The Correlation Between Smoking Eradication and the Rise of Obesity
by Don Mallonee, MS
Biological Considerations from a Philosopher of Science
The correlation could not be more clear. Recently the US Surgeon General reported that in the early 1960’s adult obesity was at 13% whereas the percentage of the adult population who smoked was at 42%. Flash forward to today and that correlation is almost perfectly inverted: Today nearly 40% of adults are obese whereas only 19% of adults are smokers. This relationship is complex and not yet well understood scientifically. Recently, lead researchers at the CDC have indicated that medical science needs to begin rigorously investigating the biological dimensions. I agree. To get to the fundamentals of this problem, it will require a well modeled epidemiological approach.
In the late 1980’s, as a graduate student Southern Illinois University I participated in the implementation of smoking cessation studies directed at rural populations in the mountain communities spanning Appalachia to the Ozark’s. Rural mountain populations offer unique organic controls for such studies because the communities tend to be poor, isolated (in the 80’s this was particularly so because of limited access to TV and radio) and therefore unaware of public health messaging etc. Why this is important is researchers need as much control as possible in order to cancel signal to noise ratio, i.e., reduce bias. They want to be able to gauge how effective such programs were and isolated communities were great control groups.
One of the major elements and considerations in both the data gathering instrument development and the intervention program was the knowledge that nicotine was both a stimulant and an appetite suppressant; that it’s both addictive and affects the genome. We had reams of data on weight gain as a result of smoking cessation. We also had a solid literature foundation on oral fixation and displacement/replacement behaviors. In other words, we anticipated weight gain as a potential outcome.
What we have found is that smoking cessation interventions are a mixed bag. Nicotine is a notoriously addictive substance and its use can become part of an entire lifestyle, many aspects of which in and of themselves are wholesome such as socializing and fraternizing. This was particularly true in rural mountain communities in the 80’s. For those communities smoking and drinking were/are treasured pastimes much in the same way that European cafe culture centered around caffein, nicotine and alcohol consumption as treasured cultural pastimes. Long term studies of smokers suggest that at any given time between 50%-70% of smokers want to quit with around 6% being successful. And there tends to be high recidivism in those who do quit. This is an important statistic we’ll come back to. Armed with the knowledge that interventions have low success rates, educators switched to smoking eradication programs.
Flash forward to 2018. Smoking eradication programs have been critically successful as stated at the onset of this essay. However, there is increasing concern as data continues to emerge showing an almost perfect correlation of rising obesity rates against a background of decreasing smoking rates in society at large that we are missing a piece of the picture. Professional researchers started to become aware of this in the mid 2000’s but it’s only recently that good data has started to emerge. The lay community is only just know beginning to become aware of the correlation.
Although the correlation between rising obesity rates to smoking eradication is clear it’s currently impossible to infer causation. We don’t know what is going on. For example, although weight gain is often an outcome from quitting smoking rarely does that weight gain lead to obesity in former smokers who were at normal weights when they quit smoking. I believe the normative weight gain range (from quitting smoking) is between 10-40 pounds, well below the threshold for obesity. The average weight gain is 12 pounds and we also know that thinner quitters gain more weight than heavier quitters. As we shall see, this is important.
Critically, our focus here is the rise of obesity in populations that never smoked or never became habitual smokers. This is key because to my knowledge nobody predicted that successfully eradicating smoking at large could be a potential factor leading to a meteoric rise in obesity in American society. I know that food titans in the 60’s did predict society would gain weight because of the explosion of processed foods but they did not predict obesity (although I don’t rule out it may have crossed their minds).
The obesity phenomenon is extremely complex. We need more data: psychological, behavioral, genetic, sociological. The emergence of the data correlating non-smoking with the rise of obesity is in fact sparking new research and giving lifelines to theories that some had thought were not as strong as supposed by their pioneers. For example, knowledge of this correlation in psychological circles is breathing new life into Freud who is enjoying a renaissance in psychology and psychiatry because of the understanding oral fixations are actually far more prevalent and powerful than had been previously anticipated.
As a biologist, it is not surprising that I would first look for a biological explanation. For your consideration, genetically there are some obvious theories and some not so obvious theories. One theory is latent hunter/gatherer behavioral expression. Hunter/Gatherers were opportunists who went for the low hanging fruit. In other words, they went after whatever was the easiest food to obtain that provided the most calories, carbohydrates, fats, and proteins and was safe to access. How this latent behavior may be playing a role in the rise of obesity is being explored in junk food addiction. Junk food is readily available, it’s tasty, it’s heavily marketed, and it’s addictive. Despite near universal understanding that junk food has many negative health outcomes the obese consume large quantities of junk food. Some theorize that it’s instinctual behavior – going for the low hanging fruit. It’s a fair line of inquiry.
A more complex and subtle theory I’ve been working on is what I call adverse genetic expression resulting from addictive substance denial in non participating populations. What does that mean? What we know is that babies of heroin addicts go through withdrawal. So, I asked myself what happens when one generation suddenly quits taking in an addictive stimulant that generations of people imbibed? In other words, what happens when we kick universal addiction? Is there some kind of withdrawal syndrome phenomenon in the generation(s) that no longer take in the stimulant?
What we know for a certainty is all of us have been exposed to hereditary genomes impacted by nicotine consumption. For example, my mother and father both smoked and I know for certain that their parents all smoked and in turn their parents all smoked. It’s highly likely that smoking goes back hundreds of years in my family tree and most of yours too. In other words, our ancestors smoked for 500 years and we know that nicotine is addictive and that our genome was impacted by 500 years of nicotine consumption. We also know that during those same 500 years our ancestors lead highly active agrarian lifestyles requiring high calorie, high carb, high protein diets. We also know nicotine is a stimulant that affects metabolic pathways. Based on discussions with colleagues across a broad spectrum of the sciences I suspect that 500 years of nicotine use impacted metabolic pathways at the genetic level and that for some of the population who never smoked, the lack of nicotine intake and absence of nicotine in the blood system leads to impaired metabolic functioning and abnormal food cravings. Further, I suspect that this genetic driver kicks in hard at puberty where well known genetic drivers kick in including increased estrogen and testosterone production that drive powerful transformations in physiological and psychological maturation. The metabolic system changes dramatically at puberty. And we know that rapid weight rise during puberty is a huge factor in adult obesity. With regard to metabolism, there are tens of thousands of metabolic pathways and we know that long exposure to stimulants and sedatives affect pathway signaling. My thought is in certain non smoking genetic populations the absence of nicotine results in impaired metabolic signal pathing and perhaps in food cravings. In other words, some populations of non smokers may be going through a kind of genetic nicotine withdrawal syndrome. For example, childhood obesity is on the rise and children born over the last 10-15 and even 20 years ago were more likely to be born to parents who did not smoke or were never regular smokers. In fact, recent studies indicate that childhood obesity is at 35%, it’s highest rate ever in children aged 2 – 12.
Another possible biological inquiry is to what extent does smoking reinforce oral fixation behaviors at the genetic level? And what happens in certain genomes when one oral behavior is taken away? In other words, are some genetic populations of non smokers more prone to oral fixation behaviors? One of the outcomes of the accumulation of knowledge is that the more we know the more we realize we don’t know. As such, I’m increasingly confident that as more data emerges one of the unanticipated negative effects of a highly successful smoking eradication program will be proven to be causal to the explosive increase in obesity. And one of the reasons I think it could be a form of substance withdrawal is we are seeing the same phenomenon happening in Europe which is a good control group because it’s a similar genome to ours but with known behavioral differences in the area of levels of activity versus sedentary lifestyles. For example, although its changing somewhat the average European walks much more than the average American and burns tens of thousand of more calories per year.
Biologically speaking, we are approaching an existentially alarming level of obesity in the population. Obesity is a pathology rich condition – The obese live lives of high morbidity. And that is a big drain on our health care resources.
As someone who was on the front lines of smoking cessation research and intervention programs, a onetime disciple and true believer of such programs, I am confronted with the unfortunate specter of unintended consequence of the rise of obesity. To quote Neil Peart too often “our causes can’t see their effects.”
As compelling as I find the promise of biological research on the rise in obesity we also have to examine socio-spiritual dimensions. I’m convinced that the sudden onset of obesity is a symptom of socio-spiritual trauma which is a very different topic. We know that obesity has a high correlation to both poverty and low educational opportunities which are both socio-spiritual issues. But that is the subject for a future essay.
In 1990, Don Mallonee finished his MS thesis titled Comparison and Contrasting of the Mechanistic and Holistic Paradigms of Science: Implications for Health Science And Health Education Research. The purpose of that work was to elevate the importance of epistemological concerns when designing instruments for the investigation into holistic aspects of health. For example, it’s hard to study, let alone design a virtuous instrument to research the spiritual dimensions of health from an epistemological paradigm that is reductionist. Upon receiving his MS, he set out for California where he began a career in the biotechnology industry. He started out doing research on metabolic signaling in E.coli genetically engineered to express human proteins. From there he moved on to process development operations; scaling technologies for large scale cell expression and then on to manufacturing operations development. Currently he is a business development professional in the biopharma industry who remains keenly interested in the philosophy of health science. This essay has not been reviewed by industry peers. His intention is to provide philosophical, theoretical observations that hopefully contribute to a broader discussion of what, in his view, can only be described as a bio-socio-spiritual public health crisis.
