What drives a person to smoke cigarettes – and keeps one out of six U.S. adults addicted to tobacco use, at a cost of 480,000 premature deaths each year despite decades of anti-smoking campaigns?
What role do emotions play in this addictive behavior?
Why do some smokers puff more often and more deeply or even relapse many years after they’ve quit?
If policy makers had those answers, how could they strengthen the fight against the global smoking epidemic?
A team of researchers based at Harvard University now has fresh insights into these questions, thanks to a set of four interwoven studies described in a new report published in the Proceedings of the National Academy of Sciences: The studies show that sadness plays an especially strong role in triggering addictive behavior relative to other negative emotions like disgust.
The studies range from analysis of data from a national survey of more than 10,000 people over 20 years to laboratory tests examining the responses of current smokers to negative emotions.
One study tested the volume and frequency of actual puffs on cigarettes by smokers who volunteered to be monitored as they smoked.
While drawing from methodologies from different fields, the four studies all reinforce the central finding that sadness, more so than other negative emotions, increases people’s craving to smoke.
“The conventional wisdom in the field was that any type of negative feelings, whether it’s anger, disgust, stress, sadness, fear, or shame, would make individuals more likely to use an addictive drug,” said lead researcher Charles A. Dorison, a Harvard Kennedy School doctoral candidate.
“Our work suggests that the reality is much more nuanced than the idea of ‘feel bad, smoke more.’ Specifically, we find that sadness appears to be an especially potent trigger of addictive substance use.”
Senior co-author Dr. Jennifer Lerner, the co-founder of the Harvard Decision Science Laboratory and Thornton F. Bradshaw Professor of Public Policy, Decision Science, and Management at Harvard Kennedy School, said the research could have useful public policy implications.
For example, current anti-smoking ad campaigns could be redesigned to avoid images that trigger sadness and thus unintentionally increase cigarette cravings among smokers.
Lerner is the first tenured psychologist on the faculty of the Kennedy School. She was the Chief Decision Scientist for the U.S. Navy in 2018-19.
Lerner has studied the impact of emotions on decision-making since the 1990s, examining issues including whether generalized negative emotions trigger substance abuse or whether a subset of specific emotions such as sadness are more important factors in addiction.
The other co-authors include Ke Wang, a doctoral student at the Kennedy School; Vaughan W. Rees, director of the Center for Global Tobacco Control at Harvard T.H. Chan School of Public Health; Ichiro Kawachi, the John L. Loeb and Frances Lehman Loeb Professor of Social Epidemiology at the Chan School; and Associate Professor Keith M.M. Ericson at the Questrom School of Business at Boston University. The work was funded by grants from the National Science Foundation and the National Institutes of Health.
The studies range from analysis of data from a national survey of more than 10,000 people over 20 years to laboratory tests examining the responses of current smokers to negative emotions.
Here are further details on the techniques and key findings of the four studies:
- Examining data from a national survey that tracked 10,685 people over 20 years, the researchers found that self-reported sadness among participants was associated with being a smoker and with relapsing back into smoking one and two decades later. The sadder individuals were, the more likely they were to be smokers. Notably, other negative emotions did not show the same relationship with smoking.
- Then the team designed an experiment to test causality: Did sadness cause people to smoke, or were negative life events causing both sadness and smoking? To test this, 425 smokers were recruited for an online study: one-third were shown a sad video clip about the loss of a life partner. Another third of the smokers were shown a neutral video clip, about woodworking; the final third were shown a disgusting video involving an unsanitary toilet. All participants were asked to write about a related personal experience. The study found that individuals in the sadness condition – who watched the sad video and wrote about a personal loss – had higher cravings to smoke than both the neutral group and the disgust group.
- A similar approach in the third study measured actual impatience for cigarette puffs rather than mere self-reported craving. Similar to the second study, nearly 700 participants watched videos and wrote about life experiences that were either sad or neutral, and then were given hypothetical choices between having fewer puffs sooner or more puffs after a delay. Those in the sadness group proved to be more impatient to smoke sooner than those in the neutral group. That result built upon previous research findings that sadness increases financial impatience, measured with behavioral economics techniques.
- The fourth study recruited 158 smokers from the Boston area to test how sadness influenced actual smoking behavior. Participants had to abstain from smoking for at least eight hours (verified by carbon monoxide breath test). They were randomly assigned to sadness or neutral control groups; smokers sat in a private room at the Harvard Tobacco Research Laboratory, watched the sad video and wrote about great loss, or watched a neutral video and wrote about their work environment. Then they smoked their own brand through a device that tested the total volume of puffs and their speed and duration. The results: smokers in the sadness condition made more impatient choices and smoked greater volumes per puff.
Lerner said the research team was motivated in part by the deadly realities of smoking: tobacco use remains the leading cause of preventable death in the United States despite five decades of anti-smoking campaigns. The global consequences are also dire, with one billion premature deaths predicted across the world by the end of this century.
“We believe that theory-driven research could help shed light on how to address this epidemic,” Dorison said.
“We need insights across disciplines, including psychology, behavioral economics and public health, to confront this threat effectively.”
There are many valuable approaches to understand addiction. Different perspectives explain its psychiatric, social, medical, historical, and psychological aspects. Addiction is about a behavior that goes beyond control.
Neurobiological models explain craving, tolerance, withdrawal syndromes, kindling and its chronic relapsing vulnerability. Yet, seldom do they take into account the subjective states associated with the different stages of addiction. Addiction feels like something; affect should be used as a bridge concept to attempt an integration of some of the findings coming from different perspectives.
Affect is felt subjectively and it can also be studied from a neurobiological point of view. It provides meanings that guide behaviors and thoughts. Emotions favor survival (Panksepp, 1998) and their regulation is compromised in addiction.
This paper suggests the hypothesis that depression constitutes a key emotional configuration that can contribute to the initial voluntary decision of a person to use drugs. Some of those depressions may be apparently asymptomatic and thus remain undiagnosed. In general terms, if they do not meet clinical criteria (e.g., DSM or ICD), they do not exist.
A psychodynamic exploration of a person’s emotional life can contribute to an early detection of problems that can later become clinical syndromes.
The earlier they can be worked with, the fewer risks for the person. From a psychoanalytic point of view, these depressions can be called “latent.” If they are felt, there are neurobiological correlates that should be used to better understand them.
This latent type of depression is proposed to exist prior to addiction and to contribute to its etiology. It relates to early experiences of ambivalence with the primary caretaker that lead to chronic separation distress.
This paper will not use clinical materials to illustrate its hypotheses; the reader can find examples in the literature (e.g., Fine, 1972; Gustafson, 1976; Johnson, 2009, 2010; Flores Mosri, 2017a).
Only a few examples will be used to illustrate some of the hypotheses and theory described throughout the paper. I suggest that ambivalent affective experiences with the primary caregiving object may result in neurochemical and subjective dysregulations that could contribute to help explain the use of psychotoxic drugs and its implicated behaviors. Such dysregulations work in cascades in which one dysregulation leads to another connection within a spiral loop that relates to depressive feelings. Some alternative aspects for treatment will be briefly discussed.
The Stages of Addiction and the Importance of Subjectivity
Addictive behaviors usually start with the voluntary decision to use a drug (Panksepp et al., 2002; Volkow and Morales, 2015). For the drug to be reinforcing, it must change a subjective state quickly, so that a direct association is established between the consumption of the drug and mood modifications.
An emotional memory will be formed and reinforced as long as the effects of the drug either produce a positive feeling or reduce a negative feeling. Adding genetic, developmental and environmental vulnerabilities, a person who has tried drugs may or may not develop an addictive disorder (see Figure 1).
Drugs of abuse increase the release of mesolimbic dopamine involving the VTA and the NAcc pathway. This initial phase of trying the effects of a psychotoxic drug may be followed by repeated and frequent use that may eventually lead to a gradual urge to use the drug, which slowly results in an involuntary decision guided by regulatory brain modifications.
Despite other factors being present, the frequent repetition of the consumption of a drug of abuse can be enough to modify the VTA-NAcc pathway and to produce a chronic acquired brain disease (Volkow et al., 2016).
At this stage, an addictive disorder can be diagnosed, characterized by a psychological and/or neurobiological dependence. Addicted people will prioritize the drug consumption over other rewarding behaviors, stimulating the mesolimbic dopamine pathway even to the point of death (Olds, 1977; Panksepp et al., 2002).
According to Volkow et al. (2016), three stages of addiction can be distinguished:
(1) binge and intoxication,
(2) withdrawal and negative affect, and
(3) preoccupation and anticipation.
The stage of binge and intoxication is characterized by an increase in dopaminergic activity; all addictive drugs increase the release of dopamine which has been interpreted as a reward signal linked to associative learning.
Dopamine is released to anticipate a response which eventually strengthens synaptic connections, leading to LTP and LTD, involving glutamatergic activity (Wright and Panksepp, 2012).
The course then goes from experimentation with drugs to addiction, which implies progressive neuroadaptations in the brain, i.e., an acquired disease of the brain (Volkow and Koob, 2015). Conditioning leads to sensitized learning and memory formation recruiting the VTA and the NAcc, which establishes habits and routines along with the dorsal striatum.
Other key structures that regulate dopaminergic activity include the amygdala and the hippocampus (Wright and Panksepp, 2012). The mesolimbic dopamine pathway is modified by the repeated use of drugs resulting in craving, which will motivate the patient to look for the drug and to use it.
The brain is gradually changing and getting ill. Addiction weakens brain regions involved in executive functions, such as decision making, inhibitory control, and self-regulation. This prefrontal function impairment contributes to repeated relapse.
The patient’s will is compromised (Johnson, 2013) and there is loss of self-control. From the subjective perspective, the users experiencing those modifications do their best to try to explain these new feelings to themselves.
They initially try to deny the loss of self-control. They frequently state that they can quit using drugs whenever they want to. But they also clarify that they do not want to stop.
This type of sentence is a clinical indicator that the patient has lost control and that the dopamine mesolimbic system may have suffered neuroadaptive modifications. As seen in Olds (1977) findings, the users’ predominant goal becomes to stimulate this pathway. Negative consequences of drug abuse will be ignored and previous interests will be left behind. Dopamine release in addictive disorders starts to feel bad when it gives the experience of a positive expectancy of satisfaction that never actually comes (Panksepp et al., 2002).
The prediction never meets real sensory input and satisfaction (Schultz, 2006, 2016). Dopaminergic neurons keep firing due to the effects of drugs. This constitutes a pathological activity that means that the drug in itself is not rewarding.
Hence, the constant firing of dopamine does not mean pleasure and object-finding; it means expectation of finding satisfaction. Dopamine release then turns into a frustrating experience, yet users continue their neurochemical stimulation.
From Panksepp’s view of a SEEKING system, only the actual finding and consumption of the satisfying object stops dopaminergic release in the mesolimbic dopamine pathway (Panksepp, 1998; Schultz, 2002), meaning that dopamine firing will only stop when the object is being consumed. Then a different pathway is activated, a “liking” system (Berridge et al., 2009) that is different from a “wanting” dopaminergic system. The satisfaction is related to the activity of several neurochemicals, including increases in opioid activity (Panksepp et al., 2002; Burgdorf and Panksepp, 2006).
The illusion experienced in addiction means that as long as dopaminergic neurons keep firing, the mu and delta opioid receptor activity related to satisfaction is not active. Thus, addicted patients only experience the expectation of a positive feeling, but not the pleasure of actually finding a satisfying object.
Addiction is a frustrating and failed illusion. The more frustration the user experiences, the less dopaminergic activity their brain shows. Neurobiologically, the dopamine system is downregulated resulting in feelings of hopelessness (Watt and Panksepp, 2009). It now has neuroadaptations that compromise its capability to fire in search of a motivated exploration of its environment.
To sum up, the first stage of addiction involves the experience of intoxication, which, if repeated, will in turn lead to a decrease in the ability to feel motivation and pleasure. The neuroplastic changes imply an increased release of glutamate that impacts the NAcc, the dorsal striatum, the amygdala, the hippocampus, and the PFC. All these structures regulate dopamine firing. Because the dopamine pathway has been modified, the user’s motivational feelings and behaviors will be compromised (see Figure 2).
The second stage for Volkow is withdrawal and negative affect. This model states that regular rewards lose their former motivational power, due to the downregulation of the dopamine mesolimbic pathway.
At the same time, there is also a hyperactive impact on the extended amygdala circuitry that produces negative affects related to withdrawal. Users will try to avoid these negative feelings, constituting a new type of negative reinforcements.
They now have a powerful reason to repeat drug use, which is to alleviate from withdrawal symptoms. Anxiety and stress are predominant feelings during this stage and they can in turn lead to irritability and aggression. Several alterations in the regulation of the HPA are observed (Volkow et al., 2016), enhancing the release of CRF.
Volkow and Morales (2015) have called the allostatic changes that lead to the use of drugs to try and alleviate withdrawal symptoms, the “dark side of addiction.” They implicate the amygdala, the BNST and the NAcc shell. There is also an upregulation of dynorphins linked to the dysphoric feelings that characterize this stage. Furthermore, neurochemicals related to positive emotions, such as enkephalins and endocannabinoids, are downregulated.
The lateral habenula is also impacted by the use of drugs since it is another regulator of dopamine firing. It is active when positive expectations fail to happen, as well as in the presence of aversive stimuli.
To summarize, this stage recruits what has also been called the “antireward” system (Volkow and Morales, 2015). It implies an enhanced reactivity to stress which yields negative emotions when the drug is withdrawn.
These dysphoric feelings result in an intense motivation to escape the discomfort, which the drug can help mitigate by a renewed increase of dopamine release. Yet, since the dopamine release gradually diminishes, the relieving feelings are also gradually less effective, leading users to increase doses and frequencies of drug consumption. They binge, which in turn deepens the dysphoria during withdrawal. Users are more prone to overdose at this stage (see Figure 3).
Withdrawal symptoms worsen previous stressful feelings, favoring some of the features of the third stage proposed by Volkow, preoccupation and anticipation. This stage emphasizes the compromise of the PFC, which impairs self-regulation and other executive functions. The PFC inhibits and regulates behavior (Anderson et al., 2016).
In addiction the user can no longer make the decision to stop. This known progress of addictive disorders enhances the importance of detecting negative affects that can lead to the initial voluntary decision of using drugs, since this stage means that treating users will represent a complex challenge. Functions such as attribution of salience, decision making, planning, and monitoring of actions are modified. The top-down regulation of emotional circuits is compromised leading to an inability to resist the urge to use drugs (see Figure 4).
Source:
Harvard
Media Contacts:
James F. Smith – Harvard
Original Research: Closed access
“Sadness, but not all negative emotions, heightens addictive substance use”. Charles A. Dorison et al.
PNAS doi:10.1073/pnas.1909888116.
