Smoking and Depression

First, let us try and understand what cigarettes do as relates to depression.

According to the American Heart Association, nicotine addiction (I prefer calling it tobacco addiction because it is not only nicotine that is addictive in the tobacco), has historically been one of the hardest addictions to break, while the pharmacological and behavioral characteristics that determine tobacco addiction are similar to those determining addiction to heroin and cocaine.

Is there anything mystical about how cigarettes are addictive? No. It is all very organic, and physical. The tobacco contains two categories of chemicals that establish addiction in addition to the conditioned reflex aspect (Pavlovian), which also fortifies the addiction. This last part is more related to the whole process of the activity itself of the cigarette touching the lips, the action of inhalation, the smell of the cigarette, holding the cigarette, etc. As nicotine enters the body, it is distributed quickly through the bloodstream and crosses the blood–brain barrier reaching the brain within 10–20 seconds after inhalation. The elimination half-life of nicotine in the body is around two hours.^[i]

Tobacco smoke contains, in addition to nicotine (the first category I alluded to above), the monoamine oxidase inhibitors harman and norharman (the second category I alluded to above). These second category compounds significantly decrease MAO activity in smokers. This was evidenced by positron emission tomography imaging that showed smokers have a much lower activity of peripheral and brain MAO-A (30%) and -B (40%) isozymes compared to non-smokers.^[ii],^[iii] MAO enzymes break down monoaminergic neurotransmitters such as dopamine, norepinephrine, and serotonin. It is thought that the powerful interaction between the MAOIs and the nicotine is responsible for most of the addictive properties of tobacco smoking.^[iv] Therefore when the activity of MAO enzymes is impeded these neurotransmitters are higher in quantity (enhancing brain function artificially), but the flip side of this is when the tobacco is gone the MAO enzymes increase and hence decrease those neurotransmitters (at least temporarily. This translates into the withdrawal syndrome from tobacco in addition to worsening of any depression state present. The magnitude and duration of these phenomena will vary with how long and how much the person has been using tobacco, and how healthy the individual is. In other words a less healthy person will take longer to renovate their brain neurotransmitter production compared to a healthier person.

As such a treatment strategy for you: target increasing the neurotransmitters in the brain by all means possible which are safe if supervised:

1. Decrease MAO enzymes activity by taking a MAO enzyme inhibitor drug. An example of this kind of drug is phenelzine (Nardil). [As a last resort only].
2. Provide the building blocks for the neurotransmitters: i.            Protein is the major component of almost all major currently recognized neurotransmitters. ii.            Vitamin C is essential for the manufacture of certain neurotransmitters. iii.            All the B-complexes play a significant role in the production of neurotransmitters and are of paramount significance for their function. iv.            Good hydration. How this works is multifactorial and I won't go into here in biochemical/physiological detail. That being said, intake sufficient fluid to maintain urine color a very light light yellow. If you are sweating in your exercise routine then replace your losses with a fluid containing sodium chloride (salt), potassium and some magnesium. The last isn't as important as the first two, so if not present in the purchased fluid then no worries.
3. Stimulate the production of adrenaline peripherally to stimulate neurotransmission and neurotransmitters in the brain. This is done by regular exercise targeting sweating 10 minutes per session in the beginning and later increasing that according to what your body tells you. Do one day per week (minimum), per decade of your age. If you are 28 years old then minimum three days exercise per week. If you are 44 years old, then five days per week, and so on.
4. Avoid food substances that inhibit adrenaline production. Any food that leads to secretion of insulin in high quantities causes inhibition of adrenaline secretion. This would be all foods that are assimilated and absorbed rapidly into the blood stream as glucose (a simple sugar). Examples are all refined sugars and all white refined starch products. (Candy, candybars, pastries, pasta, lasagna, pizza, mashed potatoes, rice, etc.)
5. Provide an environment to your body which enhances production and conservation of these neurotransmitters. In other words, sufficient regular sleep. To the tune of 8 hours per 24 hours. Preferably in one block.
6. Stop smoking, start 7 mg patch nicotine (while awake) for two weeks, start the MAO enzyme inhibitor, all in addition to above.
7. You must be off escitalopram for 10 days prior to starting MAO enzyme inhibitor. (They interact).

Comments:

1. Overcoming the conditioned reflexes will take time. Think months to a year. So the craving triggered by memory will take a while to go away.
2. The physical organic aspect of the addiction goes away quicker.
3. Taking MAO enzyme inhibitors as an antidepressant medication is serious business and must be supervised closely by the prescribing physician. Avoid over the counter medications unless cleared by physician who is aware you are on a MAO enzyme inhibitor.
4. Tobacco smoke will enhance the activity of the escitalopram in an ongoing fashion. (answering your question above.
5. The nicotine content of popular American-brand cigarettes has slowly increased over the years, and one study found that there was an average increase of 1.6% per year between the years of 1998 and 2005. This was found for all major market categories of cigarettes.^[v] So the sooner you quit the better.

References:

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[i] http://en.wikipedia.org/wiki/Nicotine

[ii] Herraiz T, Chaparro C (2005). "Human monoamine oxidase is inhibited by tobacco smoke: beta-carboline alkaloids act as potent and reversible inhibitors". Biochem. Biophys. Res. Commun. 326 (2): 378–86.

[iii] Fowler JS, Volkow ND, Wang GJ, et al. (1998). "Neuropharmacological actions of cigarette smoke: brain monoamine oxidase B (MAO B) inhibition". J Addict Dis 17 (1): 23–34.

[iv] Villégier AS, Blanc G, Glowinski J, Tassin JP (September 2003). "Transient behavioral sensitization to nicotine becomes long-lasting with monoamine oxidases inhibitors". Pharmacol. Biochem. Behav. 76 (2): 267–74.

[v] Connolly, G. N; Alpert, H. R; Wayne, G. F; Koh, H (2007). "Trends in nicotine yield in smoke and its relationship with design characteristics among popular US cigarette brands, 1997–2005". Tobacco Control 16 (5): e5. doi:10.1136/tc.2006.019695. PMC 2598548. PMID 17897974.