Freedom from Nicotine - The Journey Home

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Chapter 7: Roadmap Overview

Topics:  Starting Point | Ending Use | Recovery Layers | Recovery Time Line

Ending Nicotine Use

Photo of a crushed cigarette butt

That first courageous step is "huuuuge," the biggest baby step of all.

Mustering the courage to at last say "no" to that next nicotine fix is the only path to the wonderfulness beyond: return to a calm, quiet and beautiful mind that blind obedience to dependency wanting has for far too long keep hidden from view.

Contrary to marketing of those pushing an exploding array of nicotine delivery devices, the only way out is to stop bringing nicotine in. And the speed of natural recovery can be seen within an hour of remaining 100% nicotine-free, as the concentration of nicotine within your blood falls by 25 percent.

"Half-life" is defined as "the time required for half the quantity of a drug or other substance deposited in a living organism to be metabolized or eliminated by normal biological processes."[1] Most older cessation literature firmly fixes nicotine's elimination half-life at about two hours.[2]

But nicotine's half-life can vary substantially based upon genetic, racial, hormonal, diet, activity and age factors.[3] For now, let's ignore genetic differences, as we have no idea which genes we do or don't have.

As for racial variations, a 1998 study found an average nicotine half-life of 129 minutes in Caucasians and 134 minutes in African Americans.[4] A 2002 study compared Chinese-American, Latino and Caucasian smokers. It found that Latinos had the shortest half-life (122 minutes), Chinese-Americans the longest (152 minutes), with Caucasians in the middle (134 minutes).[5]

Nicotine's half-life is shorter in women (118 minutes) than men (132 minutes), and even faster in women taking oral contraceptives (96 minutes). This is thought to be associated with estrogen.[6]

Nicotine's half-life is shorter during pregnancy (97 minutes) than after giving birth (111 minutes).[7] Sadly, new born babies whose mothers smoked endure a nicotine withdrawal period five times longer than what their mother's would have been. Instead of the newborn having a 2-hour elimination half-life, it balloons to 11.2 hours.[8] If considering breast-feeding, nicotine's breast milk half-life averages 97 minutes.[9]

Interestingly, a 1993 nicotine patch study found that when nicotine was administered directly into the bloodstream (intravenously) it had a 2 hour elimination half-life but when administered through the skin via the nicotine patch (transdermally), once the patch was removed nicotine's half-life was 2.8 hours.[10] This finding was confirmed by a second patch study which found it to be a minimum of 3.3 hours.[11]

Most nicotine is broken-down into six primary metabolites by the liver (mostly cotinine: 70-80%). The kidneys remove (eliminate or excrete) nicotine and its metabolites from the bloodstream.[12]

Thus, any activity which increases blood flow though the liver (exercise or eating) accelerates nicotine metabolization. Liver blood flow increases by 30% after meals, with a 40% increase in the rate that nicotine is cleared from arriving blood.[13]

As we learned in Chapter 4, acidic urine accelerates the rate by which nicotine is metabolized, while alkaline urine actually allows re-absorption back into the body.

As suggested by the above half-life data, most of us had sufficient nicotine reserves to make it through 8 hours of sleep each night (4 half lives leaving us with a minimum of 6.25% of our normal daily supply).

In fact, the amount of nicotine remaining after sleep is actually higher than simple division suggests. It makes sense, as the amount of blood flow and nicotine passing through and being metabolized by the liver decreases while sleeping.

As you can see, remaining reserves become so small within 24 hours of ending use that nicotine becomes difficult to detect (.02 or just 2/100ths of our normal daily level). It's here that surgery (nicotine extraction/detox) is nearly complete and deep dependency healing begins in earnest.

Within 3 days, with absolute certainty, you will inhabit a nicotine-free body and mind.

As for detection, we often get the question, how long after I stop using nicotine will my insurance company or employer be able to detect nicotine in my system? As seen above, unless examining hair, which permanently records nicotine use, trying to measure rapidly falling nicotine levels in blood, urine and saliva is all but useless as a marker of use.

That's why insurance companies and employers normally test for cotinine, one of nicotine's longer-lasting metabolites. Cotinine's generally recognized half-life of about 17 hours.[14]

Regarding recovery, what's important is that remaining levels become so small within 24 hours of ending use that re-sensitization and the brain's adjustment to functioning without nicotine have no choice but to commence.

The mind and body begin experiencing overlapping recovery on four levels within 24 hours of ending use: physical, emotional, subconscious and conscious. Keep all nicotine on the outside and within 72 hours, regardless of your body's nicotine half-life or elimination rate, you'll stand atop withdrawal's mountain.

The most challenging portion of recovery will be behind you. While your climb was quick, the slope of the journey down the other side, although initially brisk, is continuous yet ever so gradual. Easier time with fewer bumps, the balance of the journey becomes an exercise in patience.

Yet, violate the "Law of Addiction" - just one hit of nicotine - and forget about any gradual down slope or doing easy time. It's called relapse. You'll either resume life as an actively feeding addict or need to again endure nicotine detox and another climb to the top.

The price of each climb is further depletion of core dreams and desires. Although able to rest and rejuvenate once at or over the top, amazingly few have the stamina of purpose needed to make back-to-back climbs.

Expect to be teased during both your climb and descent by those selling chemicals that stimulate brain dopamine pathways (tobacco products, cigarettes, e-cigarettes, replacement nicotine, bupropion and varenicline). Expect them to try to discourage you.

Listen for the false and deceptive implication that few succeed in stopping on their own. Truth is, it's how the vast majority will succeed this year, and they know it.

Clearly, they want your money. And sadly, nearly all are willing to lie to get it.

Expect their tease to falsely suggest that their product makes the climb easy, or as suggested by recent Nicorette commercials, that it makes quitting "suck less." Don't listen. If the product stimulates dopamine pathways, physical withdrawal's climb cannot be completed until product use ends.

Continued stimulation does not aid recovery but delays it. That's why advertising the product's cessation results while study participants were still under the chemical's influence (varenicline's half-life is 24-hours, 12 times longer than nicotine's), isn't about science but salesmanship.

As Joel Spitzer says, we'd only have ourselves to blame for intentionally extending what should have been a few days of withdrawal into weeks or months.

Not only do users face the side-effect risks posed by each product, they face having to someday adjust to living without the dopamine stimulation the product provides.

Let's turn our attention to what happens once fright musters the courage to say "no." Let's start with the body's physical response to ending use.

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1. half-life. (n.d.). The American Heritage Dictionary of the English Language, Fourth Edition. Retrieved August 22, 2008 from
2. Benowitz NL, et al, Interindividual variability in the metabolism and cardiovascular effects of nicotine in man, The Journal of Pharmacology and Experimental Therapeutics, May 1982, Volume 221(2), Pages 368-372; also see Feyerabend C, et al, Nicotine pharmacokinetics and its application to intake from smoking, British Journal of Clinical Pharmacology, February 1985, Volume 19(2), Pages 239-247.
3. Benowitz NL, Clinical pharmacology of nicotine: implications for understanding, preventing, and treating tobacco addiction, Clinical Pharmacology & Therapeutics, April 2008, Volume 83(4), Pages 531-541.
4. Perez-Stable EJ, et al, Nicotine metabolism and intake in black and white smokers, Journal of the American Medical Association, July 8, 1998, Volume 280(2), Pages 152-156.
5. Benowitz NL, et al, Slower metabolism and reduced intake of nicotine from cigarette smoking in Chinese-Americans, Journal of the National Cancer Institute, January 16, 2002, Volume 94(2), Pages 108-115.
6. Benowitz NL, et al, Female sex and oral contraceptive use accelerate nicotine metabolism, Clinical Pharmacology & Therapeutics, May 2006, Volume 79(5), Pages 480-488.
7. Dempsey D, et al, Accelerated metabolism of nicotine and cotinine in pregnant smokers, Journal of Pharmacology Exp Therapeautics, May 2002, Volume 301(2), Pages 594-598.
8. Dempsey D, et al, Nicotine metabolism and elimination kinetics in newborns, Clinical Pharmacology Therapeutics, May 2000, Volume 67(5), Pages 458-465.
9. Luck W, Nicotine and cotinine concentrations in serum and milk of nursing smokers, British Journal of Clinical Pharmacology, July 1984, Volume 18(1), Pages 9-15.
10. Gupta SK, et al, Bioavailability and absorption kinetics of nicotine following application of a transdermal system, British Journal of Clinical Pharmacology, September 1993, Volume 36(3), Pages 221-227.
11. Keller-Stanislawski B, et al, Pharmacokinetics of nicotine and cotinine after application of two different nicotine patches under steady state conditions, Arzneimittel-Forschung, September 1992, Volume 42(9), Pages 1160-1162.
12. Benowitz NL, et al, Nicotine chemistry, metabolism, kinetics and biomarkers, Handbook of Experimental Pharmacology 2009; Volume 192), Pages 29-60.
13. Hukkanen J, et al, Metabolism and disposition kinetics of nicotine, Pharmacological Reviews, March 2005, Volume 57(1), Pages 79-115.
14. Swan GE, et al, Saliva cotinine and recent smoking--evidence for a nonlinear relationship, Public Health Reports, Nov-Dec 1993, Volume 108(6), Pages 779-783.

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