Craving
Addiction has been sitting in the wiki as a table row — one of the conditions the Khalsa roadmap lists under interoceptive-psychopathology, with “craving/withdrawal interoception” as its interoceptive sign and no page to hold it. Bonaz et al. (2021), with Rajita Sinha and Paul Kenny on the author list, supply enough to justify one.
Craving as a feeling, not a cognition
The framing worth recording is that craving is treated as an interoceptive motivational feeling rather than a belief or a decision — and specifically as one that is state-dependent:
In substance use disorders, craving is an interoceptive motivational feeling that varies as a function of drug state (acute intoxication, tolerance, withdrawal, abstinence, and long-term recovery).
Interoception enters addiction as the conduit for several constructs at once: physiological arousal, motivational drive, impulsivity, and representations of stress and reward (Paulus & Stewart 2014). Binge and chronic psychoactive drug use produces adaptations across corticolimbic (including insula), striatal and prefrontal networks contributing to interoception, altering emotional and reward processing.
Verdejo-Garcia et al.’s (2012) proposal — cited here — is that models of interoception applied to addiction should be extended by considering (i) the multiple components of the bodily feedback system (signal, perception, appraisal) and (ii) how individual differences in those three components affect cognitive-affective processing. That tripartite split is the taxonomy problem arriving in addiction research independently.
The insula lesion finding
The strongest evidence on this page, and it is not from this review. Among the specific emotional and motivational deficits produced by acquired focal lesions to the insula, Bonaz et al. list — alongside disgust insensitivity, acquired alexithymia and psychopathy — loss of drug-craving.
This is the well-known observation that smokers who suffer insular damage can quit without effort or relapse, and it is unusually clean for a field built on correlations: damage a specific interoceptive cortex, and a specific motivational feeling disappears while the rest of the person’s motivational life continues. It is about as close as the literature comes to a causal demonstration that a felt bodily state is constitutive of a motivational drive rather than accompanying it. Relevant to where-are-feelings-constituted and to the body-loop question of whether a signal must be felt to bias behaviour — here, apparently, yes.
The wiki holds this at one remove; the primary insular-lesion smoking literature (Naqvi et al.) is not in raw/ and Bonaz et al. give it a clause, not a section.
The provenance improves with Jones, Ward & Critchley (2010), which is still secondhand but supplies the design. Naqvi et al. (2007): 19 patients whose stroke involved the insula, either hemisphere (right n=6, left n=13), who “reported greater ease in giving up smoking, without relapse or persistent urge to smoke, in contrast to smokers with strokes affecting other areas.” Note the control comparison is what does the work — other stroke patients, not healthy quitters.
Jones et al. offer two mechanisms and decline between them, which the clause version concealed:
- a reduced ability to detect interoceptive states linked to craving, or
- a reduction in the hedonic feelings induced by smoking (Gray & Critchley 2007).
Those are different theories. The first says the drive is intact and the patient can no longer read it; the second says the reward is gone. Only the first is the interoceptive claim this page has been leaning on, and nothing in the lesion data separates them. The wiki should stop stating the finding as though the first reading were established. The review also flags that whether the effect generalizes to other addictions is unknown — still true.
The somatic-marker reading Jones et al. prefer is a third framing again: exposure to or recollection of a drug-associated experience reactivates an “interoceptive memory” state (Naqvi & Bechara 2009), which is the as-if loop applied to addiction.
The other lesion literature on addiction, and the two do not meet
The somatic marker programme reached addiction two decades earlier from a different lesion and a different logic, and the wiki should hold the two side by side because they disagree about what the body contributes.
Bechara, Damasio & Damasio (2000): substance abusers resemble VM patients in that, offered an immediate reward at the risk of losing reputation, job, home and family, they take the reward and ignore the consequences. Supported by iowa-gambling-task deficits in drug-abusing samples (Grant et al. 1997; Petry et al. 1998; Bechara et al. 1999b; Rogers et al. 1999) — impaired decision-making proposed as standing “at the core of the problem of substance abuse.” See acquired-sociopathy for the family of extensions this belongs to.
The contrast with the insula finding above is sharp and nobody in this wiki draws it:
| somatic marker account | insular-lesion account | |
|---|---|---|
| lesion | ventromedial prefrontal | insula |
| what is lost | the bias that would have deterred the choice | the craving itself |
| effect on the addiction | a model of why the addict chooses badly | the addict stops wanting the drug |
| direction | body signal absent → worse choices | body signal absent → the drive disappears |
Both are lesion arguments about bodily signals and addiction, and they point opposite ways on whether removing the body’s contribution helps or hurts. The reconciliation is available in principle — different signals, different structures, one marking outcomes and one constituting a drive — but no source here makes it, and the somatic marker literature’s own extension to addiction was made by behavioural resemblance without measuring interoception in anyone. Recorded as an open seam.
The humoral route: stress hormones as conditioned cues
Sinha’s contribution, and the part that is genuinely interoceptive rather than generically neurobiological. Alcohol stimulates release of stress hormones via the hpa-axis and upregulates glucocorticoid receptor expression across limbic forebrain and medial prefrontal circuits (Blaine & Sinha 2017). This humoral interoceptive route is proposed to contribute to the development and progression of alcohol use disorders — severity, chronicity, and relapse risk.
The mechanistically interesting claim:
Stress hormone release and alcohol cues can both serve as conditioned interoceptive cues motivating alcohol consumption.
So the body’s own endocrine stress response becomes a learned cue for drinking. That is a conditioning account in which the conditioned stimulus is internal, which is exactly the structure interoceptive-exposure assumes for panic and schema-guided-symptom-perception assumes for symptom report — the same architecture in a third clinical literature. The therapeutic inference drawn is that treatments improving prefrontal function and/or normalizing HPA function may assist in treatment and relapse prevention.
Treatment, and the interoceptive target
Current practice combines pharmacotherapy and behavioural counselling. Bonaz et al. flag growing evidence for brain stimulation targeting the insula, “through its involvement in interoception, decision-making, pain perception, cognitive control, mood, anxiety, threat, and conscious urges” (Ibrahim et al. 2019) — see bioelectronic-medicine. Note the loop: the insula is proposed as a stimulation target because lesioning it abolishes craving.
The review also records that cognitive-behavioural strategies attenuating negative cognitions and interoceptive/emotional arousal suppress coactivation of anterior insula with amygdala and orbitofrontal cortex, across both addiction and mood disorders — and that compassion meditation elicits similar changes, by cultivating “an equanimous and nonreactive dissociated form of attention to depictions of suffering.” Those citations are Weng et al. (2018) and Laneri et al. (2017); see compassion-meditation and lutz-2008-compassion-meditation, where the wiki holds the contemplative side of this first-hand.
Treating craving through a different interoceptive system: the ghrelin route
Weng et al. (2021), with Lorenzo Leggio contributing this section, make the most concrete proposal on the page and it is a cross-system one: treat substance use by manipulating hunger. The rationale is that craving is itself an interoceptive feeling (as this page’s opening framing has it, from a different review), that addiction and feeding neurocircuitry overlap substantially, and that medications approved for addiction routinely affect appetite and food intake.
The target is the ghrelin system. (Acyl-)ghrelin is a stomach-derived peptide — the “hunger hormone” — acting at growth hormone secretagogue receptor 1a (GHS-R1a). The evidence as summarized:
| level | finding |
|---|---|
| rodent, genetic | deleting the ghrelin peptide or receptor gene reduces alcohol intake and other alcohol-related outcomes |
| rodent, pharmacological | ghrelin administration increases alcohol intake, preference, self-administration and conditioned place preference; GHS-R1a blockade reduces them |
| human, observational | endogenous ghrelin concentrations correlate with alcohol craving, subjective alcohol effects, and brain response to alcohol cues |
| human, experimental | ghrelin administration increases cue-induced craving for alcohol but not for juice, and increases progressive-ratio alcohol self-administration |
| human, therapeutic | PF-5190457, a GHS-R1a blocker, safe and tolerable with alcohol; may reduce cue-elicited craving for alcohol and food in heavy drinkers |
The alcohol-not-juice dissociation is what makes this more than an appetite story. If ghrelin merely raised general wanting, juice craving should rise too. That it does not suggests a gut peptide is acting on a specific learned motivational target rather than on drive in general — which is the interoceptive claim, and the one thing here that the wiki’s body-loop material can actually make use of.
Two connections worth holding. First, this is the second peripheral metabolic peptide on this page doing motivational work centrally (GLP-1 is the other, below), and ghrelin recurs in gut-hippocampal-memory as a signal of energy need rather than satiation. Second, the therapeutic logic is the opposite of MABT’s: block the interoceptive signal pharmacologically, rather than train the person to notice and reinterpret it. Weng et al. put both in the same framework as different levels of one intervention space, and suggest combining them. The wiki notes that no study does.
The authors’ own verdict is appropriately thin: “significant additional work is needed.”
The nicotine circuit, recorded and held apart
Kenny’s section is the most detailed mechanism in the whole review and the least connected to anything else in this wiki. Glucagon-like peptide-1 (GLP-1), secreted by intestinal enteroendocrine cells, is also present in the nucleus tractus solitarius — the first brainstem site where spinal and vagal interoceptive afferents converge. Nicotine activates NTS GLP-1 neurons, which excite medial habenular projections to the interpeduncular nucleus; activating this circuit in mice attenuates nicotine reward and reduces hyperglycemic responses. Chronic nicotine exposure alters habenular cholinergic signalling, fostering dependence.
Recorded as mouse circuit work with an interoceptive framing. It is the review’s clearest instance of a peripheral metabolic peptide doing motivational work in the brain, and its clearest instance of evidence the wiki cannot situate — no human data, no interoceptive measurement in the wiki’s sense, and no bridge to any other page here.