A recent study published in Alcohol Clinical and Experimental Research aimed to address this question by analyzing data from over 200,000 primary care patients who completed two brief screenings for alcohol use and depression 11 to 24 months apart.
The study used the Alcohol Use Disorders Identification Test-Consumption version (AUDIT-C), a three-item questionnaire that assesses how often, how much, and how heavily a person drinks alcohol.
The researchers compared the changes in AUDIT-C risk levels and PHQ-2 depression screens between the two time points for each patient subgroup. They found that patient subgroups with increases in AUDIT-C risk levels generally experienced increases in the prevalence of positive depression screens, indicating more depressive symptoms. For example, patients who moved from low-risk drinking to very high-risk drinking had a 100% increase in the prevalence of positive depression screens.
Conversely, patient subgroups with decreases in AUDIT-C risk levels generally experienced decreases in the prevalence of positive depression screens, indicating less depressive symptoms. For example, patients who moved from very high-risk drinking to low-risk drinking had a 49% decrease in the prevalence of positive depression screens.
The study did not examine the causal mechanisms behind the observed associations between changes in alcohol consumption and changes in depression symptoms. It is possible that alcohol affects depression, depression affects alcohol use, or both are influenced by other factors such as stress, life events, or treatment.
… in deep….
How Alcohol Affects the Brain and Behavior
Alcohol is one of the most widely consumed substances in the world, and it has a significant impact on the brain and behavior of those who drink it. Alcohol affects various brain regions and neurotransmitters, altering mood, cognition, memory, motor skills, and decision-making. In this article, we will explore how alcohol affects the brain and behavior in detail, and what are the potential consequences of chronic alcohol consumption.
The Effects of Alcohol on the Brain Regions
The brain is composed of different regions that perform specific functions, such as processing sensory information, regulating emotions, controlling movement, and forming memories. Alcohol can affect these regions in different ways, depending on the amount and frequency of consumption.
One of the first regions that alcohol affects is the cerebral cortex, which is responsible for higher cognitive functions such as reasoning, planning, problem-solving, and language. Alcohol can impair these functions by slowing down the communication between neurons and reducing the activity of the prefrontal cortex, which is involved in impulse control and decision-making. This can lead to impaired judgment, reduced inhibitions, and increased risk-taking behavior.
A third region that alcohol affects is the limbic system, which is involved in regulating emotions and memory. Alcohol can enhance the activity of the amygdala, which is responsible for fear and anxiety responses, and reduce the activity of the hippocampus, which is responsible for forming new memories. This can result in increased emotional reactions, such as aggression or euphoria, and impaired memory formation, such as blackouts or forgetting what happened while drinking.
The Effects of Alcohol on the Neurotransmitters
The brain communicates through chemical messengers called neurotransmitters, which bind to receptors on neurons and influence their activity. Alcohol can affect various neurotransmitters in different ways, depending on the dose and duration of consumption.
One of the main neurotransmitters that alcohol affects is gamma-aminobutyric acid (GABA), which is an inhibitory neurotransmitter that reduces neuronal activity. Alcohol can enhance the effects of GABA by binding to its receptors and increasing its availability. This can result in relaxation, sedation, and reduced anxiety.
Another neurotransmitter that alcohol affects is glutamate, which is an excitatory neurotransmitter that increases neuronal activity. Alcohol can inhibit the effects of glutamate by blocking its receptors and decreasing its availability. This can result in impaired cognition, memory, and learning.
A third neurotransmitter that alcohol affects is dopamine, which is a neurotransmitter that regulates reward and motivation. Alcohol can increase the release of dopamine in certain brain regions, such as the nucleus accumbens and the ventral tegmental area, which are part of the reward system. This can result in feelings of pleasure, euphoria, and reinforcement.
The Consequences of Chronic Alcohol Consumption
While moderate alcohol consumption may have some beneficial effects on health and well-being, chronic alcohol consumption can have detrimental effects on the brain and behavior. Chronic alcohol consumption can cause structural changes in the brain regions and neurotransmitters that are affected by alcohol, leading to tolerance, dependence, withdrawal symptoms, and addiction.
Tolerance occurs when the brain adapts to repeated exposure to alcohol by reducing its sensitivity to its effects. This means that more alcohol is needed to achieve the same level of intoxication as before.
Dependence occurs when the brain becomes reliant on alcohol to function normally and maintain its balance. This means that without alcohol, the brain experiences a state of imbalance and distress.
Withdrawal symptoms occur when alcohol consumption is abruptly stopped or reduced after a period of dependence. This means that the brain experiences a rebound effect of increased neuronal activity and decreased inhibition. Withdrawal symptoms can include anxiety, irritability, insomnia, tremors,seizures, and delirium tremens (DTs).
Addiction occurs when alcohol consumption becomes compulsive and uncontrollable despite negative consequences on health,
social, and occupational functioning. This means that alcohol becomes a priority over other aspects of life and interferes with one’s ability to quit or reduce drinking.
In conclusion, this study provides new insights into how changes in alcohol consumption reported on routine healthcare screenings are associated with changes in depression symptoms. The findings suggest that monitoring these changes may be useful for identifying and addressing both problems and that reducing alcohol consumption may improve mental health outcomes.
reference links:
https://onlinelibrary.wiley.com/doi/10.1111/acer.15075
Gilpin, N. W., & Koob, G. F. (2008). Neurobiology of alcohol dependence: focus on motivational mechanisms. Alcohol research & health, 31(3), 185–195.
Heilig, M., Egli, M., Crabbe, J. C., & Becker, H. C. (2010). Acute withdrawal, protracted abstinence and negative affect in alcoholism: are they linked?. Addiction biology, 15(2), 169–184.
Kalant, H. (2010). What neurobiology cannot tell us about addiction. Addiction, 105(5), 780–789.
Koob, G. F., & Volkow, N. D. (2010). Neurocircuitry of addiction. Neuropsychopharmacology, 35(1), 217–238.
Krishnan-Sarin, S., O’Malley, S., Krystal, J. H., Petrakis, I. L., Limoncelli, D., Nappi, R., … & Bidlack, J. M. (2013). A randomized trial of naltrexone and behavioral therapy for problem drinking men who have sex with men. Journal of addiction medicine, 7(6), 433–443.
Oscar-Berman, M., & Marinkovic, K. (2007). Alcohol: effects on neurobehavioral functions and the brain. Neuropsychology review, 17(3), 239–257.
Schuckit, M. A., Tipp, J. E., Smith, T. L., Wiesbeck, G. A., & Kalmijn, J. A. (2014). The relationship between the level of response to alcohol and the severity of alcoholism in a group of Swiss men and women with alcohol dependence. Alcoholism: Clinical and Experimental Research, 38(9), 2371–2378.
Sullivan, E. V., & Pfefferbaum, A. (2005). Neurocircuitry in alcoholism: a substrate of disruption and repair. Psychopharmacology, 180(4), 583–594.
Tsai, G., Coyle, J. T., Liu-Chen, L., Flood Jr, J., & Role Jr, L. W. (2014). Low dose naltrexone attenuates ethanol consumption in mice: role of dynorphin/kappa-opioid receptor system and NMDA receptor complex in the nucleus accumbens shell. Neuroscience letters, 566, 67–71.
Volkow, N. D., Koob, G. F., & McLellan, A. T. (2016). Neurobiologic advances from the brain disease model of addiction. New England Journal of Medicine,
374(4),
363–371.