The relationship between nicotine and the brain has been a topic of interest for decades. Intriguing though, is what on the surface appears to be benefits of smoking to the brain. Such a link is puzzling though, given the many known detrimental effects of smoking in other parts of the body. The basis of the notion is two observations based on research. They are the following:
- Decreased prevalence of Parkinson’s disease among people who smoke compared to those who do not
- Decreased prevalence of Alzheimer’s disease in smokers reported in older but not current literature
Is it reasonable however, to surmise that cigarette smoking – the number one preventable cause of death – is so harmful in most respects yet of benefit to the brain? Or is it possible that the quasi benefit is the result of misinterpretation of the data? Just maybe the consensus interpretation of the presumed statistical facts is a matter of putting the cart before the horse. If so, accurate insight might rest in an understanding of the role of the reward center of the brain with respect to nicotine addiction and the effect of Parkinson’s disease and Alzheimer’s disease on it.
It is common knowledge that the most striking pathology of Parkinson’s disease is death and degeneration of dopamine-producing cells in the substantia nigra of the brain. What is not common knowledge though is that the same type of cell loss involving the nicotine-binding dopamine-producing cells also occurs in the ventral tegmental area of the midbrain according to past research. Similar research has also shown that the pathology in Alzheimer’s disease seems to be more limited to the nucleus accumbens except when there is associated Parkinson’s disease. In either case there is a disruption of the reward center of the brain.
Without cells in parts of the brain’s reward center that bind nicotine and/or release dopamine, there is a failure to generate and transmit addictive signals – the sine qua non for addiction. Thus, the decreased rate of Parkinson’s disease in smokers is probably not due to a protective effect of nicotine or one of the other chemicals in tobacco as some are prone to think. Rather, it is probably due to the fact that people with these diseases are just less prone to becoming or remaining addicted to nicotine. The probable reason is they lack the full anatomy to do so.
The conflicting data with respect to the effect of cigarette smoking on the rate of Alzheimer’s disease probably has more than one explanation. An often cited one is the contribution of the tobacco industry to the earlier research and the effect it had on the outcomes and conclusions. Other commonly reported reasoning is that many of the patients in the earlier studies died from other diseases caused by smoking before having a chance to develop Alzheimer’s disease.
Be that as it may, comparative differences and flaws in the design are shortcomings of many research studies in general. The factors involved might be the criteria for diagnosing a condition under study, the population studied and the recording of the data.
Unlike the diagnosis of Parkinson’s disease, the diagnosis of Alzheimer’s disease is not quite as clear cut. Parkinson’s disease is a clinical diagnosis based on signs, symptoms and response to treatment. Absolute proof of Alzheimer’s disease on the other hand, requires an autopsy and inspection of brain tissue with a microscope. In fact, 20% of individuals diagnosed with it on clinical grounds end up not having it at the time of autopsy. They have either another form of dementia or another disorder causing their cognitive problems.
There are many variables within study populations that can cause differences in study results. Some of them are age, geography, ethnicity and socioeconomic status. Foremost with respect to the link between smoking and Alzheimer’s disease are the number of years and the time frame during which one has smoked. Recent studies have shown a definite increased risk in individuals who have smoked heavily during their midlife years.
Undoubtedly, the prevalence of Alzheimer’s disease might be less among active smokers compared to nonsmokers if the brain reward center damage theory holds true. If so, more detailed analysis would probably show that many of the nonsmokers with the disease are former smokers who quit.
Chronic illnesses don’t develop in one day. They do so gradually over years and sometimes decades. Because the degree of degeneration of neurons in the reward center of the brain varies depending upon the stage of development of disease the potential for addiction also varies. One person might have been a smoker for years prior to diagnosis but able to easily quit. Another might have never had the desire to smoke at all.
I remember an aunt who smoked most of if not all of her adult life. To the delight of her daughter, she quit abruptly and with ease in her 80s. She died a few years later from clinically diagnosed Alzheimer’s disease.
It is much more likely that certain brain diseases protect against smoking, if you will, than that smoking protects the brain. If this premise is correct, it applies to degenerative diseases of the central nervous system in general as they begin to involve the reward center of the brain. To date, there is no cogent explanation of how or why cigarette smoking would protect the brain. This topic is a fertile area for future research.