Sugar addiction

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Sugar addiction is the state of addiction to sugar consumption.

Sugar has been shown to induce ΔFosB in D1-type medium spiny neurons in the nucleus accumbens (NAcc).[1][2] Consequently, regular consumption of large quantities of sugar can result in a state of addiction to sugar.[1][2]

Summary of addiction-related plasticity[edit]

This section is transcluded from FOSB. (edit | history)
Form of neural or behavioral plasticity Type of reinforcer Sources
Opiates Psychostimulants High fat or sugar food Sexual intercourse Physical exercise
(aerobic)
Environmental
enrichment
ΔFosB expression in
nucleus accumbens D1-type MSNs
[2]
Behavioral plasticity
Escalation of intake Yes Yes Yes [2]
Psychostimulant
cross-sensitization
Yes Not applicable Yes Yes Attenuated Attenuated [2]
Psychostimulant
self-administration
[2]
Psychostimulant
conditioned place preference
[2]
Reinstatement of drug-seeking behavior [2]
Neurochemical plasticity
CREB phosphorylation
in the nucleus accumbens
[2]
Sensitized dopamine response
in the nucleus accumbens
No Yes No Yes [2]
Altered striatal dopamine signaling DRD2, ↑DRD3 DRD1, ↓DRD2, ↑DRD3 DRD1, ↓DRD2, ↑DRD3 DRD2 DRD2 [2]
Altered striatal opioid signaling μ-opioid receptors μ-opioid receptors
κ-opioid receptors
μ-opioid receptors μ-opioid receptors No change No change [2]
Changes in striatal opioid peptides dynorphin dynorphin enkephalin dynorphin dynorphin [2]
Mesocorticolimbic synaptic plasticity
Number of dendrites in the nucleus accumbens [2]
Dendritic spine density in
the nucleus accumbens
[2]

See also[edit]

References[edit]

  1. ^ a b Robison AJ, Nestler EJ (November 2011). "Transcriptional and epigenetic mechanisms of addiction". Nat. Rev. Neurosci. 12 (11): 623–637. doi:10.1038/nrn3111. PMC 3272277. PMID 21989194. ΔFosB has been linked directly to several addiction-related behaviors ... Importantly, genetic or viral overexpression of ΔJunD, a dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-1-mediated transcriptional activity, in the NAc or OFC blocks these key effects of drug exposure14,22–24. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is also induced in D1-type NAc MSNs by chronic consumption of several natural rewards, including sucrose, high fat food, sex, wheel running, where it promotes that consumption14,26–30. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states. 
  2. ^ a b c d e f g h i j k l m n o Olsen CM (December 2011). "Natural rewards, neuroplasticity, and non-drug addictions". Neuropharmacology 61 (7): 1109–22. doi:10.1016/j.neuropharm.2011.03.010. PMC 3139704. PMID 21459101.