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 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.
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.