy’s Hospital Campus, London SE1 1UL, UK

b Biochemical Neuropharmacology Group, Centre for Neuroscience Research, GKT School of Biomedical Sciences, King’s College London, Hodgkin Building, Guy’s Hospital Campus, London SE1 1UL, UK

Accepted 6 October 2000.
Available online 10 January 2001.

References and further reading may be available for this article. To view references and further reading you must purchase this article.

Abstract

Acute nicotine administration (0.5 mg/kg i.p.) significantly decreased BDNF mRNA levels in dentate gyrus, CA3 and CA1 subfields of the rat hippocampus 2 h and 24 h after administration. However, with 7 days nicotine treatment, tolerance developed to the inhibitory effect of nicotine on BDNF mRNA expression and there was a significant increase in BDNF expression 2 h after the final injection in the CA1 region. These data suggests that changes in expression of hippocampal BDNF may be involved in the behavioural effects of nicotine observed after acute and chronic treatment.

Author Keywords: Neurotrophin; Withdrawal; In situ hybridisation; Acetylcholine; Drug dependence

Neuroscience classification codes: Development and regeneration, Neurotrophic factors: expression and regulation


Repeated nicotine injections actually sensitize D3 neurons in nucleus accumbens (very atypical for reinforcing dopaminergics):

QUOTE
http://biopsychiatry.com/nicotine-dopamined3.htm

Disruption of nicotine conditioning
by dopamine D(3) receptor ligands
by
Le Foll B, Schwartz JC, Sokoloff P
Mol Psychiatry 2003 Feb;8(2):225-30

ABSTRACT

Tobacco smoking is the first cause of preventable death in modern countries. Nicotine replacement therapy or sustained release bupropion helps smoking cessation, but relapse rates are still very high. Nicotine, like other drugs of abuse, activates the dopamine mesolimbic system, which originates in the ventral tegmental area and projects notably to the nucleus accumbens. Situations or environmental stimuli previously associated with cigarette smoking, for example, smell of cigarette smoke, can elicit craving in abstinent smokers and promote relapse. Reducing the effects of nicotine-associated cues might therefore have potential therapeutic utility for smoking cessation. Such an approach has been validated for cocaine in animals, by using the dopamine D(3) receptor-selective partial agonist BP 897, which inhibits cocaine cue-induced drug-seeking behavior. Here we show that rats repeatedly injected with nicotine in a particular environment develop nicotine-conditioned locomotor responses, accompanied by an increase in D(3) receptor expression in the nucleus accumbens. This conditioned behavior was inhibited by BP 897 or a selective D(3) receptor antagonist, suggesting that antagonizing dopamine selectively at the D(3) receptor disrupts nicotine-conditioned effects and might represent a novel therapeutic approach for smoking cessation

[Colin]

To add some anecdotal feedback on jacking up the potency of topicals....

Usnic acid is effing killer.

I tried this a while back with old school Lipoderm-Y and I vividly remember LOCALIZED SWEATING where I applied the Lipoderm-Y,on my pecs.I would wake up in the morning and my bedsheets would be soaked from sweat,right around where my chest was resting.

It's much more difficult to come by nowadays then it was a few years back but a Google searched turned up a supplier,the last time I looked a few months ago.

[thesinner]

I think they're volatile enough and this is something that I would not take my chances with.

As far as the patches,I'd opt for rolling tobacco as outlined in the post below.FWIW,Heavylifter_85 is a high school chemistry teacher (or college,can't remember) and the dude knows his ****.

[quote name='Heavy_Lifter85' date='Feb 15 2008, 04:55 PM' post='458358']

[/QUOTE]

Ok, that was a little different (or more detailed) than what I read in the opening post of the M&M thread.

I can totally understand that method working, and I don't think we want people to be playing with chloroform in their kitchen.

[Colin]

Ok, that was a little different (or more detailed) than what I read in the opening post of the M&M thread.

I can totally understand that method working, and I don't think we want people to be playing with chloroform in their kitchen.[/QUOTE]

Dichloromethane can be used instead of chloroform but either way I would suggest performing the extraction in say,your garage with the doors/windows open.

This is what I did,in a well ventilated area,I wore two pairs of gloves.While it won't yield a 100% extraction it will be pretty close to the results you'd see with HeavyLifter85's method.

Ground nic lozenges,with a hammer.

Soak in isopropyl for a week.

Strain through a coffee filter.

Let that evaporate down a good amount,to a point where it won't thin out the transdermal base.

Done,shake Napalm before each application.

[jmh80]

Capsacin brings entirely too much pain for the results.

The juice ain't worth the squeeze in that case.

[thesinner]

I wouldn't think DCM is much safer.

The lozenge idea is definitely a better way to do it.

[jmh80]

DCM isn't very nice, from what I remember. But I may be thinking of trichloro ethylene.

Anyway - halogens, bah.

[thesinner]

DCM isn't very nice, from what I remember. But I may be thinking of trichloro ethylene.

Anyway - halogens, bah.

DCM is a carcinogen.

Supposedly companies used to decaffinate coffee that way, but not anymore.

[Colin]

Capsacin brings entirely too much pain for the results.

The juice ain't worth the squeeze in that case.

I wasn't suggesting cap and yeah,topically applied cap is effing nuts IMO,tried it once and that was enough for me.

The inclusion of raspberry ketones in Napalm makes cap redundant as they act on the same pathways.I strongly suggest procuring usnic acid,to add to Lipoderm Ultra or Napalm though.It is quite safe,when applied topically,as very little is absorbed systematically.I cannot stress enough how good my results were on old school Lipoderm-Y with caffiene and usnic acid.Topical usage of UA blows topical clen away,IME.

I wouldn't think DCM is much safer.

The lozenge idea is definitely a better way to do it.

The former method is for those with a good amount of experimentation under their belt,I wouldn't suggest this to *most* people who post on BB discussion boards.I chose the latter as it requires less prep materials and works nearly as good as Heavy's method.

Damn....I shoulda made a seperate thread for usnic acid + Napalm/Lipo Ultra because i know this is going to be overlooked....

I'll do so,with some supporting research,as time allows.

[grocker]

Damn....I shoulda made a seperate thread for usnic acid + Napalm/Lipo Ultra because i know this is going to be overlooked....

I'll do so,with some supporting research,as time allows.

That would be great. I'm interested in finding out more about this since I will be using Napalm very soon.

[Colin]

That would be great. I'm interested in finding out more about this since I will be using Napalm very soon.

Well,the "supporting research" I have is really just a post by someone on M&M whose opinion I respect,there haven't been any studies done on UA as a topical fat loss aid.Anecdotally,I can tell you it has a profound effect.It's a also pretty cheap,once you actually find it,just don't use it orally as liver toxicity is a real issue when taken systematically.

[jmh80]

I wasn't suggesting cap and yeah,topically applied cap is effing nuts IMO,tried it once and that was enough for me.

The inclusion of raspberry ketones in Napalm makes cap redundant as they act on the same pathways.I strongly suggest procuring usnic acid,to add to Lipoderm Ultra or Napalm though.It is quite safe,when applied topically,as very little is absorbed systematically.I cannot stress enough how good my results were on old school Lipoderm-Y with caffiene and usnic acid.Topical usage of UA blows topical clen away,IME.

REALLY?? I loved Napalm and clen.

I've got a Napalm - I'ma give the UA a shot. What amount did you add of usnic to a bottle of Napalm?
Did it mix easily or pain in the azz?

[Colin]

REALLY?? I loved Napalm and clen.

I've got a Napalm - I'ma give the UA a shot. What amount did you add of usnic to a bottle of Napalm?
Did it mix easily or pain in the azz?

Well,I appear to be the only one who's tried topical UA and I also haven't really given topical clen much of a shot.I have used Lipo Ultra with clen but my diet wasn't as aggressive as it was while on Lipo/UA.By the end of the Lipo/UA run I was the leanest I have ever been,not so ripped at the end of the Lipo/clen stint.

I can tell you that UA made my chest SWEAT,that is a distinct and undeniable sign of thermogenesis.I applied the Lipo/UA to my pecs and my bedsheets would be soaked with sweat (only the sheets around where my chest was) the next morning.Kinda like the fat cells on my chest were up all night partying,dancing and doing jumping jacks.

This was with old school Lipoderm-Y,the first version without caffiene.Mixing it wasn't difficult.

It was an 8-oz. bottle IIRC and I put in around 5 grams of UA and about a gram of caffiene.You may be able to get 3 grams into Napalm or Lipo Ultra but that is asking a lot of the carrier.I'd add 1.5 grams at a time to insure the carrier will absorb it,following the outline below.

As an aside,UA in either Lipo Ultra or Napalm would make for a sweet topical to rotate in clen's place,if you already have a bottle of Lipo Ultra or Napalm with clen in it.

Here is how to figure dosing:


Take number of grams you will put in the fluid times 1000, which will convert it to milligrams. So, let’s say you have 10 grams. 10 * 1000 = 10,000mg. Next, divide by 240, which is the amount of fluid in milliliters. So, 10,000 /240= 41.6mg per ml of fluid.


Take half of the fluid out in a seperate container. Heat up the remaining gel in the Lipo/Napalm bottle for about 10 seconds, add half your desired powder, then heat again. Next add the remaining powder, heat once again. Next heat the fluid that was originally taken out and then add to the Lipo/Napalm bottle, shake, powder should be dissolved and ready for use.


Please keep us updated if you follow through and try this.

[munique]

That would be great. I'm interested in finding out more about this since I will be using Napalm very soon.

same here. please do update us.