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Posts: 104
Reply with quote  #1 
After years of trying the wrong way, a reconstructed attitude turned the trick on first try. 

Each failed attempt caught me counting how many days I had the strength to deny myself the habit. Way down deep, I knew that after five days or so, the reward for failure was a wild blast of nicotine punch that took me back as a loyal smoker. It was all like holding a bungee cord stretched out until collapsed effort brought welcome relief.

What worked was to estimate the half-life of aggravation in days. Picking three days (it didn't matter) as the half-life, it was clear that after three days of no smoke, the next try would be twice the misery. At nine days, I faced eight times the present misery if I gave up giving up. It just never ever  made sense to ever light up again.

Two's a crowd.

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Posts: 501
Reply with quote  #2 
That's an exceptional method. I quit 27 years ago. The price went up over a buck and I drew the line. Quit cold turkey. Your method makes mine seem so mundane...[rolleyes]
The universe is a hairball. It was created by Fritz the Cat. :P Einstein said the universe was like a plate of spaghetti. Still, you don't want to know what transpired between him and Elsa to bring about that idea.

Posts: 104
Reply with quote  #3 

Back in my day, Lucky Strikes were still dirt cheap.

I even tried self hypnosis. A trick took my usage rate from a pack a day to half a pack. It worked immediately, but fell off after some five weeks. Yet, it worked so well that it scared me to use something (hypnosis) totally beyond my comprehension.

Didn't dare to try that again.

Two's a crowd.

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Posts: 501
Reply with quote  #4 

Patty, my other half, kicked it about 5 years ago, pretty much the same way I did. Both of us have a Karate background, so the willpower that accompanies such.

Just a thought, but maybe if you took up Karate and/or Tai Chi, it might provide the replacement one needs to displace the Freudian urge to devour, while the nicotine fades out of your system.

Systematic (IUPAC) name
Clinical data
Trade namesNicorette, Nicotrol
Pregnancy cat.D (US)
Legal statusUnscheduled (AU) GSL (UK) OTC (US)
Dependence liabilityVery high
Routessmoked (as smoking tobacco, mapacho, etc.), insufflated (as tobacco snuff or nicotine nasal spray), chewed (as nicotine gum, tobacco gum or chewing tobacco), transdermal (as nicotine patch, nicogel or topical tobacco paste), intrabuccal (as dipping tobacco, snuffs, dissolvable tobacco or creamy snuff), vaporized (as electronic cigarette, etc.), directly inhaled (as nicotine inhaler), oral (as nicotini), buccal (as snus)
Pharmacokinetic data
Bioavailability20 to 45% (oral)
Half-life2 hours; 20 hours active metabolite (cotinine)
CAS number54-11-5 YesY
ATC codeN07BA01 QP53AX13
PubChemCID 942
IUPHAR ligand2585
ChemSpider80863 YesY
KEGGD03365 YesY
ChEBICHEBI:18723 [svg]N
Chemical data
Mol. mass162.12 g/mol
Physical data
Density1.01 g/cm³
Melt. point-79 °C (-110 °F)
Boiling point247 °C (477 °F)
 [svg]N (what is this?)  (verify)

Nicotine is a potent parasympathomimetic alkaloid found in the nightshade family of plants (Solanaceae) and a stimulant drug. It is a nicotinic acetylcholine receptor agonist. It is made in the roots and accumulates in the leaves of the plants. It constitutes approximately 0.6–3.0% of the dry weight of tobacco[1] and is present in the range of 2–7 µg/kg of various edible plants.[2] It functions as an antiherbivore chemical; therefore, nicotine was widely used as an insecticide in the past[3][4] and nicotine analogs such as imidacloprid are currently widely used.

In smaller doses (an average cigarette yields about 1 mg of absorbed nicotine), the substance acts as a stimulant in mammals, while high amounts (30–60 mg[5]) can be fatal.[6] This stimulant effect

It is being determined that nicotine does nerve damage, especially in fetuses. If you look at that nitrogen radical in the molecule, you can see it's lurking in wait for almost any of several candidate radicals to attach to. As the blurb above depicts, it is generally a nerve receptor, but could just as easily attach to a cholinesterase receptor, inhibiting its activity, thus causing nervous tremors. VX or Mustard Gas, among others, do this to convulsive extremes.

acetylcholinesterase (Yt blood group)
Acethylcholinesterase TC 1EA5.png
Diagram of Pacific electric ray acetylcholinesterase. From PDB 1EA5.
Alt. symbolsYT
Other data
EC number3.1.1.7
LocusChr. 7 q22
Butyrylcholinesterase 1P0I.png
Cartoon diagram of human butyrylcholinesterase. From PDB 1P0I.
Alt. symbolsCHE1
Other data
EC number3.1.1.8
LocusChr. 3 q26.1-26.2

In biochemistry, cholinesterase is a family of enzymes that catalyze the hydrolysis of the neurotransmitter acetylcholine into choline and acetic acid, a reaction necessary to allow a cholinergic neuron to return to its resting state after activation.


There are two types:

  • Acetylcholinesterase (EC (AChE), also known as RBC cholinesterase, erythrocyte cholinesterase, or (most formally) acetylcholine acetylhydrolase, found primarily in the blood on red blood cell membranes, in neuromuscular junctions, and in neural synapses. Acetylcholinesterase exists in multiple molecular forms. In the mammalian brain the majority of AChE occurs as a tetrameric, G4 form (10) with much smaller amounts of a monomeric G1 (4S) form.[1]
  • Pseudocholinesterase (EC (BChE or BuChE), also known as plasma cholinesterase, butyrylcholinesterase, or (most formally) acylcholine acylhydrolase, is produced in the liver and found primarily in plasma.

The difference between the two types of cholinesterase has to do with their respective preferences for substrates: the former hydrolyses acetylcholine more quickly; the latter hydrolyses butyrylcholine more quickly.

The half-life of pseudocholinesterase is approximately 8–16 hours. Pseudocholinesterase levels may be reduced in patients with advanced liver disease. The decrease must be greater than 75% before significant prolongation of neuromuscular blockade occurs with succinylcholine.[2][3]


In 1968, Walo Leuzinger et al. successfully purified and crystallized the enzyme from electric eels at Columbia University, NY.[4][5]

The 3D structure of acetylcholinesterase was first determined in 1991 by Joel Sussman et al. using protein from the Pacific electric ray.[6]

Clinically useful quantities of butyrylcholinesterase were synthesized in 2007 by PharmAthene, through the use of genetically modified goats.[7]

Clinical significance[edit]

An absence or mutation of the pseudocholinesterase enzyme leads to a medical condition known as pseudocholinesterase deficiency. This is a silent condition that manifests itself only when people that have the deficiency receive the muscle relaxants succinylcholine or mivacurium during a surgery.

Pseudocholinesterase deficiency may also affect local anaesthetic selection in dental procedures. The enzyme plays an important role in the metabolism of ester-based local anaesthetics, a deficiency lowers the margin of safety and increases the risk of systemic effects with this type of anaesthetic. The selection of an amide-based solution is recommended in such patients.

Elevation of plasma pseudocholinesterase was observed in 90.5% cases of acute myocardial infarction.[8]

The presence of acetylcholinesterase in the amniotic fluid may be tested in early pregnancy. A sample of amniotic fluid is removed by amniocentesis, and presence of AChE can confirm several common types of birth defect, including abdominal wall defects and neural tube defects.[9]

Butyrylcholinesterase can be used as a prophylactic agent against nerve gas and other organophosphate poisoning.[7]

Cholinesterase inhibitors[edit]

A cholinesterase inhibitor (or "anticholinesterase") suppresses the action of the enzyme. Because of its essential function, chemicals that interfere with the action of cholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death (examples are some snake venoms, and the nerve gases sarin and VX). One counteracting medication is pralidoxime. The so-called nerve gases and many substances used in insecticides have been shown to act by combining with a residue of serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. The enzyme acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop.


So you can see just what is taking place in your body.

Patty's dad kicked it with acupuncture. He died from diabetes, though, in 1994, so can't be here to add his 2 cents worth. I recommend an activity that can increase your will power.

The universe is a hairball. It was created by Fritz the Cat. :P Einstein said the universe was like a plate of spaghetti. Still, you don't want to know what transpired between him and Elsa to bring about that idea.

Posts: 104
Reply with quote  #5 

My original posting was made only to acknowledge the simplicity encountered by accident when just an attitude alteration took me out of the losers' circle of smokers. Dropping cigarettes after some three decades of smoking was no bother at all and the habit never came back these last 30 or 40 years.

No will power was wasted upon that mundane accomplishment.

Two's a crowd.

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Posts: 501
Reply with quote  #6 
I read your launch post again. Don't know how, now, I got the idea you were still struggling to quit. Glad that isn't the case. Yes. Attitude has everything to do with it, although quitting comes easier to some than others.
The universe is a hairball. It was created by Fritz the Cat. :P Einstein said the universe was like a plate of spaghetti. Still, you don't want to know what transpired between him and Elsa to bring about that idea.
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