Dr Lee Hogarth

Office hours Term 1 2024: Mondays 2-3 (MS Teams) and Tuesday 3-4 (in office WSL232). But feel free to email me to arrange a meeting anytime. I can offer general guidance and welfare to tutees, and module specific guidance for PSY3437, PSY1202, PSY2212 and PSYM231. Exceptions in week 6 (starting 28 Oct), where office hours will be Thursday at 2 (online) and Friday at 2 (online).

Postgraduate Research opportunities: Lee Hogarth is open to email enquires from students with their own funding  interested in pursuing an MSc by Research or PhD. I am also open to supporting students who would like to apply to the China Scholarship Council, Commonwealth Scholarship, or other PhD funding scheme.

About me:

Lee Hogarth is a critical addiction psychologist who studies risk factors, treatment mechanisms and epistemic harms in addiction psychology. His work encompasses epidemiology, experimental assessment of risk and protective factors, small scale randomised controlled trials evaluating treatment components, secondary data analysis, critical evaluation of animal to human translational pipelines and grand theoretical models of addiction, and exploration of scientific integrity. He is a critic of the compulsive brain disease model of addiction, which envisages drug users as constitutionally damaged and helpless. Instead, he argues that addiction stems from the interaction of social, economic, environmental and market forces, promoting goal-directed drug choice. He advocates structural and political reform to nurture individual agency, unbiased drug knowledge, and quality of life in marginalised groups.

Interests:

I am an associate professor in the Department of Psychology at the University of Exeter UK. My work focuses on individual risk factors, pathways and mechanisms that confer risk of transitioning from recreational substance use to dependence, protective factors that reduce risk by diverting vulnerable groups, and mechanisms that mediate recovery from addiction. My work has been funded by the Wellcome Trust, BBSRC, ESRC, MRC and Alcohol Change UK. At the start of my career, I focused on translating animal associative learning theory and behavioral neuroscience methods to humans to test whether vulnerability mechanisms found in animals were also found in humans. My PhD and early post-doctoral work tested the prediction of incentive salience theory that drug related cues command selective attention which controls automatic drug-seeking. I developed conditioning procedures to measure acquired attentional bias for drug paired cues with eye tracking. However, this learned attentional bias was not reliably associated with level of dependence severity and could be abolished without affecting the capacity of drug stimuli to elicit drug-seeking behavior suggesting the attentional bias for drug cues does not underpin dependence vulnerability and is not a viable target for treatment. Consequently, I moved on to test cue reactivity theory which claims that dependence liability is conferred by greater sensitivity to drug cue priming of drug-seeking behavior. For this purpose, I was first person to develop a human Pavlovian to instrumental transfer procedure with drug rewards, translating method in animal behavioral neuroscience. However, there was no evidence that dependence was associated with greater capacity of drug cues to prime drug-seeking behavior above baseline, so cue reactivity could not underpin individual vulnerability to dependence, contrary to this widely held assumption (Hogarth, 2022). I then returned to test the preferred hypothesis of my one-time PhD supervisor, Anthony Dickinson (FRS) – that drug dependence is driven by excessive habit learning, that is, the tendency to engage in well-practiced drug-seeking behavior without forethought for the consequences. For this purpose, I was the first person to develop an outcome-devaluation procedure for humans with drug reinforcers. However, once again, the predictions of animal behavioral neuroscience failed to translate to humans – I consistently found no evidence that variation in human dependence severity was associated with greater habit learning. I have since positioned myself as a vocal critic of habit theory of addition, on the grounds that habit effects in animals occur in such narrow experimental conditions that this effect lacks ecological validity for humans. Moreover, the minority of human studies which do report greater habit learning in drug users are flawed because the users also report greater disengagement from the tasks (reduced task contingency knowledge), suggesting the observed impairment in performance does not stem form habit learning, but from a trivial, non-specific reduction in task motivation. My recent critical review of habit theory won the journal of Neuropsychopharmacology’s NEAR award at the 2021 ACNP meeting in Puerto Rico (Hogarth, 2020).

My most recent findings suggest that dependence liability can be attributed to preferential goal-directed drug choice governed by greater expected value of the drug in vulnerable individuals (Hogarth & Field, 2020). Across 23 studies, the average correlation between preferential goal-directed drug choice and dependence severity was r=0.51, suggesting this mechanism can account for 26% of the variance in dependence severity (probably the most reliable behavioral marker yet published). Additionally, experimentally induced adverse states (negative mood and stress) motivate further goal-directed drug choice above the baseline preference, and this negative induction effect is powerful enough to overrule the reduction in drug choice produced by devaluation through specific satiety. This powerful effect suggests that negatively motivated goal-directed drug choice could explain the persistence of drug-seeking despite harms/costs. Most importantly, individuals who self-report using substances to cope with negative affect are reliably more susceptible to negatively motivated goal-directed drug choice in laboratory paradigms. Given that self-reported coping motives mediate the greater risk of dependence in individuals who have experienced poverty, discrimination, bullying, adverse childhood events, trauma, and mental health problems, it can be argued that susceptibility to negatively motivated goal-directed drug choice underpins the greater risk of addiction seen in these vulnerable groups. Regarding interventions, whereas the automatic, habit, and compulsion theories of addiction inspire biomedical interventions to correct supposed constitutional learning abnormalities, the negatively motivated goal-directed account inspires interventions that target coping motives as well as systemic reforms to reduce adversity in disadvantaged groups, fitting with a social justice agenda which I find personally rewarding (Hogarth, 2022; Shuai et al., 2022).

Hogarth, L. (2020). Addiction is driven by excessive goal-directed drug choice under negative affect: translational critique of habit and compulsion theory. Neuropsychopharmacology, 45(5), 720-735. https://doi.org/10.1038/s41386-020-0600-8

Hogarth, L. (2022). The persistence of addiction is better explained by socioeconomic deprivation related factors powerfully motivating goal-directed drug choice than by automaticity, habit or compulsion theories favored by the brain disease model. In N. Heather, M. Field, A. Moss, & S. Satel (Eds.), Evaluating the Brain Disease Model of Addiction. Routledge.

Hogarth, L., & Field, M. (2020). Relative expected value of drugs versus competing rewards underpins vulnerability to and recovery from addiction. Behavioural Brain Research, 394, 112815. https://doi.org/10.1016/j.bbr.2020.112815

Shuai, R., Anker, J. J., Bravo, A. J., Kushner, M. G., & Hogarth, L. (2022). Risk pathways contributing to the alcohol harm paradox: Socioeconomic deprivation confers susceptibility to alcohol dependence via greater exposure to aversive experience, internalizing symptoms and drinking to cope [Original Research]. Frontiers in Behavioral Neuroscience, 16. https://doi.org/10.3389/fnbeh.2022.821693

Contributions to Science

1. Incentive salience theory of addiction in humans

My PhD and early Postdoctoral research tested Robinson and Berridge’s (1993) incentive salience theory of addiction in humans. This account predicts that (a) drug addicts should have their attention captured by drug cues, (b) attentional capture by drug cues should play a causal role in driving drug-seeking behavior, and therefore (c) abolishing the attentional bias should reduce cue-elicited drug-seeking. My first publication was one of the earliest demonstrations that drug cues do in fact capture addicts’ attention, using a reaction time measure of attention(A) and is in the top 10% for citations relative to comparable articles based on Scopus data. My subsequent work demonstrated that this attentional bias could be conditioned to arbitrary stimuli and measured more sensitively by eye tracking(B). However, I later discovered that abolishing the attentional bias did not reduce the ability of drug cues to elicit drug-seeking behavior, suggesting that abolishing the attentional bias will not provide a viable therapeutic intervention for addiction(C,D). This latter paper is in the top 30% for citations despite contradicting a core tenet within addiction theory. My prediction from this pre-clinical work, that attentional bias retraining would not yield therapeutic benefits, has been confirmed by clinical trials.

A. Hogarth LC, Mogg K, Bradley BP, Duka T, Dickinson A. Attentional orienting towards smoking-related stimuli. Behav Pharmacol. 2003 Mar;14(2):153-60. PMID: 12658076.

B. Hogarth L, Dickinson A, Hutton SB, Elbers N, Duka T. Drug expectancy is necessary for stimulus control of human attention, instrumental drug-seeking behaviour and subjective pleasure. Psychopharmacology (Berl). 2006 May;185(4):495-504. PMID: 16547713.

C. Hogarth L, Dickinson A, Janowski M, Nikitina A, Duka T. The role of attentional bias in mediating human drug-seeking behaviour. Psychopharmacology (Berl). 2008 Nov;201(1):29-41. PMID: 18679657.

D. Hogarth L, Dickinson A, Duka T. Detection versus sustained attention to drug cues have dissociable roles in mediating drug seeking behavior. Exp Clin Psychopharmacol. 2009 Feb;17(1):21-30. PMID: 19186931.

2. Drug cue-reactivity

Having discovered that attentional bias for drug cues is not a viable target for therapy, I switched to studying the decision mechanisms underpinning drug cue-reactivity. My first aim was to test whether cue elicited drug-seeking is automatic as predicted by implicit accounts, or driven by an expectation of the drug as predicted by decision making accounts. To test these predictions, I was the first person to develop an outcome-specific Pavlovian to instrumental transfer (PIT) procedure for humans with drug reinforcers (a method only previously used in animal behavioural neuroscience). My human procedure demonstrated that a drug stimulus could transfer selective control over a separately trained drug-seeking response, but not over a response trained with a different reinforcer(A) (top 6% cited). To produce this effect, the drug stimulus must have retrieved an expectation of the drug which selectively primed drug-seeking. This effect cannot be explained by automatic, habitual or implicit accounts of drug cue-reactivity.

Paradoxically, I later found that the selective control by a tobacco stimulus over a tobacco-seeking response was not attenuated by nicotine replacement therapy (NRT)(B) (top 7% cited). Furthermore, Dr. Hitsman and I extended this result, finding that that cue-elicited tobacco craving was also not attenuated by varenicline(C) (top 25% cited). The implication of these findings is that drug cues elicit drug-seeking by retrieving an expectation that the drug-seeking response has a higher probability of being reinforced, irrespective of whether the drug outcome currently has low value. I subsequently, confirmed this view experimentally and outlined the implications for cue-retraining therapies(D) (top10% cited).

The crucial observation across all of these studies, however, was that the capacity of drug cues to prime drug-seeking in the PIT procedure was not associated with individual differences in level of dependence(A,B,D). Thus, drug cue-reactivity is not the principal mechanism underpinning risk of dependence, so I turned my research program away from this outcome measure.

A. Hogarth L, Dickinson A, Wright A, Kouvaraki M, Duka T. The role of drug expectancy in the control of human drug seeking. J Exp Psychol Anim Behav Process. 2007 Oct;33(4):484-96. PMID: 17924795.

B. Hogarth L. Goal-directed and transfer-cue-elicited drug-seeking are dissociated by pharmacotherapy: evidence for independent additive controllers. J Exp Psychol Anim Behav Process. 2012 Jul;38(3):266-78. PMID: 22823420.

C. Hitsman B, Hogarth L, Tseng LJ, Teige JC, Shadel WG, DiBenedetti DB, Danto S, Lee TC, Price LH, Niaura R. Dissociable effect of acute varenicline on tonic versus cue-provoked craving in non-treatment-motivated heavy smokers. Drug Alcohol Depend. 2013 Jun 1;130(1-3):135-41. PubMed PMID: 23201174.

D. Hogarth L, Retzler C, Munafò MR, Tran DM, Troisi JR 2nd, Rose AK, Jones A, Field M. Extinction of cue-evoked drug-seeking relies on degrading hierarchical instrumental expectancies. Behav Res Ther. 2014 Aug;59:61-70. PMID: 25011113.

3. Habit learning theory of addiction in humans

My PhD supervisor, Anthony Dickinson, had previously developed the habit learning theory of addiction in animals, and this account has since become a popular account of addiction in humans. On this view, drug-seeking is at first goal-directed (driven by the expected value of the drug), and progressively becomes habitual through practice (automatically elicited by drug related contexts without forethought for the consequences). Individual differences in vulnerability to dependence is driven by a propensity for drug-seeking to shift from being goal-directed to habitual, making the behaviour less amenable to cognitive regulation. To test this prediction, I was the first person to develop an outcome devaluation protocol for humans with drug reinforcers based on the animal model (A,B) (top 5% and 6% cited respectively). This work revealed that although drug-seeking could be rendered habitual under conditions of acute alcohol intoxication(C) (top 9% cited) or cognitive load (D) (top 20% cited), under normal conditions, drug-seeking is goal-directed rather than habitual. Furthermore, more dependent individuals were not more susceptible to drug-seeking becoming habitual(A,B,C,D). Instead, they engage in higher frequency of goal-directed drug-seeking, suggesting dependence is driven by greater expected reward value of the drug (consistent with behavioural-economic accounts). I have concluded from these findings that the evidence for habitual drug-seeking in animals is a product of the invariant nature of their laboratory experience, and that habit theory does not account for addiction in human.

A. Hogarth L, Chase HW. Parallel goal-directed and habitual control of human drug-seeking: implications for dependence vulnerability. J Exp Psychol Anim Behav Process. 2011 Jul;37(3):261-76. PMID: 21500933.

B. Hogarth L. Goal-directed and transfer-cue-elicited drug-seeking are dissociated by pharmacotherapy: evidence for independent additive controllers. J Exp Psychol Anim Behav Process. 2012 Jul;38(3):266-78. PMID: 22823420.

C. Hogarth L, Attwood AS, Bate HA, Munafò MR. Acute alcohol impairs human goal-directed action. Biol Psychol. 2012 May;90(2):154-60. PMID: 22406757.

D. Hogarth L, Field M, Rose AK. Phasic transition from goal-directed to habitual control over drug-seeking produced by conflicting reinforcer expectancy. Addict Biol. 2013 Jan;18(1):88-97. PMID: 23167442.

4. Negative reinforcement theory of drug dependence

My previous work had suggested that individual differences in sub-clinical dependence is driven by the greater expected reward value of the drug driving higher rates of goal-directed drug-seeking. The suspicion, however, was that a second process contributed to clinical addiction. According to negative reinforcement theories, negative states such as depression, anxiety, withdrawal, cognitive deficits etc., powerfully motivate drug-seeking to acutely mitigate those states. Dr. Hitsman and myself hypothesized that individual sensitivity to such negative triggers motivating goal-directed drug-seeking would be the crucial process underpinning clinical dependence. In testing this hypothesis, we adapted the outcome-devaluation procedure to demonstrate that acute negative mood can powerfully motivate drug-seeking behavior, fully countermanding the capacity of drug satiety to reduce goal-directed drug-seeking(A). We then demonstrated that smokers with current major depression are more sensitive to negative mood and withdrawal induced motivation of tobacco-seeking(B) and young adult drinkers with depression symptoms are more sensitive to negative mood-induced increases in alcohol-seeking(C). We have also synthesized this goal-directed account of drug dependence vulnerability in a high profile review article(D). Overall, we argue that individual differences in sub-clinical dependence are driven by the greater expected reward value of the drug driving higher rates of goal-directed drug-seeking. This process is amplified by negative motivational states in groups with comorbid psychiatric symptoms, which powerfully promote goal-directed drug-seeking producing the pathological character of clinical addiction. Our current work focuses on hypersensitivity to negative triggers for drug use in groups with comorbid psychiatric illness, to inform understanding of mechanisms, as well as treatment and prevention strategies for vulnerable drug user groups.

A. Hogarth, L., He, Z., Chase, H. W., Wills, A. J., Troisi, J., II, Leventhal, A. M., (…), Hitsman, B. (2015). Negative mood reverses devaluation of goal-directed drug-seeking favouring an incentive learning account of drug dependence. Psychopharmacology, 232(17), 3235-3247. PMID: 26041336.

B. Hogarth, L., Mathew, A. R., & Hitsman, B. (2017). Current major depression is associated with greater sensitivity to the motivational effect of both negative mood induction and abstinence on tobacco-seeking behavior. Drug and Alcohol Dependence, 176, 1-6. PMID: 28460322

C. Hogarth, L., Hardy, L., Mathew, A. R., & Hitsman, B. (in press) Negative mood-induced alcohol-seeking is greater in young adults who report depression symptoms, drinking to cope, and subjective reactivity. Experimental and Clinical Psychopharmacology.

D. Mathew, A. R., Hogarth, L., Leventhal, A. M., Cook, J. W., & Hitsman, B. (2017). Cigarette smoking and depression comorbidity: systematic review and proposed theoretical model. Addiction, 112(3), 401-412. PMID: 27628300.

Qualifications:

BSc Hons 1st, Sussex,
PhD, Cambridge

Career:

I received my PhD from Cambridge University in 2000 for research on conditioning processes in human addiction supervised by Prof Anthony Dickinson. I then obtained two grants (Wellcome, BBSRC) supporting 7 years of postdoctoral research on attentional learning at Sussex University with Prof Theodora Duka. I obtained a lectureship at Nottingham University in 2007 and shortly after was awarded an MRC young investigators award for 3 years of research on individual differences in associative learning underlying addiction vulnerability. I took up a Senior Lectureship at the University of New South Wales (UNSW), Australia, in 2012, under the academic lead of Prof Simon Killcross. Finally, I returned home in 2013 to take up an Associate Professorship at Exeter University under the academic lead of Prof. Ian McLaren.