Dipendenza dal cibo

La dipendenza dal cibo o dipendenza dal mangiare è una dipendenza comportamentale che si caratterizza per il consumo compulsivo di alimenti appetibili (per esempio, cibi ad alto contenuto di grassi e zucchero) - i tipi di cibo che marcatamente attivano il sistema di ricompensa negli esseri umani e in altri animali - nonostante le conseguenze negative^[5]^[6].

Il cibo molto zuccherato e ad alto contenuto di grassi ha dimostrato di aumentare l'espressione de ΔFosB, un biomarcatore di dipendenza, nei neuroni medi spinosi tipo-D1 del nucleo accumbens;^[6] tuttavia, ci sono ancora scarse ricerche sulla plasticità sinaptica da consumo compulsivo di cibo, un fenomeno che è noto per essere causato dalla sovra espressione del ΔFosB^[6].

Si è osservata la dipendenza psicologica anche con la presenza di sintomi di astinenza quando il consumo di questi alimenti si interrompe con la sostituzione di cibi a basso contenuto di grassi o di zucchero.^[6]^[7] I professionisti dedicati (in genere psicologi e dietologi) affrontano questo disturbo utilizzando la terapia comportamentale.

^ Nestler EJ, Cellular basis of memory for addiction, in Dialogues Clin. Neurosci., vol. 15, n. 4, December 2013, pp. 431–443, PMC 3898681, PMID 24459410.
«Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.⁴¹. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.»
^ Malenka RC, Nestler EJ, Hyman SE, Chapter 15: Reinforcement and Addictive Disorders, in Molecular Neuropharmacology: A Foundation for Clinical Neuroscience, 2nd, New York, McGraw-Hill Medical, 2009, pp. 364–375, ISBN 978-0-07-148127-4.
^ Glossary of Terms, su Mount Sinai School of Medicine, Department of Neuroscience. URL consultato il 9 febbraio 2015 (archiviato dall'url originale il 10 maggio 2019).
^ Volkow ND, Koob GF, McLellan AT, Neurobiologic Advances from the Brain Disease Model of Addiction, in N. Engl. J. Med., vol. 374, n. 4, January 2016, pp. 363–371, DOI:10.1056/NEJMra1511480, PMID 26816013.
^ Olsen CM, Natural rewards, neuroplasticity, and non-drug addictions, in Neuropharmacology, vol. 61, n. 7, December 2011, pp. 1109–1122, DOI:10.1016/j.neuropharm.2011.03.010, PMC 3139704, PMID 21459101.
«Functional neuroimaging studies in humans have shown that gambling (Breiter et al, 2001), shopping (Knutson et al, 2007), orgasm (Komisaruk et al, 2004), playing video games (Koepp et al, 1998; Hoeft et al, 2008) and the sight of appetizing food (Wang et al, 2004a) activate many of the same brain regions (i.e., the mesocorticolimbic system and extended amygdala) as drugs of abuse (Volkow et al, 2004). ... As described for food reward, sexual experience can also lead to activation of plasticity-related signaling cascades. ... In some people, there is a transition from “normal” to compulsive engagement in natural rewards (such as food or sex), a condition that some have termed behavioral or non-drug addictions (Holden, 2001; Grant et al., 2006a). ... the transcription factor delta FosB is increased during access to high fat diet (Teegarden and Bale, 2007) or sucrose (Wallace et al, 2008). ...To date, there is very little data directly measuring the effects of food on synaptic plasticity in addiction-related neurocircuitry. ... Following removal of sugar or fat access, withdrawal symptoms including anxiety- and depressive-like behaviors emerge (Colantuoni et al, 2002; Teegarden and Bale, 2007). After this period of “abstinence”, operant testing reveals “craving” and “seeking” behavior for sugar (Avena et al, 2005) or fat (Ward et al, 2007), as well as “incubation of craving” (Grimm et al, 2001; Lu et al, 2004; Grimm et al, 2005), and “relapse” (Nair et al, 2009b) following abstinence from sugar. In fact, when given a re-exposure to sugar after a period of abstinence, animals consume a much greater amount of sugar than during previous sessions (Avena et al., 2005).»
"Table 1"
^ ^a ^b ^c ^d Hebebrand J, Albayrak Ö, Adan R, Antel J, Dieguez C, de Jong J, Leng G, Menzies J, Mercer JG, Murphy M, van der Plasse G, Dickson SL, "Eating addiction", rather than "food addiction", better captures addictive-like eating behavior, in Neurosci Biobehav Rev, vol. 47, November 2014, pp. 295–306, DOI:10.1016/j.neubiorev.2014.08.016, PMID 25205078.
«
•Evidence for addiction to specific macronutrients is lacking in humans.
•'Eating addiction' describes a behavioral addiction. ...
We concur with Hone-Blanchet and Fecteau (2014) that it is premature to conclude validity of the food addiction phenotype in humans from the current behavioral and neurobiological evidence gained in rodent models. ... To conclude, the society as a whole should be aware of the differences between addiction in the context of substance use versus an addictive behavior. As we pointed out in this review, there is very little evidence to indicate that humans can develop a “Glucose/Sucrose/Fructose Use Disorder” as a diagnosis within the DSM-5 category Substance Use Disorders. We do, however, view both rodent and human data as consistent with the existence of addictive eating behavior.»
^ Karen S. I. Ho, Milton Z. Nichaman, Wendell C. Taylor, Eun Sul Lee e John P. Foreyt, Binge eating disorder, retention, and dropout in an adult obesity program, in International Journal of Eating Disorders, vol. 18, n. 3, 1995, pp. 291–4, DOI:10.1002/1098-108X(199511)18:3<291::AID-EAT2260180312>3.0.CO;2-Y, PMID 8556026.

[Cellular_basis-1] Nestler EJ, Cellular basis of memory for addiction, in Dialogues Clin. Neurosci., vol. 15, n. 4, December 2013, pp. 431–443, PMC 3898681, PMID 24459410.
«Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.⁴¹. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.»

[Addiction_glossary-2] Malenka RC, Nestler EJ, Hyman SE, Chapter 15: Reinforcement and Addictive Disorders, in Molecular Neuropharmacology: A Foundation for Clinical Neuroscience, 2nd, New York, McGraw-Hill Medical, 2009, pp. 364–375, ISBN 978-0-07-148127-4.

[Nestler_Labs_Glossary-3] Glossary of Terms, su Mount Sinai School of Medicine, Department of Neuroscience. URL consultato il 9 febbraio 2015 (archiviato dall'url originale il 10 maggio 2019).

[Brain_disease-4] Volkow ND, Koob GF, McLellan AT, Neurobiologic Advances from the Brain Disease Model of Addiction, in N. Engl. J. Med., vol. 374, n. 4, January 2016, pp. 363–371, DOI:10.1056/NEJMra1511480, PMID 26816013.

[Natural_and_drug_addictions-5] Olsen CM, Natural rewards, neuroplasticity, and non-drug addictions, in Neuropharmacology, vol. 61, n. 7, December 2011, pp. 1109–1122, DOI:10.1016/j.neuropharm.2011.03.010, PMC 3139704, PMID 21459101.
«Functional neuroimaging studies in humans have shown that gambling (Breiter et al, 2001), shopping (Knutson et al, 2007), orgasm (Komisaruk et al, 2004), playing video games (Koepp et al, 1998; Hoeft et al, 2008) and the sight of appetizing food (Wang et al, 2004a) activate many of the same brain regions (i.e., the mesocorticolimbic system and extended amygdala) as drugs of abuse (Volkow et al, 2004). ... As described for food reward, sexual experience can also lead to activation of plasticity-related signaling cascades. ... In some people, there is a transition from “normal” to compulsive engagement in natural rewards (such as food or sex), a condition that some have termed behavioral or non-drug addictions (Holden, 2001; Grant et al., 2006a). ... the transcription factor delta FosB is increased during access to high fat diet (Teegarden and Bale, 2007) or sucrose (Wallace et al, 2008). ...To date, there is very little data directly measuring the effects of food on synaptic plasticity in addiction-related neurocircuitry. ... Following removal of sugar or fat access, withdrawal symptoms including anxiety- and depressive-like behaviors emerge (Colantuoni et al, 2002; Teegarden and Bale, 2007). After this period of “abstinence”, operant testing reveals “craving” and “seeking” behavior for sugar (Avena et al, 2005) or fat (Ward et al, 2007), as well as “incubation of craving” (Grimm et al, 2001; Lu et al, 2004; Grimm et al, 2005), and “relapse” (Nair et al, 2009b) following abstinence from sugar. In fact, when given a re-exposure to sugar after a period of abstinence, animals consume a much greater amount of sugar than during previous sessions (Avena et al., 2005).»
"Table 1"

[Food/eating_addiction_review-6] Hebebrand J, Albayrak Ö, Adan R, Antel J, Dieguez C, de Jong J, Leng G, Menzies J, Mercer JG, Murphy M, van der Plasse G, Dickson SL, "Eating addiction", rather than "food addiction", better captures addictive-like eating behavior, in Neurosci Biobehav Rev, vol. 47, November 2014, pp. 295–306, DOI:10.1016/j.neubiorev.2014.08.016, PMID 25205078.
«
•Evidence for addiction to specific macronutrients is lacking in humans.
•'Eating addiction' describes a behavioral addiction. ...
We concur with Hone-Blanchet and Fecteau (2014) that it is premature to conclude validity of the food addiction phenotype in humans from the current behavioral and neurobiological evidence gained in rodent models. ... To conclude, the society as a whole should be aware of the differences between addiction in the context of substance use versus an addictive behavior. As we pointed out in this review, there is very little evidence to indicate that humans can develop a “Glucose/Sucrose/Fructose Use Disorder” as a diagnosis within the DSM-5 category Substance Use Disorders. We do, however, view both rodent and human data as consistent with the existence of addictive eating behavior.»

[7] Karen S. I. Ho, Milton Z. Nichaman, Wendell C. Taylor, Eun Sul Lee e John P. Foreyt, Binge eating disorder, retention, and dropout in an adult obesity program, in International Journal of Eating Disorders, vol. 18, n. 3, 1995, pp. 291–4, DOI:10.1002/1098-108X(199511)18:3<291::AID-EAT2260180312>3.0.CO;2-Y, PMID 8556026.

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