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It has been shown that the majority of cigarette users want to stop smoking. However, by one year over 85% of smokers have returned to smoking unless they have pharmacological help and that the average smoker has made about ten attempts to quit before long term success. Even with treatment, so many smokers return to using. Why is it so difficult?
One important thing to remember before a discussion of treatments is that 99% of the harm of cigarettes comes from the burning of tobacco and the inhalation of carbon monoxide, formaldehyde and over 70 other oxidants and cancer causing chemicals. The nicotine may be the addictive component but it does not cause cancer, atherosclerosis or lung disease. This is why it is considered safe to replace nicotine even though it may maintain the addiction. Interestingly, a recent study of marijuana smokers found relatively low complications from smoke (but not necessarily zero). This suggests that chemical treatment of the tobacco or the tobacco paper is a cause of much of the toxicity from smoking.
Another thing to remember is that the cigarette industry has had centuries and billions of dollars to perfect the attractiveness of their product by increasing the addictive potential. The industry has added various chemicals to enhance the burning of the leaf. This creates a smoke with extremly small particles that penetrate deep into the lung. This allows an extremely rapid and significant uptake which makes the tobacco particularly addictive. Most treatments cannot reproduce either the speed of nicotine uptake or the peak nicotine levels obtained
Patients often like to brag about having reduce the number of cigarettes they smoke. The problem is that their technique of smoking almost always changes. They breathe deeper, hold their breath longer and smoke more of the cigarette. Therefore, unless there is more than a 70% reduction in the number of cigarettes, they are usually not seeing less nicotine or toxic chemicals.
Nicotine substitution is often what most patients turn to first. I feel nicotine patches, such as Nicoderm, are the most ideal nicotine option as they eliminate nicotine on-demand and has the best chance to eliminate the use of nicotine completely. Anyone using more than a half pack starts on the highest dose of 21 mg. Of course the problem is the slow nicotine uptake and relatively low blood levels. To partially solve this problem, I advise my heavier tobacco users to use more than one patch. I routinely go up to two 21 mg patches. Alternatively, nicotine gum or lozenge or e-cigarette on top of the patch may help stop cigarette use. This helps many, many patients. Of course, many other patients still find this option less than satisfying because they are looking for that on-demand nicotine surge
Of course, all the agents have issues with low speed of nicotine uptake. Although the nicotine inhaler as well as the e-cigarette are inhaled, the nicotine particles are relatively large and they do not get as deep into the lung. Therefore, nicotine uptake is slower and less satisfying. One agent that comes close to mimicking the rapid uptake of cigarettes is the Nicotrol nasal spray. Yes- this is snorting nicotine and yes it maintains the addiction but at least we avoid all the harmful effects of smoke.
IMPORTANT: it is okay to use patches or any nicotine product indefinitely. Although the idea is to stop since no more than 3 months of treatment are recommended by the company, there is no clear cut harm to long term continued use. It is infinitely better to do nicotine substitution of any type than tobacco.
People want to know how safe the e-cigarettes are. These devices work by misting nicotine in warm water. The devices contain propylene glycol, which is used to keep the nicotine in solution. It is not known to be harmful. Other chemical have been found that are potentially harmful but no one knows if they are harmful in this case due to the fact they exist in very low levels. E-cigarettes are not a prescription medicine, they have not been studied long term with the rigor that the medical establishment usually approaches such a task. Nevertheless, I am reasonably certain that the e-cigarette is far safer than a real cigarette.
Most users will tell you that the slower uptake of nicotine requires more time spent "smoking" or "misting". This can be overcome with higher concentrations of nicotine. However, one must be careful, I have seen a couple of instances of nicotine poisoning
People find e-cigarettes effective and if it works, that is fine, but I still prefer an NON ON-DEMAND approach with the hope that the addiction can be completely overcome. In addition to patches there are several non-nicotine medications that are effective.
If one wants to use only nicotine agents, the combination of a long acting agent such as a patch with a breakthrough agent of any type, is more effective as any single agent and the majority of people will stop using cigarettes.
Buproprion is the active ingredient in Wellbutrin and Zyban. It works by increasing dopamine levels in critical parts of the brain and has been found to be effective in curbing cravings. About a third of patients benefit and stop smoking. When combined with nicotine patches, almost 50% of smokers will stop smoking. Buproprion is also an anti-depressant and has the additional benefit of reducing appetite and weight gain sometimes seen with quitting smoking.
Chantix is a chemical structurally similar to nicotine. It sits in the nicotine and gives about 60% of the effect that nicotine does. The less-than-maximal effect is important since a maximal effect would cause the Chantix to be addictive as well. Chantix stays in the body for up to twelve hours allowing steady stimulation of the receptor and avoiding withdrawal. It also blocks the receptor from nicotine should the patient smoke while on it. For these reasons, it is considered a partial agonist/antagonist. For those of you familiar with Suboxone, you will know it has the same effects and classification related to the opioid receptor.
Chantix is by far and away the most effective medication for terminating the tobacco habit. I find a third of my patients stop smoking immediately and another third stop smoking eventually. Many patients smoke on Chantix; however, the number of cigarettes smoked is reduced by over 75% and often the inhalations that are done on Chantix are fewer, more shallow and shorter. When Chantix is stopped, there may be a very mild nicotine withdrawal; yet, I have numerous patient who have stopped the medication after a few months and have not returned to smoking.
Chantix has other benefits. Since it increases dopamine levels on a slow steady basis, it has broader benefits with impulse control disorders. Alcohol use and cravings go down, so do those for cocaine. It reduces hunger and may lead to weight loss.
A number of patients have side effects. Vivid dreams are likely and due to dopamine release during the REM state of our sleeping. Some nausea is also common. Irritability is seen but it is unclear if this is due to Chantix or not smoking. Constipation, also reported,is likely due to not smoking as nicotine induces bowel movements.
Unfortunately, depression has gotten a lot of publicity as a complication of treatment. Yet it is unclear that Chantix causes this as opposed to just failing to prevent it. Nicotine is a stimulant. Any withdrawal of stimulants is associated with depression which is occasionally severe. When a smoker, who is trying to quit, gets very depressed, they may grab a cigarette. If Chantix is on board, the cigarette has no effect. While I would not recommend unstable psychiatric patients to start this, I would not avoid it for stable patients. Most patients do not get depressed. Even the few that do become "depressed" seemed to have overly anticipated the problem and quickly blame any bad feelings on Chantix-right or wrong. Many just use the publicity as an excuse to avoid making any attempts to stop.
Other drugs that are not approved for nicotine addiction have been found to be useful in stimulant withdrawal use in general. They include naltrexone, baclofen and low-dose zofran. The also provide benefit.
It is very easy to be dismissive of nicotine when we use other substances. We are aware of its' problematic use, but we fail to give it proper respect as a drug. Its legal status, and its' familiarity, creates a tendency for us to minimize the significance of its use.
I am not going to discuss the health issues of smoking. There are more complete discussions elsewhere in the internet. Rather, I want to discuss the issues of tobacco use in relation to how it affects other drug use. Does giving up smoking make it harder to give up other drugs?
I recall, years age, when smoking was allowed on inpatient drug treatment units. The counselors would evaluate the new clients while both clients and counselors smoked cigarettes. "Give up alcohol" the counselor would say, "Wait to give up cigarettes. Only do one thing at a time." However, I could never recall an instance where a patient drinking and using heroin or crack or pot was told to continue the other drugs because they should only concentrate on one thing at a time.
And the assumption became a reality. Patients are convinced that they should wait to give up cigarettes. After all, many smokers live and work in society without seeming to be intoxicated. They may be putting their health at risk, but they are not perceived as addicts. They are reliable and accomplish all they need to do for work and home. Therefore cigarettes are not perceived as so bad.
Nevertheless, the smoker is aware of the distress caused by giving up nicotine. Wouldn't attempting to give up cigarettes while trying to give up other drugs make the whole process too difficult?
What do the studies show? Believe it or not, there are very few studies addressing this. I am not a person given to conspiracies but there is a curious absence of desire to study whether ongoing nicotine use increased or decreased withdrawal syndromes from other drugs. A curious lack of money and a curious lack of interest.
To be fair, these studies are hard to do. The best studies are double-blind studies: in these studies, neither the patient nor the researcher knows who is getting the intervention or a placebo. How do you do a double-blind a study in which a patient would know they were smoking?
So what do we know? We know that the heaviest smokers are more likely to drink. We know that active alcoholics who are also smokers are almost certainly going to continue to smoke. We know that lab animals, exposed to nicotine, are more likely to drink.
However, none of these situations address the real question. That is: Does stopping tobacco use early in abstinence make us more or less likely to relapse with our drug of choice.
The best studies have focused on simply encouraging patients to stop smoking. Forcing the issue has been associated with poor outcomes. Most studies set up a smoking intervention group. These interventions encourage smoking cessation- some offered medications and others did not.
The groups that were encouraged to stop smoking had better success rates with alcohol cessation than the group where smoking cessation was not stressed.
On particularly good study, (Burling et al) showed a 10% nicotine abstinence rate in the intervention group (vs. none in the usual care group). The patients who stopped smoking were twice as likely to have maintained abstinence as those who continued smoking.
When substances, other than alcohol are looked at, the results are even better. This includes studies with adolescent populations. Also, in those specific studies where smoking cessation medication was used, we also saw improvement in total abstinence rates.
There was one single study where patients had increased alcohol cravings while giving up tobacco, but this is the sole conflicting study.
I encourage all my patients to stop smoking. It only makes sense. The mechanism that leads to nicotine craving is a relatively low level of dopamine activity. Each time we smoke, our dopamine level becomes low 1-2 hours later and we want another cigarette. However, the mechanism of cocaine and other stimulant cravings is also low dopamine. How does a smoker, trying to get off drugs, know what to crave for when his dopamine level drops?
I have also had patients, given Chantix for smoking, who noted fewer cravings for their substance of choice. It is to be noted that there have not been any studies using Chantix for smokers in early recovery. If my own office experience is representative, than this would significantly improve both tobacco and over-all abstinence rates.
The stimulant withdrawal process is often minimized by the public, medical professionals and even by those who suffer from stimulant dependence. Afterall, alcohol and opioid withdrawal can be observed and even measured. In fact, alcohol withdrawal has dire, even fatal, consequences if not appropriately treated. None of this occurs in stimulant withdrawal. Therefore, the tendency to relapse is often dismissed as a psychological dependence which relegates it to a behavioral disorder. Many people consider it nothing more than a character flaw.
I do not understand the meaning of the term: psychological dependence. When you get right down to it, neither does anyone else. It is a dismissive term designed to characterize neurological phenomenon we do not understand. It is embroiled with popular misconceptions and used to disparage behaviors that fall out cultural norms,
I often use the term limbic circuit which refers to all the brain structures that contribute to our emotional and motivational drives. In my mind, using this term emphasizes that there are biological/neurological abnormalities that are identifiable, potentially measurable and treatable.
In stimulant dependence, dopamine biology figures prominently in the disease state. All stimulants boost dopamine activity. The euphoria, or 'high', is a result of excess stimulation of a certain type of dopamine receptor call the D1. D1 stimulation is normally involved with pleasure, learning and focus. However, when drugs excessively stimulate dopamine, there is an intense euphoria or "high".
However the excess dopamine activity is a temporary phenomenon. Soon the targeted cells become less sensitive to dopamine. In addition, dopamine levels drop for a variety of reasons. This is often why cocaine and amphetamine binges become less rewarding as time goes by; there is less dopamine to modulate their effect.
Unfortunately, this has consequences on a second type of dopamine receptor, the D2. This type of dopamine receptor affects nerve cells that are paramount in maintaining our baseline emotional state. Let's call it contentment as opposed to euphoria. When the activity of these go down, we become depressed, unmotivated and unable to focus. We really suffer. Many refer to this as a crash.
This state of "ill feeling" causes us to do whatever is needed to feel normal. Such behavior may include only thoughts as we obsess about ways to feel better (ie. drugs). Often, he behavior includes drug foraging and drug taking. Many times, the substance user will find themself using drugs without being aware of obsessing of foraging about them. All this is craving behavior. Saying no is really difficult.
In sum, low dopamine activity is significant cause of cravings. However, it is probably not the only cause. Elsewhere on this website, I discuss imbalance of endorphins in the prefrontal cortex, weakening of goal directed circuitry , and relative strengthening of habit circuitry. These all contribute to cravings. However, in those using stimulants, low dopamine remains quite important.
Since low dopamine is such an important craving mechanism, we might ask ourselves what else, other than our drug of choice, exacerbates low dopamine. All stimulants cause low dopamine. This includes nicotine. Low dopamine caused by the use of one stimulant can trigger cravings for a second. That is why tobacco use goes up in most people during a cocaine binge; the low dopamine from cocaine leads to nicotine cravings. For the same reason, the reverse will be true. Low dopamine seen in nicotine withdrawal will lead to cravings for cocaine, amphetamine and most other substances. Abstinence from our drug of choice is most likely when we abstain from any form of nicotine.
Also medications that lower D2 activity have the potential to stimulate cravings. This unfortunately, is the mechanism of action for most anti-psychotics including seroquel, olanzepine, risperdal, abilify and many others. Many people are able to use these drugs without consequence; however, others develop increased cravings for tobacco and other stimulant drugs.
The treatment of cravings includes trying to normalize dopamine activity. Wellbutrin, Chantix, antabuse as well as other drugs increase dopamine effects and are potentially anti-craving.