Some pigment migrates from a tattoo site to lymph nodes, where large particles may accumulate.

For some reason my intuition went into overdrive and I got a message to go slowly with him. I put on one point to test his sensitivity and within less than 30 seconds, his throat swelled completely closed.  He was basically suffocating - it was pretty dramatic! I removed the point and washed the area with water and administered basic first aid (something all practitioners should know) and used a special 'opening the throat'  breathing technique to keep him breathing until it wore off.

Not typical but it just goes to show how careful you need to be.

Lobeline, an alkaloid from Indian tobacco (Lobelia inflata), is classified as a nicotinic agonist and is currently used as a smoking cessation agent. However, our previous in vitro studies demonstrate that lobeline does not act as a nicotinic agonist but alters presynaptic dopamine (DA) storage by potently inhibiting DA uptake into synaptic vesicles. Recently, d-amphetamine has been reported to act at the level of the synaptic vesicle to alter presynaptic function. The present in vitro studies further elucidate the mechanism of lobeline's action and compare its effects with those of d-amphetamine. [3H]Dihydrotetrabenazine ([3H]DTBZ), used routinely to probe a high-affinity binding site on the vesicular monoamine transporter (VMAT2), bound to vesicle membranes from rat striatum with a KD of 1.67 nM and Bmax of 8.68 pmol/mg of protein. Lobeline inhibited [3H]DTBZ binding with an IC50 of 0.90 microM, consistent with its previously reported IC50 of 0.88 microM for inhibition of [3H]DA uptake into vesicles. These results suggest that lobeline specifically interacts with DTBZ sites on VMAT2 to inhibit DA uptake into synaptic vesicles. Interestingly, d-amphetamine inhibited [3H]DTBZ binding to vesicle membranes with an IC50 of 39.4 microM, a concentration 20 times greater than reported for inhibition of VMAT2 function, suggesting that d-amphetamine interacts with a different site than lobeline on VMAT2 to inhibit monoamine uptake. Kinetic analysis of [3H]DA release from [3H]DA-preloaded synaptic vesicles in the absence of drug revealed a t1/2 of 2.12 min. Lobeline and d-amphetamine evoked [3H]DA release with EC50 values of 25.3 and 2.22 microM, respectively. At a concentration 10 times the EC50, lobeline and d-amphetamine significantly decreased the t1/2 of [3H]DA release to 1.58 and 1.48 min, respectively. Thus, in contrast to d-amphetamine, which is equipotent in inhibiting DA uptake and promoting release from the synaptic vesicles, lobeline more potently (28-fold) inhibits DA uptake (via an interaction with the DTBZ site on VMAT2) than it evokes DA release to redistribute presynaptic DA storage.

The present study tested the hypothesis that pretreatment with LOB would attenuate heroin self-administration in rats. The findings from this investigation demonstrated that LOB pretreatment effectively attenuates opiate self-administration in a dose dependent manner. The lowest dose of LOB (0.3 mg/kg) had no effect, while attenuation of heroin self-administration was demonstrated with LOB doses of 1.0 and 3.0 mg/kg. Our findings are in agreement with the findings of Miller et al. (2007) where lobeline was found to be a μ opioid receptor antagonist, due to having a high affinity for μ opioid receptors, thereby producing an inhibitory effect on opiate pharmacology.

A notable occurrence found in the data from the dose effect testing was the level of active (heroin) lever pressing on the subsequent baseline (saline) days (See Figure 1). After the ineffective dose of LOB (0.3 mg/kg), lever presses for heroin infusions on the following baseline days (3 and 4) stayed steady or slightly increased. Following the first effective dose of LOB (1.0 mg/kg) we observed a decrease in the average number of active lever presses on baseline days 5 and 6. This likely was due to carry-over effects and resulted from feed-forward (Pavlovian) conditioning cues that may have contributed to the antagonistic effects of LOB on heroin reinforcement.

Heroin, once it reaches the brain, is converted to morphine, which then binds to μ opiate receptors acutely expressed on GABAergic ventral tegmental area (VTA) interneurons and on nucleus accumbens (NAc) neurons (Hyman, Malenka, and Nestler, 2006). These inhibitory GABA neurons in the region of the VTA modulate tonic glutamate (Glu) activation of dopamine neurons projecting to the NAc, therein producing reward effects. In this cascade, when opiates bind to the μ receptors on GABA fibers they operate as antagonists. The resulting disinhibition of Glu stimulation permits elevated levels of DA to accrue in the NAc, thereby defining the rewarding properties of heroin. It is possible that LOB may competitively or noncompetitively antagonize opiate action at the μ receptor site (cf. Miller et al., 2007), thus interfering with the disinhibitory effects of heroin that would otherwise occur. Of course, LOB may act more directly on DA in the mesolimbic pathway of the brain. As discussed, LOB interrupts the activity of VMAT2, preventing vesicular DA transport within the pre-synaptic terminal (Felpin and Lebreton, 2004) and the attendant compromise in DA activity in the NAc may challenge the reward properties of heroin. This potential direct interference with the activation of the DA reward circuit may lessen heroin drug-seeking, and could account for the pattern of results observed in this study.

Whatever the mechanism(s), the results from the present study increase our understanding of potential chemical interventions and therein add opiates to the growing list of abused drugs for which LOB could potentially become part of an extensive pharmacotherapy regimen. The implications along these lines are profound. Currently, methadone is the treatment of choice for heroin addiction (see Fugelstad et al., 2007), but it comes with established risks. Specifically, methadone overdose (death) is much more common than many people realize (Srivastava and Kahan, 2006; Zador, 2007), and the development of potentially safer, substitute pharmacotherapy’s is desired. In this regard, the fact that LOB acts antagonistically on the opiate system may offer a reliable and less dangerous way to manage selective addiction profiles.

i took a good amount of 3-mmc , 125 mg ( calculated and weighted out) 45 minutes after ingesting i used lobelia sessilifolia. 15 minutes after chewing and ingesting lobelia sessilifolia the 3-mmc trip completely altered. i completely sobered up and felt no effects of 3-mmc whatsoever aside from some anti-depressant effects and stimulation. i went from fuzzy and euphoric high to clear headed and sober within a few minutes, the trip turned into something that would like like a lower dose of psilocybin truffles but without any hallucinogenic effects.

i also noticed that most side effects also decreased, like 3-mmc got the shit kicked out of it. One hour after this i redosed 3-mmc - do note that i had 0 % desire to redose - somehow lobelia took away the desire to redose it became a rational choice instead of a compulsive one, this time the 3-mmc overtook the lobelia but the small amount of lobelia alkaloids made me very clear headed ( no scattered thoughts ) without decreasing the euphoria too much. the peak came way later then it should - probably have sometimes to so with lobelia delaying the absorption and metabolism of 3-mmc.

i was out of lobelia sessilifolia leaves so i used other lobelia species after the redose ( cardinalis, siphilitica etc ) and used a larger amount of them ( 18 leaves total, don't do this if you do not have tolerance ) and 3-mmc got the shit kicked out of it again - however serotonin effects and stimulating effects were present ( not impressive but still ) however the dopamine release was completely inhibited. during the comedown i had no desire to redose ( i wouldn't redose anyway after using such amount .. yuk :/ but there was no underlaying biochemical will to redose ). the comedown was a bit easier as wel.

the day after i did feel sluggish and a bit down like you normally do when you used something that work on serotonin , however i did not have that cracked out feeling from dopamine depletion. late morning or early afternoon i start feeling better and in fact felt better than the days before i used 3-mmc with lobelia ( i kept using lobelia until 2 days after ). i also didn't had that drone smell you normally would when you use cathinones ( a little bit but not as bad as usual which is a plus. )

somehow lobelia decreased the toxic effects ( the whole thing just felt less toxic, no horrible vasoconstriction) , prevented neurotransmitter depletion ( no cracked out feeling like i usually would have ) and reversed the moreishness )

i already tried lobelia cardinalis with pentadrone ( was a long time ago, i fell asleep after i took lobelia while being on pentadrone ) and 4-Fa and had similar effects. lobeline and related alkaloids seem to inhibit the effects of these psychoactive drugs which is good with OD or bad reactions on these types of drugs, the fact that it stopped the desire to redose or the addiction like behaviour is pretty cool as well.

I tried lobelia with mushrooms and syrian rue ( 3 gram wet mass shrooms, 0,5 gram syrian rue + lobelia ) and had a increase in psychedelic effects compared to no lobelia. lobelia works with interacts with cannabis, mushrooms and syrian rue. i never had negative effects from combining lobelia with anything, i only had decreases in negative side effects.

Lobelia is one of my most favorite of herbs because of its skill in healing.  It’s so delicate to see in nature, however, the energy it gives off to me is not delicate and not meek at all.  It gives off energy of pure strength and intelligence. This brings me to mind its medicinal use that few know about and that is the application of its intelligence.  Known as the thinking herb, by some herbalists such as the famed Dr. Christopher, Lobelia added to a formula has a way of thinking where healing is needed in the body, and then directing other herb ingredients where they are most needed.