Freedom from Nicotine - The Journey Home


Chapter 1: Nicotine Addiction 101

Topics:  Aaah | Slavery | Tolerance | Nicotine | Heroin | Industry | Admitting

Chemical Slavery's Onset

What would happen if, by chance, an external chemical so closely resembled the properties of the neuro-chemical responsible for activating brain dopamine pathways (acetylcholine), that once inside the brain it was capable of generating a stolen and unearned dopamine "aaah" wanting relief sensation?

Unfortunately, entirely by chance, nicotine is such a chemical.

Nicotine's polarities and chemical structure are so similar to acetylcholine, the brain's natural chemical messenger responsible for initiating normal dopamine pathway stimulation, that it bonds to acetylcholine receptors.

In those of us whose genetics or development made us susceptible to nicotine addiction, our dopamine pathways began to document and record nicotine use as though a pre-programmed species survival event.

Clearly, no inner "wanting" or desire existed when we first used nicotine. But if susceptible to dependency, it probably didn't take using too many times before repeated activation caused physical changes within our dopamine pathways.

Those changes would combine with constantly falling blood serum nicotine levels to cause our tonic dopamine level to decline. This would trigger subtle background wanting, wanting that would motivate us to use again and again and again.

Each new supply of nicotine would be followed by a phasic dopamine release. The lower our tonic dopamine level, the more noticeable our "aaah" wanting relief sensation, the more vivid our newest use reinforcement memory.

Soon, an increasing number of high definition nicotine use memories would themselves begin suggesting that we use early and often, so as to avoid sensing the onset of wanting.

As though bars to a prison cell, our thinking, planning and day became surrounded by hundreds and then thousands of durable use memories, each forcing us to vividly recall how wanting gets satisfied.

We had developed a physical need that we couldn't then possibly understand. We found ourselves inventing reasons to explain and justify our continued use. Those reasons (false use rationalizations) would act as additional bars in our prison cell.

Collectively, our wanting satisfaction memories quickly became more durable and vivid than any negative memory of any toxic unpleasantness felt during our first few uses of tobacco. In fact, it wasn't long before a growing number of high definition use memories buried all remaining memory of what life was like without nicotine.

Try recalling the calm, quiet and relaxed mind you enjoyed before getting hooked. Try hard to remember going entire days and weeks without once wanting to use nicotine. You can't do it, can you! Don't feel alone. None of us can. It's a drug addiction hallmark.

Prisoners of hijacked pay-attention circuitry, wanting's satisfaction became our #1 priority.[9] We quickly forgot that it was ever possible to function without nicotine.

Our priorities teacher had been taken hostage. If we resisted and delayed using, we were disciplined with anxieties for failure to apply the lessons taught.

The brain's control room for coordinating and routing dopamine pathway functions appears to be the right insula. It's an oval, prune-sized brain structure above our ear.

The insula receives a wide range of input from our senses, emotions, dopamine pathways, and from the prefrontal cortex, home to previously recorded "pay attention" memories.

A 2007 study found that smokers who sustained brain damage to the right insula actually lost the urge to smoke,[10] suggesting that it also routes or coordinates use urges, craves and anxieties.

Thank goodness it doesn't take traumatic brain injury or a stroke to make us stop craving nicotine. Thank goodness that recovery isn't nearly as difficult as our brain wanting disorder suggests.

Whether heroin, cocaine, methamphetamines, alcoholism or nicotine, drug addiction is about the brain's dopamine pathways being taken hostage by an external chemical.

We nicotine smokers didn't suck tissue destroying tars that included ammonia, formaldehyde, arsenic, butane, hydrogen cyanide, lead, mercury, vinyl chloride, methane or vast quantities of carbon monoxide into our bodies because we wanted to watch each puff destroy a bit more of our capacity to receive and circulate life-giving oxygen. We did so to replenish constantly falling nicotine reserves.

Nicotine is a small molecule. This allows it to cross through our protective blood-brain filter. Once through, it docks with acetylcholine receptors and stimulates dopamine flow.

Smoked nicotine contains at least one other as yet unidentified chemical that somehow diminishes dopamine cleanup enzymes MAO A and MAO B. Diminished MAO means delay in normal dopamine cleanup following a phasic release. It means that smoked nicotine's wanting relief sensation is allowed to linger longer than normal.

Think about how short-lived the "aaah" sensation is following a single potato chip or a sip of water when thirsty. Longer wanting relief is thought to make smoked nicotine possibly the most perfectly designed form of addiction.

It may also help explain why oral tobacco users generally have higher blood nicotine concentrations than smokers. Smokeless tobacco does not inhibit MAO or normal dopamine clean-up. It may be that users of all non-smoked forms of nicotine require higher levels of nicotine in order to keep their wanting at bay.

Whether smoked or oral, an endless cycle of wanting and its brief absence following use left us totally yet falsely convinced that nicotine was essential to survival.

Animated gif showing the nicotine dependency feeding cycle

Our nicotine feeding cycle left many of us believing that use defined who we were, that nicotine gave us our edge, helped us cope, and that life without it would be horrible or even meaningless.

Punished with wanting that was satisfied by use, we quickly grew to believe that we could not function comfortably without it.

Why can't we starve ourselves to death? Not only is wanting for food satisfied with dopamine "aaah" relief sensations when we anticipate eating or actually do so, we are punished with anxieties and cravings when we wait too long between meals.

As for nicotine levels, like food, what goes up must come down. As our body slowly metabolized and rid itself of nicotine, we gradually experienced increasing mood deterioration and escalating distress, punctuated by anxiety, anger and depression.

In fact, it's work living life as a nicotine addict. We endured greater extremes in daily mood swings than non-users, greater problematic anger,[11] and the greater our dependency the more unstable our moods.[12]

Our hijacked priorities teacher was fooled and started teaching a false lesson, that bringing a new supply of nicotine into the bloodstream was every bit as important as eating.

Extensive dopamine circuitry overlap,[13] nicotine cravings became as real as food cravings. Nicotine "aaah" wanting relief sensations became as important as food "aaah"s. Nearly indistinguishable, we experienced the same anxiety beatings, and similar dopamine wanting relief sensations upon surrender.

But there is one massive difference between dependency upon food and dependency upon nicotine. Without food we starve, without nicotine we thrive!

Unfortunately, our hostage dopamine circuitry is incapable of distinguishing fact from fiction. By design, it has buried and suppressed the beauty of never wanting or needing that existed prior to nicotine's arrival.

Would coming home to your calm and quiet yet forgotten mind be a good thing or bad? If good, what sense does it make to fear it?

The problem is that attempts to end nicotine use are often met with a rising tide of anxieties. Soon, our thousands of old nicotine use "aaah" relief memories begin looking like life jackets.

While we only needed to remain nicotine-free and stay afloat for a maximum of three days in order to navigate the roughest seas and move beyond peak withdrawal, hungry for calm, most of us took the hook and bit on our "aaah" memory bait.

We obeyed the false lessons generated by our chemically hijacked teacher. In doing so, we abandoned the only path home in exchange for a few minutes of relief.

When trying to stop using, it isn't unusual to find our mind's addiction chatter insanely trying to convince us that things will be fine if we just have a little more nicotine now, that we can stop using while using more.

I hate to think about how many times I told myself during a prior attempt that using just once more was my reward for having briefly succeeded in going without.

Obviously, this quick fix isn't a solution at all. It shows a total lack of understanding as to the purpose and function of brain dopamine pathways, to make circuitry activating activities nearly impossible, in the short term, to forget or ignore.

But bondage is more than a rising tide of anxieties being fostered by a diminishing tonic dopamine level, in response to constantly declining blood-serum nicotine reserves. And it's more than thousands of old use memories screaming the wrong way out.

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9. McGowan, K, Addiction: Pay Attention, Psychology Today Magazine, Nov/Dec 2004, Article ID: 3571; also see, Rosack, J, Volkow May Have Uncovered Answer to Addiction Riddle, Psychiatric News June 4, 2004, Volume 39 Number 11, Page 32.
10. Naqvi, NH, et al, Damage to Insula Disrupts Addiction to Cigarette Smoking, Science, January 2007, Vol. 315 (5811), Pages 531-534.
11. Cougle JR, Delineating a Relationship Between Problematic Anger and Cigarette Smoking: A Population-Based Study, Nicotine and Tobacco Research, May 13, 2012.
12. Parrott AC, Cigarette-derived nicotine is not a medicine, The World Journal of Biological Psychiatry, April 2003, Volume 4(2), Pages 49-55.
13. Blum K, et al, Reward circuitry dopaminergic activation regulates food and drug craving behavior, Current Pharmaceutical Design, 2011; Volume 17(12), Pages 1158-1167; also Kelley AE, et al, Neural systems recruited by drug- and food-related cues: studies of gene activation in corticolimbic regions, Physiology & Behavior. 2005 September, Volume 15:86(1-2):11-14.

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Page created June 15, 2015 and last updated June 24, 2015 by John R. Polito