Applying understanding of psychology, neurological pathways and social inequality to smoking cessation
Vulnerability to many drugs results from their ability to give a “false signal” of an evolutionary fitness advantage. Drug addiction is often associated with different neurological pathways for ‘liking’ and ‘wanting’ where a drug that is liked comes to be ‘wanted’ even where, after sustained drug use, the drug no longer gives pleasure.
Smoking is addictive biochemically (cessation of use triggers withdrawal symptoms). ‘Liking’ and ‘wanting’ neurological pathways are divergent and addiction has a strong psychological (wanting) element unrelated to both biochemical addiction and any genuine pleasure (liking) it can give. The cue for the desire for tobacco may be stress, however it can also be simply a ‘wanting’ that persists long after any real ‘liking’ for tobacco.
Smoking cessation programmes can be based on understanding of behavioural psychology and the way smoking addictions result from the “hijacking” of neurological pathways that evolved in ancient times as adaptive (survival) advantages. People place more value on what they have (and stand to lose) than what they might potentially gain in future. How choices to smoke or not are framed, and the salience (vividness) with which possible losses and gains from smoking are perceived, will influence behaviour. Money rewards for smoking cessation can be designed to overwhelm exploitation by smoking of neurological pathways, and turn the emotions and behaviours associated with these pathways in more productive directions.
There are associations between low perceived social rank and stress-related health problems, including those associated with smoking. For historical reasons, because of modern socio-economic inequalities, and because of the effects over generations of family influences, Maori have become disproportionately vulnerable to smoking. However, Maori do have social structures that could underpin an administrative basis to implement incentives-based smoking cessation programmes. These programmes can also deliver other secondary benefits, such as good savings habits.
An incentives-based smoking cessation programme is proposed based on behavioural psychology, of the neurological pathways underlying addiction,
and understanding of the relationship between socio-economic status and ranking and behaviour.
Keywords Smoking psychology. Addiction. Smoking cessation. Maori smoking.
Cahill & Perera’s 2009 Cochrane Review of seventeen studies of competition and incentives-based smoking cessation programmes concluded that:
“Incentives and competitions have not been shown to enhance long-term cessation rates, with early success tending to dissipate when the rewards are no longer offered…”
However, Volpp et al (2009) report more promising findings from studies and recommend further replication. More importantly, this paper contends incentive programmes for smoking cessation can be effective if they are informed by behavioural psychology, the neurological pathways underlying addiction, and the effects of social rank and inequality.
The evolutionary, biochemical, social and psychological factors underlying addiction need to be understood:
Evolution occurs because variations exist in populations and those conferring a fitness (survival) advantage will be selected for and increase in frequency in populations. People’s psychology and biochemistry is hard-wired with those traits that conferred a survival advantage over evolutionary time, even where they may be harmful now. In evolutionary times, finding a high fat or sugar source would be a matter of life or death and so we evolved a taste for such foods. In modern times our excessive taste for such foods can be harmful.
Many modern drugs give a false signal of increased fitness by exploiting neurological pathways that evolved in evolutionary times when an elevated mood was associated with surviving short-term risks (Saah 2005). The neurological pathways that evolved to favour behaviours (such as liking for certain foods) that had Pleistocene-era advantages is effectively highjacked by tobacco even though tobacco (unlike food) confers no survival advantages. Being addictive, nicotine and other chemicals in smoke then create a dependence that locks in biochemically what began as a neurological liking.
Hard-wired emotions create the linkage between evolved neurological pathways and how people behave in modern times. Emotions are shaped by natural selection to coordinate physiological, cognitive and behavioural responses to meet adaptive challenges that recurred over evolutionary time (Plutchik 2003, Nesse & Ellsworth 2009). For example, in evolutionary times fear would be an emotion that would enhance survival prospects by increasing alertness and “fight or flight” responses. Not surprisingly, we evolved to like drugs that give a short-term boost in alertness and other physiological responses that were fitness advantages in evolutionary times but may be maladaptive now.
Many psychological defences that protected our ancestors in evolutionary times (such as anxiety in a risky environment or fear of strange noises) are akin to “smoke detectors” where false alarms are tolerable because the cost of responding to one is low compared to the possibly fatal consequences of the alarm not going off. Mechanisms associated with stress, and with temporarily enhanced alertness, are therefore inexpensive where they protect against fatal threats whose presence is signalled by unreliable cues – so even an optimal system will produce false alarms.
When an emotion such as anxiety becomes pervasive and goes beyond even the false alarms of a smoke detector, then people become vulnerable to drugs, including tobacco. People under stress are vulnerable to smoking because of nicotine’s ability to produce small but reliable adjustments in relevant cognitive and behavioural functions (Pomerleau 1997).
Biochemical determinants of addiction
Smoking addiction results from constituents in smoke that deliver a range of sensory effects. Because nicotine in smoke can be substituted with nicotine replacement therapy (NRT) using gum, patches or nasal spray, we would expect NRT to be highly effective in smoking cessation. However, NRT by itself is not very effective, largely because it does not address non-nicotine components of smoking reinforcement (Rose 2006). Some smoke constituents such as acetaldehyde, ammonia, menthol and monoamine oxidase (MAO) inhibitors strengthen addiction, in some cases through their interaction with nicotine (Rose 2006).
Smoking can heighten heart rate, alertness, and reaction time. Dopamine and later endorphins are released, which are often associated with reward and pleasure. However, after addiction occurs, pleasure fades, and people continue smoking to avoid withdrawal symptoms.
For some addictions as they develop, drug-induced pleasure declines or remains constant, even as cravings increase and negative consequences accumulate.
Addicts often crave drugs that no longer reliably give pleasure. They return to them even after extended periods of abstinence despite the lack of both biochemical addiction and drug-induced pleasure. One likely reason is the separation of mammalian brain reward systems into components that correspond roughly to “liking” (pleasure on receiving a reward) and “wanting” (motivation and behavioural pursuit of reward).
‘Liking’ (of sweet foods for example) is mediated by forebrain systems whereas ‘wanting’ is mediated by ascending mesolimbic dopamine-containing neurons and associated opoioid receptors. The separate neural mediation of liking and wanting may have evolved so that “likes” for different things could be compared within a common currency of utility. The liking system is activated by receiving the reward, while the wanting system anticipates reward and motivates behaviours. When these two systems are exposed to some drugs, the liking system provides the initial “hook” that encourages ongoing drug use and turns it into a habit. The “wanting” system cuts in later, and motivates persistent pursuit of drugs that no longer give pleasure.
Many drugs induce positive emotions that give a false signal of a fitness benefit. This signal hijacks incentive mechanisms for ‘liking’ and ‘wanting’ and can result in continued use of drugs that no longer bring pleasure (Nesse & Berridge 1997).
Given this, how can we exploit neurological pathways to negate or override smoking addictions? Buchanan (2009) provides evidence that our brains process ideas about money using the same neurological pathways as have evolved to think about food. People react to money at an emotional level rather than purely as an exchange medium. It is associated with status and reproductive fitness and enables people to manipulate their position in a social hierarchy.
The neurological pathways that make money a powerful motivator of behaviour have similarities with those relating to food and to tobacco. Therefore, pathways associated with both money and tobacco can be dominated by money and this can crowd out the desire for tobacco. Using money to trump the desire for tobacco can be effective if we exploit behavioral psychology, especially loss aversion, salience (vividness) and framing (or “choice architecture”).
Social aspects of smoking
Individuals have different responses to drugs. Individuals differ in their vulnerability to smoking, which is influenced by interactions among at least five genes, each of which exists in several variants (Stearns, Nesse & Haig 2008). Variation is affected by social as well as genetic factors.
The literature (e.g. Sloan & Wang 2008, Mungasinghe & Sicherman 2000, Terracciano & Costa 2004) suggests smokers have an excessive focus on short-term behaviours. Where children and young people receive erratic and unreliable care they may focus more on managing short-term risks. In an evolutionary environment this may have been an adaptive fitness advantage, however in modern times it is maladaptive. Children and young people who suffer from low parental investment and supervision know their parents cannot be trusted to protect them. This shapes their psychology and behaviour to focus on short-term risks and is associated with higher stress levels and short-term behaviours, including smoking and other addictions.
Peer pressure and its association with risk taking and boundary stretching influence smoking, however an even greater influence comes from rank-based social stress.
There is overwhelming evidence of causative correlations between perceived low social status and unhealthy behaviours such as smoking (Fuller 2006, Price et al 2007, Wilkinson & Pickett 2009). The Whitehall 1 Study set up in 1967 showed that among British public servants low status strongly correlated with poor health (Wilkinson & Pickett 2009). Key sources of stress are low social ranking, and threats to lower this ranking further.
Low status in a hierarchy has been shown to cause damaging physiological stress in monkeys as well as humans (Offer 2006). Experiments with macaque monkeys show that those that are more dominant (and therefore less stressed by ranking inequality) had more dopamine activity in their brains (Wilkinson & Pickett 2009).
Health inequalities are associated with relative income and status differences rather than absolute wealth (Offer 2006, Wilkinson & Pickett 2009). The relative status is more about subordination or hierarchy than income as such. Lower income people often suffer more stress not because they are at the bottom of the financial heap but because they are at the bottom of a social scale they perceive for themselves. That is, relative status and inequality within a social rank order are more important than income inequality.
People can of course be of multiple status or rank in the same way they have multiple identities. Someone may have low status in their job but high status in volunteer work, sporting or community organization, or at home. People in occupations others perceive as humble may take great pride in their work, so what matters is how a person perceives their status.
Stress is debilitating if it is not seen as manageable. It can be invigorating if resources are there to marshal it productively. However stress mechanisms, if they are activated excessively, can be damaging both directly and through their tendency to lead to harmful stress-alleviating behaviours, such as drug taking.
Stress mechanisms are unleashed by cues that trigger stress unnecessarily, such as the effects of perceived social ranking. A low status person is subject to environmental triggers that may now be trivial but in ancient times might legitimately have triggered emotional reactions of fear, anger, or “fight or flight” response.
Stress mechanisms are therefore triggered excessively compared to actual threats in the modern environment. When someone is stressed, the brain releases cortisol, a central stress hormone that helps prepare physiologically to deal with threats (Wilkinson & Pickett 2009). Cortisol increases blood pressure and blood sugar and reduces immune responses. Long-term exposure to cortisol can damage cells in the hippocampus and this can impair learning.
Maori health problems are associated with stress and the drugs (including tobacco) used to alleviate it. This has its roots in low perceived rank and social inequality. It may also have some deeper historical origins. Charles Darwin characterized Maori society as the most warlike on earth (Darwin 1997). James Cook’s journals (Cook 1999) observed “…the New Zealanders must live under perpetual apprehensions of being destroyed by each other…One hardly ever finds a New Zealander off his guard.”
These high stress levels continued through the early 19th century tribal wars and the later land wars, and were later reinforced by perceived low social rank that persists for some Maori today. It is not therefore surprising that Maori are vulnerable to smoking, and the persistence of smoking within Maori is further compounded by family environments pre-disposing children to smoking.
Barnett, Pearce & Moon (2009) concluded that over the period 1981-2006 smoking became ethnically more polarised, with greater levels of cessation among higher socio-economic groups and Pakeha than Maori. These differences could not be accounted for by socio-economic differences between ethnic groups. That is, even when socio-economic factors are accounted for, Maori are disproportionately affected by smoking. It is contended this difference can be explained partly by perceived social rank as opposed to socio-economic position (though of course there are relationships between the two). This may also suggest that “mana-enhancing” initiatives that address low perceived social ranking may be legitimately considered as part of health policy for Maori.
Behavioural psychological determinants of smoking
People are influenced by loss aversion and status quo bias. Loss aversion means people are more motivated by fear of loss than the desire to gain something additional (Kahneman et al 1991). Status quo bias means that people will continue with an established state in preference to changing it. So, a voluntary superannuation scheme such as Kiwisaver will have quite different outcomes depending on whether it is opt-in or opt-out, that is, whether people are automatically enrolled and have to opt out, or whether they have to actively opt in. Sustained conditions become the norm and people adjust to them. People are also “present biased”, that is they place value on smaller immediate rewards than on larger ones more distant in time. Positive financial incentives can therefore provide short-term rewards for behaviours that have longer term health (and financial) benefits.
Choices people make depend on the way things are framed, for example where money is held in different “mental accounts” (Thaler 1990). Money in a superannuation fund or house is treated differently to cash, and people perceive credit card expenditure differently to paying in cash. Mental accounts interact with the salience (vividness) with which things are perceived. For example, people spend more through credit cards than they do in cash because the delayed nature of the card payment and bundling of several individual purchases into one payment reduces salience (in effect, the spending becomes less obvious and therefore less painful).
Given the above, how should we design smoking cessation programmes?
We need to stop smoking hijacking evolved liking and wanting systems by offering a cessation reward that directs neurological pathways away from smoking to money. Cessation needs to be maintained long enough to end biochemical dependency. We must make the financial cost of returning to smoking too high by exploiting loss aversion.
The proposal is for a modified version of a scheme run by the CARES (campaign to reduce and end smoking) programme offered by the Green Bank of Caraga in Mindanao, Philippines (see Thaler & Sunstein 2008). In this scheme, someone wanting to stop smoking opens an account with a minimum balance of $1. For six months she deposits the amount of money she would otherwise spend on smoking into this account. She then takes a urine test, and if this proves she has ceased smoking she keeps the money. If she fails the test the money is given to charity. MIT’s Poverty Action lab has done an assessment of this initiative and early results suggest that participation makes those who want to quit over 50% more likely to achieve their goal.
A model to build on may be Ngai Tahu’s Whai Rawa savings fund based on individualized accounts. The savings are locked in until age 50 but can be drawn down for tertiary education and first-time home deposits. While Whai Rawa targets children with the aim of building good lifetime savings habits, this type of initiative could be adapted to adult smoking cessation, using the CARES approach.
Assuming an individual spends $40 a week on cigarettes, then this $40 saved by ceasing smoking would be credited into an account and allowed to accumulate, with interest, over a six month period. The “six month rule” sets a predictable enough timeframe for people to visualize the (salient) financial benefits while being long term enough for substantial money to accumulate. Over $1000 plus substantial interest could be collected at the end of each six month period. This provides a strong abstinence incentive since the marginal cost of (or rather loss from) one cigarette is over $1000.
It is acknowledged that some cessation programmes have used a range of pharmacological interventions (such as nicotine replacement therapy) and short- term as well as longer-term rewards. In contrast, in this proposal the only financial reward comes at the end of the programme. Pharmacological intervention could be a valuable complement to this proposal. The salient appeal of short-term rewards could be partly replicated by making more vivid to participants the real time accumulation of savings, for example through frequent financial reports on the money being saved. Alternatively, a small part of the savings could be used for tangible short-term rewards to complement the great bulk of the savings accumulating in the longer-term account.
A key feature of this proposal is it exploits evolutionary psychology and its behavioural manifestations, especially in relation to framing, status quo bias and loss aversion. It also exploits the emotions associated with money in ways that trumps those hijacked by smoking. The accumulated money, plus interest, would be in a “capital” rather than spending “mental account”. The endowment and mental account effects would reinforce the status quo bias and increase the likelihood of the money being saved.
A spin-off benefit from the proposal would be the encouragement of good savings habits. The above scheme could be modified to make this an explicit secondary objective. For example, after the six months accumulation the money could be either withdrawn or, as the default condition, automatically saved in a longer-term account that could end up contributing to a home purchase, education, retirement savings or whatever. Automatic long-term re-investment would be the default condition, exploiting status quo bias. The “locking in” psychology of this might well reinforce the pressures for long-term and permanent smoking cessation. This is an important point, as many incentives-based smoking cessation programmes that achieve early success with short-term rewards tend to have high relapse rates over the longer term.
A scheme such as this would lend itself to a trial within a Maori organisation, after which the results could be evaluated. If successful, it could then be rolled out more widely in the community.
This paper sought to integrate understanding of the neurological pathways underlying addiction, behavioural psychology, and social ranking aspects of vulnerability to addiction. It focused on Maori because of their health inequalities, and proposed a practical initiative to reduce smoking rates. Because it highlighted the relationships between social ranking and health, it allowed us to reflect on why indigenous people (even where there is no absolute poverty) suffer from relatively poor socio-economic outcomes, despite often massive social welfare and affirmative action expenditure.
Could poor outcomes for Maori have some of their fundamental origins in perceptions of social rank within a hierarchy? Defining symbolic events such as the seabed and foreshore dispute, debates over the naming of towns and mountains, the very conception of mana (and mana whenua itself) surely have associations with emotions of standing, rank and perceived position within hierarchies. Together with research on self-identity and memetics this could well be a fruitful field for future research into reducing Maori socio-economic inequality.
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