Exploring the munchies: An online survey of users' experiences of cannabis effects on appetite and the development of a Cannabinoid Eating Experience Questionnaire.

BACKGROUND: Cannabis intoxication is commonly reported to increase appetite and enhance appreciation of food (the 'munchies'). These effects are attributed to activation of the endocannabinoid system. However, the psychological changes that underlie these phenomena are under-researched. We report here the results of an extensive online survey of cannabis users with an exploratory Cannabinoid Eating Experience Questionnaire (CEEQ). METHOD: Frequent cannabis users completed a 46-item questionnaire about their eating behaviour under the influence of cannabis. An English-speaking sample (n=591) provided data for the initial exploratory validation of the scale. A second Dutch-language survey (n=163) was used for confirmatory factor analysis. Test-retest reliability was based on a third English-speaking sample (n=40) who completed the revised, 28-item CEEQ twice across 2 weeks. RESULTS: Principal components analysis provided a two-factor solution. Factor 1 (hedonic) comprised 14 items that related primarily to the enjoyment and altered sensory aspects of eating. Factor 2 (appetitive) comprised a further 14 items related to motivational factors that instigate or promote eating. The two-factor structure was supported by confirmatory factor analysis. Both the hedonic and appetitive subscales had good internal reliability (α=0.92 for each subscale, in two independent samples). Good test-retest reliability was obtained for the revised 28-item questionnaire (ps<.01 for Total CEEQ and each subscale). CONCLUSION: The Cannabinoid Eating Experience Questionnaire provided a valid, reliable assessment of the psychological features of cannabis-induced alterations to appetite. Our data confirm that cannabis principally influences the motivational factors that lead to the initiation of eating and the hedonic factors implicated in maintaining eating.

The effect of Korean pine nut oil (PinnoThin) on food intake, feeding behaviour and appetite: a double-blind placebo-controlled trial.

Certain free fatty acids have been shown to have potent effects on food intake and self-reported changes in appetite; effects associated with increases in the release of endogenous cholecystokinin (CCK) and glucagon like peptide-1 (GLP-1). In the current study, the effects of a Korean pine nut oil product, PinnoThin, at doses 2 g, 4 g and 6 g triglyceride (TG) and 2 g free fatty acid (FFA), on food intake and appetite were examined in a cross-over double-blind placebo-controlled randomised counter-balanced design in 42 overweight female volunteers. 2 g FFA PinnoThin, given 30 minutes prior to an ad-libitum buffet test lunch, significantly reduced food intake (gram) by 9% (F(4,164) = 2.637, p = 0.036) compared to olive oil control. No significant effect of PinnoThin on macronutrient intake or ratings of appetite were observed. Given the recent data showing that the TG form of PinnoThin may also reduce appetite by increasing CCK release, the lack of any effect of the TG form found in this study could be attributed to the timing of the dosing regime. Collectively, these data suggest that PinnoThin may exert satiating effects consistent with its known action on CCK and GLP-1 release, and previously observed effects on self-reported appetite ratings.

Cannabinoids and ghrelin have both central and peripheral metabolic and cardiac effects via AMP-activated protein kinase.

Endocannabinoids and ghrelin are potent appetite stimulators and are known to interact at a hypothalamic level. However, both also have important peripheral actions, including beneficial effects on the ischemic heart and increasing adipose tissue deposition, while ghrelin has direct effects on carbohydrate metabolism. The AMP-activated protein kinase (AMPK) is a heterotrimeric enzyme that functions as a fuel sensor to regulate energy balance at both cellular and whole body levels, and it may mediate the action of anti-diabetic drugs such as metformin and peroxisome proliferator-activated receptor gamma agonists. Here we show that both cannabinoids and ghrelin stimulate AMPK activity in the hypothalamus and the heart, while inhibiting AMPK in liver and adipose tissue. These novel effects of cannabinoids on AMPK provide a mechanism for a number of their known actions, such as the reduction in infarct size in the myocardium, an increase in adipose tissue, and stimulation of appetite. The beneficial effects of ghrelin on heart function, including reduction of myocyte apoptosis, and its effects on lipogenesis and carbohydrate metabolism, can also be explained by its ability to activate AMPK. Our data demonstrate that AMPK not only links the orexigenic effects of endocannabinoids and ghrelin in the hypothalamus but also their effects on the metabolism of peripheral tissues.

Endocannabinoid levels in rat limbic forebrain and hypothalamus in relation to fasting, feeding and satiation: stimulation of eating by 2-arachidonoyl glycerol.

Endocannabinoids are implicated in appetite and body weight regulation. In rodents, anandamide stimulates eating by actions at central CB1 receptors, and hypothalamic endocannabinoids may be under the negative control of leptin. However, changes to brain endocannabinoid levels in direct relation to feeding or changing nutritional status have not been investigated. We measured anandamide and 2-arachidonoyl glycerol (2-AG) levels in feeding-associated brain regions of rats, during fasting, feeding of a palatable food, or after satiation. Endocannabinoid levels were compared to those in rats fed ad libitum, at a point in their daily cycle when motivation to eat was absent. Fasting increased levels of anandamide and 2-AG in the limbic forebrain and, to a lesser extent, of 2-AG in the hypothalamus. By contrast, hypothalamic 2-AG declined as animals ate. No changes were detected in satiated rats. Endocannabinoid levels in the cerebellum, a control region not directly involved in the control of food intake, were unaffected by any manipulation. As 2-AG was most sensitive to variation during feeding, and to leptin regulation in a previous study, we examined the behavioural effects of 2-AG when injected into the nucleus accumbens shell, a limbic forebrain area strongly linked to eating motivation. 2-AG potently, and dose-dependently, stimulated feeding. This effect was attenuated by the CB1 receptor antagonist SR141716. These findings provide the first direct evidence of altered brain levels of endocannabinoids, and of 2-AG in particular, during fasting and feeding. The nature of these effects supports a role for endocannabinoids in the control of appetitive motivation.