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Healthy Neurochemical Reactions to LifeNicotine's two-hour half-life inside the human body was the basic clock that not only set the deadline for that next mandatory feeding but also which feedings we'd consider our "best."
Imagine sleeping through four nicotine half-lives (8 hours) and awaking the next morning with our nicotine level somewhere down around our socks. No wonder that morning fix was one of the "best." Although the clock could not be slowed, acid generating events such as stress, anxiety, alcohol and mega doses of vitamin C could accelerate the clock by more rapidly depleting the body's reserves of the alkaloid nicotine. Such events would more rapidly transport us to the brink of onset of early withdrawal. No wonder we made such deep rooted yet false conclusions about nicotine's relationship to stress and alcohol. No wonder these groups of feeding memories are some of our "best!"
Living life on nicotine's clock totally ignored our body's own natural and healthy neurochemical timetables. As you've probably read here at Freedom, nicotine caused the brain to release stores of adrenaline and noradrenaline that prepared our body for the fight or flight survival mode. An amazing cascade of fight or flight neurochemicals would temporarily shut down all non-essential systems and functions, constrict extremity blood vessels to help control any bleeding during battle or escape, accelerate the heartbeat to pump greater volumes of blood, stimulate the lungs to process more oxygen, would heighten the senses, and dump stored fats and sugars into the bloodstream to provide an instant source of energy. Question: Is that what our body really needed when life's moment begged for deep deep relaxation like just before climbing into bed to sleep?
Recovery can be a wonderful adventure in self-discovery as we begin to appreciate that our body's neurochemicals each had purpose and their flow had natural controls, controls that, by coincidence, the chemical nicotine was able to completely bypass. Was it time for a nicotine induced dopamine ahhhhh reward sensation upon learning the tragic news of the death of a close friend or loved one? Was it then time to smoke a chemical that would diminish the flow of serotonin, a mood and critical anxiety busting neurochemical?
All that matter are the next few moments and each is entirely doable. The accomplishment induced dopamine ahhhhh sensation resting just beyond that next challenge is not only yours to enjoy, it's "you," it's beautiful, and it's an honest message that this recovery is a keeper. You're going home! There was always only one rule, no nicotine today - Never Take Another Puff! John
Nicotine renal excretion rate influencesJ Pharmacol Exp Ther. 1985 July;234(1):153-5.
nicotine intake during cigarette smoking.
Benowitz NL, Jacob P 3rd.
We examined the hypothesis that rate of elimination of nicotine affects nicotine intake during cigarette smoking. Elimination rate was altered by administering ammonium chloride or sodium bicarbonate throughout the day. Nicotine intake during unrestricted cigarette smoking was measured using metabolic clearance data obtained after i.v. nicotine infusion together with blood and urinary nicotine concentrations measured during 24-hr periods of cigarette smoking. Compared with placebo treatment (urine pH 5.6), urinary acidification (pH 4.5) increased (208%) renal clearance and, to a lesser extent (41%), total clearance and increased (by 7.2 mg) daily urinary excretion of nicotine. Urinary alkalinization (pH 6.7) resulted in a decrease (78%) in renal clearance with a small decrease (3.7 mg) in daily nicotine excretion. Average blood nicotine concentrations were similar in placebo and bicarbonate treatment conditions, but were 15% lower during acid loading. Daily intake of nicotine was 18% greater during acid loading. The compensatory increase in nicotine consumption was only partial, replacing about half the excess urinary nicotine loss. This is the first direct demonstration that rate of elimination can influence self-determined drug consumption in humans.
PMID: 4009497 [PubMed - indexed for MEDLINE]
Effects of urinary pH on the behavioral
responses of squirrel monkeys to nicotine.Pharmacol Biochem Behav. 1983 Sep;19(3):553-7.
Grunberg NE, Morse DE, Barrett JE.
The present study evaluated the behavioral effects of nicotine under conditions that manipulated urinary pH. The effects of nicotine were examined on the responding of squirrel monkeys under a multiple fixed-interval, fixed-ratio schedule of stimulus-shock termination when nicotine was administered alone or together with the gastric administration of an acidifier (ammonium chloride) or an alkalinizer (sodium bicarbonate). Responding under the FI schedule was increased markedly across a range of doses of nicotine (0.02-0.20 mg/kg). Responding under the FR was increased to a lesser extent by the lower doses of nicotine (0.02-0.05 mg/kg) and was decreased by doses of nicotine that increased responding under the FI (0.10-0.20 mg/kg). Generally, administration of the acidifier attenuated the effects of nicotine while administration of the alkalinizer potentiated those effects. These findings support the argument that changes in cigarette smoking under conditions that alter urinary pH involve nicotine per se. In addition, a new interpretation of the relationship between urinary pH and cigarette smoking is offered.
PMID: 6314394 [PubMed - indexed for MEDLINE]
Protons enhance the gating kinetics of the alpha3/beta4 neuronal nicotinic acetylcholine receptor by increasing its apparent affinity to agonists.Mol Pharmacol. 2002 February;61(2):369-78.
Abdrakhmanova G, Dorfman J, Xiao Y, Morad M.
Department of Pharmacology, Georgetown University School of Medicine, Washington DC 20007, USA.
Neuronal nicotinic acetylcholine receptors (nAChRs) are widely distributed in the nervous system. Although there is a vast literature on the molecular, structural and pharmacological properties of neuronal nAChR, little is known of their pH regulation. Here we report that rapid acidification (pH 6.0) enhances the current through the alpha3/beta4 recombinant nAChRs expressed stably in human embryonic kidney 293 cells and accelerates its activation kinetics without altering selectivity. Acidification also strongly accelerates the decay kinetics ("desensitization") of cytisine- and nicotine-evoked currents (pK(a) approximately 6.1), but the effect is somewhat smaller with acetylcholine and carbachol (undetermined pK(a) values), suggesting that protonation of the agonist contributes to the relaxation of the current. Transient increases of [H(+)](o) from pH 7.4 to 6.0, during the time course of decay of the current, enhances the current and accelerates its decay kinetics in a manner similar to reactivation of current by higher concentrations of agonists. We suggest that protons interact with multiple extracellular sites on alpha3/beta4 nAChRs, decreasing the effective EC(50) values of the agonist and accelerating gating kinetics, in part by promoting agonist-induced block. We speculate that corelease of protons with ACh from the secretory vesicles may induce rapid and reversible conformational changes in the slowly "desensitizing" alpha3/beta4 nAChRs, leading to accelerated signaling.
PMID: 11809862 [PubMed - indexed for MEDLINE]
New reactions, old expectationsNot only did stressful acid producing events quickly neutralize and deplete the body's reserves of the alkaloid nicotine, forcing us to service our addiction before addressing the underlying stressful event (if it were addressed at all), we also have to take care not to intentionally use anxiety driven recovery anger as a tool to try and replace the central nervous system stimulation (CNS) that came with each new puff.
and a junkie mind at work
Via acetylcholine receptor sites, nicotine released adrenaline and a host of other fight or flight neurochemicals designed to prepare the body to attack or run from the sabertooth tiger. Although not addictive (as is with stealing from the dopamine reward pathways) we were each conditioned to expect instant CNS stimulation as part of each new nicotine feeding. So how can a recovering nicotine addict stop using nicotine and yet still experience regular adrenaline releases? Can it be done by picking fights with those around us? Can it be done by inventing our very own sabertooth tiger?
On yet another level the conscious mind can intentionallye employ and use anxiety driven recovery anger to the point that it knows it can cause family or friends to want us to relapse.
Sadly, my junkie mind used this tactic on more than one occasion to not only force my loved ones to again want me to smoke nicotine but to actually get them to purchase my relapse smokes for me. It was almost too perfect. It allowed my junkie mind to employ the most destructive form of blame transference imaginable. "Maybe someday my loved ones would be strong enough to allow me to go the distance and succeed at quitting," I told myself.
Such destructive garbage could only flow from the mind a true drug addict. But this time I have a much fuller understanding of my now arrested dependency. Fool me once shame on you, fool me twice shame on me! Millions of words here at Freedom but only one rule ... no nicotine just one day at a time, Never Take Another Puff!
John (Gold x5)
It's Clean-up Time!
We can continue to sell our mind on the rationalization that smoking the alkaloid nicotine helped relieve stress or dig a bit deeper and conclude that we were instead doing was adding the onset of early withdrawal to each and every stressful acid producing event that life threw our way.
Imagine facing daily challenges without being forced to flee into your addiction. It is far far easier being "you" than the neurochemical mess that nicotine has for far too long been allowed to make of your mind.
John (Gold x5)