Biological explanation for alcohol addiction

Mode of action

Empirical evidence

Li et al (2014)
GABA as an inhibitory neurotransmitter in the brain of mammals

1. Inhibitory neurotransmitters, GABA, are active throughout the brain, controlling neural activity along brain pathways and reducing energy levels.

2. Glutamate acts as the brain's excitatory neurotransmitter.

3. When alcohol enters the brain, it delivers a double sedative punch, interacting with GABA receptors to make them even more inhibitory and slowing down the CNS.

4. It binds to glutamate receptors, preventing the glutamate from exciting the cell.

5. Reduces serotonin activity - serotonin associated with emotions, low levels in the brain create feelings of depression, alcohol considered a depressant.

6. Increased release of dopamine in the brain's reward centre. Continuation of drinking occurs to get more dopamine release, till the effect is gone.


  • Carried out a meta-analysis of GABA-a receptor genes using 4,739 people dependent on alcohol, opioids or methamphetamine and 4,924 controls
  • Found associations between variants of GABA-a receptor genes and alcohol dependence (GABRA2) and associations between GABRAG2 and both alcohol and heroin dependence
  • Concluded that give GABA-a receptor genes were implicated
    • This is evidence for genetic involvement in alcoholism
  • Many clinical drugs target GABA-a receptors, such as benzodiazepines and barbiturates and GABA is known to be an inhibitory neurotransmitter
    • The evidence that GABA is involved in alcohol dependence confirms a role for neurotransmission in alcohol addiction

Study of twins showed a genetic link to alcohol and smoking

  • Maes et al (1999) looked at 1,412 MZ and DZ twins pairs and found genetic influence in smoking and drinking alcohol
    • If there is a genetic link to alcohol addiction, this doesn't mean a neurotransmitter explanation is wrong
    • There can be a neurotransmitter explanation that can be explained by looking at genes

Evaluation

Strengths

Weaknesses

  • A lot of evidence that neurotransmitter functioning, particularly in the brain's reward system, relates to drug misuse, including alcoholism
    • Noble (1996) confirmed there are reduced dopamine levels and reduced numbers of D2 dopamine receptors in animals that prefer alcohol, suggesting a neurotransmitter explanation for alcoholism as well as a genetic one
  • Studies often animal lab experiments with strong controls and careful testing
    • Cause-and-effect conclusions drawn and conclusions have credibility
  • Studies using human support animal studies, lending credibility to findings
    • Noble (1996) used animal studies as evidence and also showed that brain scanning in humans shows lowered dopamine in alcoholics
    • Treating alcoholics with a dopamine receptor agonist reduces alcohol drinking, giving evidence for dopamine in alcoholism
  • Use of animal lab experiments can be seen as a strength, but there is the criticism that humans aren't the same as animals in their brain functioning
    • Evidence for an explanation from animal studies might not be generalisable to humans
  • Neurotransmitter functioning as an explanation for alcohol misuse doesn't seem to be separate from genetic or learning explanations
    • Genes can affect neurotransmitter functioning
    • The reward system in the brain rewards the individual in a positive way, which leads to more of the behaviour that gives the reward, relates to operant conditioning
    • Neurotransmitter, genetic and learning explanations seem to link
  • Weiner et al (1997)
    • Alcohol works to reduce glutamate activity at the NMDA glutamate receptor and increases the inhibiting effect of GABA at the GABA-a receptor, reducing brain activity in general
  • Roberto et al (2004b)
    • Alcohol suppressed the transmission of signals using glutamate in the central nucleus of the amygdala