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|
|Trade names||Nicorette, Nicotrol|
|Pregnancy cat.||D (US)|
|Legal status||Unscheduled (AU) GSL (UK) OTC (US)|
|Dependence liability||Very high|
|Routes||smoked (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)|
|Bioavailability||20 to 45% (oral)|
|Half-life||2 hours; 20 hours active metabolite (cotinine)|
|CAS number||54-11-5 Y|
|ATC code||N07BA01 QP53AX13|
|Mol. mass||162.12 g/mol|
|Melt. point||-79 °C (-110 °F)|
|Boiling point||247 °C (477 °F)|
| 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 and is present in the range of 2–7 µg/kg of various edible plants. It functions as an antiherbivore chemical; therefore, nicotine was widely used as an insecticide in the past 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) can be fatal. 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.
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 220.127.116.11) (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.
- Pseudocholinesterase (EC 18.104.22.168) (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.
In 1968, Walo Leuzinger et al. successfully purified and crystallized the enzyme from electric eels at Columbia University, NY.
The 3D structure of acetylcholinesterase was first determined in 1991 by Joel Sussman et al. using protein from the Pacific electric ray.
Clinically useful quantities of butyrylcholinesterase were synthesized in 2007 by PharmAthene, through the use of genetically modified goats.
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.
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.
Butyrylcholinesterase can be used as a prophylactic agent against nerve gas and other organophosphate poisoning.
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.