Excess sugar consumption ‘similar to cocaine addiction', says study
FAB RESEARCH COMMENT:
This new study confirms and extends previious research showing that excessive, intermittent sugar consumption can activate brain pathways and systems involved in addiction to drugs of abuse.Read the associated research here:
The idea of 'addiction' to food, or to sugar or fructose in particular remains controversial, although interest - and evidence - in this area has been developing rapidly in recent years. Much debate arises from the fact that the term 'addiction' is difficult to define, as it involves both biological and psychological / behavioural mechanisms that can be difficult to separate out in practice (particularly in human studies).
In addition, while much research focuses on specific ingredients such as sugar, other evidence indicates that a combination of fat and sugar is characteristic of most foods that are consumed to excess.
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And for more articles on this subject, please see the following lists, which are regularly updated.
An over consumption of sugar sets in motion a reward mechanism in the brain that mimics other drugs such as tobacco and cocaine, a study has suggested.
The study identified that excessive sugar consumption increases the dopamine levels in the brain with higher levels of sugar needed to achieve the same reward levels and avoid mild states of depression.
The researchers believe that since the pathways of each drug are so similar, drugs used to treat nicotine addiction could be used to treat addiction to sugar.
The team from the Queensland University of Technology (QUT) used animal models to investigate the efficacy of varenicline, a drug that that can regulate dopamine in the reward pathway of the brain, and its effect of reducing long-term sucrose consumption.
Wistar rats were divided into groups of 10–12 and varenicline was administered to each animal to assess short-term exposure (4 weeks) and, long-term exposure (12 weeks)
Study details
Results revealed that in the short-term only 2 mg/kg of vareniciline significantly decreased sucrose consumption. In contrast, in the long-term both 1 and 2 mg/kg varenicline decreased sucrose consumption.
They demonstrated that long-term sucrose consumption increases a certain receptor (α4β2) and decreases another (α6β2) receptor in the key brain region associated with reward.
“The present study shows that systemic administration of varenicline produced a reduction of sucrose consumption, especially after long-term sucrose consumption,” the study’s authors said.
“Interestingly, varenicline did not affect sucrose consumption in the short-term suggesting that intermittent access to sucrose may contribute to neurological changes for which varenicline is effective.”
Binging on sugar has repeatedly been shown to elevate dopamine levels in the reward part of the brain, an observation also seen in drug abuse. Chronic intermittent sugar intake also causes an increase in the expression of dopamine (D1) receptors and decrease in the expression of D2 receptors in these brain regions. Similar changes have also been noted in cocaine and morphine responses.
Source: PLOS one
Published online ahead of print, doi.org/10.1371/journal.pone.0150270
“Neuronal Nicotinic Acetylcholine Receptor Modulators Reduce Sugar Intake.”
Authors: Masroor Shariff, Maryka Quik, Joan Holgate, Michael Morgan, Omkar L. Patkar, Vincent Tam, Arnauld Belmer, Selena E. Bartlett
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