Neuroimaging techniques provide a window on the active brain and a glimpse at regions with structural damage. Alcohol directly stimulates release of the neurotransmitter serotonin, which is important in emotional expression, and of the endorphins, natural substances related to opioids, which may contribute to the “high” of intoxication and the craving to drink. Alcohol also leads to increases in the release of dopamine (DA), a neurotransmitter that plays a role in motivation and in the rewarding effects of alcohol (Weiss and Porrino 2002).
“If drinking allows you to engage in behavior you wouldn’t engage in otherwise, maybe you shouldn’t be doing it,” said Pagano. “And if you always use it to have a good time, you won’t learn how to be okay in social situations without it.” According to the CDC, binge drinking is defined as consuming four or more alcoholic drinks for women or five or more alcoholic drinks for men on the same occasion. The impaired judgment you have when drinking alcohol may cause you to think that you can still drive, regardless of your BAC. Drivers with a BAC of 0.08 or more are 11 times more likely to be killed in a single-vehicle crash than non-drinking drivers.
Effects of alcohol on the brain
Drinking to avoid feeling bad leads to higher and higher levels of consumption, which can cause greater damage to the brain and the rest of the body. Alcohol kills cells and damages cellular networks in the brain, for example, and it’s not entirely clear to what extent they can grow back. The good news is that within a year of stopping drinking, most cognitive damage can be reversed or improved.
- Some of the previously mentioned factors that are thought to influence how alcoholism affects the brain and behavior have been developed into specific models or hypotheses to explain the variability in alcoholism-related brain deficits.
- A blood alcohol level of 0.08, the legal limit for drinking, takes around five and a half hours to leave your system.
- Doctors have not yet established a safe level of alcohol consumption during pregnancy, so the best strategy for preventing fetal alcohol syndrome is to abstain altogether from alcohol at this time.
- Furthermore, genetic analysis in humans indicated that GSK3β is an alcohol dependence risk factor, suggesting a central role of GSK3β in AUD [58].
- Importantly, the neurobiological basis of AUD appears in many cases to manifest in a sex-specific manner.
Furthermore, brain changes can be correlated with neuropsychological and behavioral measures taken at the same time. Brain imaging can aid in identifying factors unique to the individual which affect that person’s susceptibility to the effects of heavy drinking and risk for developing dependence, as well as factors that contribute to treatment efficacy. Alcohol use disorder (AUD) affects about 10–15% of the global population, causing significant medical, social, and economic burdensi. While most drinkers consume alcohol for years without escalating to excessive use, a subset of people develop harmful drinking patterns [1]. Unfortunately, efficacious treatment options are limited [2], due in part to the complex and multi-faceted ways by which intake of alcohol affects the nervous system. Both acute and chronic alcohol exposure produce molecular and cellular neuroadaptations influencing the activity of discrete brain regions and cell types [3–5].
Drinking and Driving
Another example is the transcriptional regulator, LIM Domain Only 4 (Lmo4), which was shown to drive vast changes in gene expression in the basolateral amygdala (BLA) of mice in response to repeated exposure to alcohol and to the regulation of alcohol intake [30]. In addition to contributing to the mechanisms that drive excessive drinking (GO signaling), transcription factors are likely to contribute to the gating of alcohol intake (STOP signaling). For example, the activity-dependent neuroprotective protein (Adnp) is a transcription factor that protects against excessive alcohol intake and relapse in female rodents [31]. The frontal lobes are connected with all other lobes of the brain (i.e., the parietal, temporal, and occipital lobes on both halves of the brain; see figure 1), and they receive and send fibers to numerous subcortical structures.
Another serine/threonine kinase that participates in neuroadaptations underlying AUD is GSK3β [58]. Specifically, Gsk3β in the mPFC participates in mechanisms underlying motivation to consume alcohol and alcohol withdrawal-induced anxiety [58]. Furthermore, genetic analysis in humans indicated that GSK3β is an alcohol dependence risk factor, suggesting a central role of GSK3β in AUD [58].
Health Topics: Alcohol and the Brain
Surprisingly however, Gsk3β in the NAc is inhibited by alcohol in rats [40], emphasizing the region-specificity of alcohol’s action. Like Fyn, the kinase mTORC2 is specifically activated by alcohol in the DMS of mice [59]. Alcohol-dependent activation of mTORC2 in the DMS promotes F-actin assembly, the formation for mature spines and alcohol intake [59].
The brain’s hippocampus region—which helps create new memories—is also affected by alcohol, which contributes to blackouts and short-term memory lapses while drinking. According to a 2020 review in the journal Alcohol Research, men and women experience alcohol-induced 5 expert tips to quit benzos for good fhe health blackouts at equal rates, even though women tend to drink less often and less heavily than men. These include your age, gender, overall health, body weight, how much you drink, how long you have been drinking and how often you normally drink.
Alcohol abuse can increase your risk for some cancers as well as severe, and potentially permanent, brain damage. It can lead to Wernicke-Korsakoff syndrome (WKS), which is marked by amnesia, extreme confusion and eyesight issues. During alcohol withdrawal, glutamate receptors that have adapted to the long-term presence of alcohol may become overactive, and this overactivity has been repeatedly linked to neuronal death, which is manifested by conditions such as stroke and seizures. Deficiencies of thiamine caused by malnutrition may contribute to this potentially destructive overactivity (Crews 2000). According to a 2021 study in Scientific Reports, heavy drinking could lead to loss of brain volume. The researchers found that people with alcohol use disorder (AUD) had less brain matter than people without AUD.
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
The bed nucleus of the stria terminalis (BNST) also exhibits plasticity in endocannabinoids and CRF- expressing neurons due to chronic alcohol use, and these alterations modulate drinking, withdrawal-induced negative affect, and stress-induced alcohol seeking in mice [85,86]. Furthermore, the CeA and BNST regions are anatomically connected, and inhibition of CRF neurons projecting from the CeA to the BNST decreases escalation of alcohol intake and somatic withdrawal symptoms in rats [87]. Several recent studies have built on classic literature to further detail the mechanisms by which presynaptic dopamine signaling and postsynaptic activity of medium spiny neurons (MSNs) orchestrate motivated behavior and its dysregulation by chronic alcohol drinking [71,72]. In addition, alcohol also engages feeding circuits in the hypothalamus which in turn indirectly modulates dopamine neuron activity [74]. Studies in animal models indicate that following long-term use of alcohol, striatal circuits and receptors undergo a range of adaptations [75,76].
However, it is not known whether this comparison between men and women holds among older populations (Oscar-Berman 2000). An alternate version suggests that older patients (age 50 and older) are especially susceptible to the cumulative effects of alcoholism, and aging is accelerated only later in life. The preponderance of scientific evidence suggests that although alcoholism-related brain changes may mimic some of the changes alcohol use disorder and timeline of alcohol withdrawal symptoms seen in older people, alcoholism does not cause premature aging. Rather, the effects of alcoholism are disproportionately expressed in older alcoholics (Oscar-Berman 2000). “They become much more likely to seek alcohol and to rely on it to cope with negative feelings,” said Ray. “Often when people start drinking, they drink to feel good—but as they drink more chronically, they have to drink to avoid feeling bad.”
“For starters, alcohol slows down the neurotransmitter GABA, and that’s what drives the sluggish movement, slurred speech, and slower reaction time in someone who’s intoxicated,” said Pagano. At the same time, Pagano added, alcohol speeds up a neurotransmitter called glutamate, which is responsible for regulating dopamine in the brain’s reward center. Blackouts are gaps in a person’s memory of events that occurred while they were intoxicated. These gaps happen when a person drinks enough alcohol that it temporarily blocks the transfer of memories from short-term to long-term storage—known as memory consolidation—in a brain area called the hippocampus. A 2018 study that followed 9,087 participants for 23 years found that people who did not drink alcohol in midlife were more likely to develop dementia.
Also, studies examining brain functioning in people with and without a positive family history of alcoholism have shown that there are clear differences between the groups on measures of brain electrical activity (Porjesz and Begleiter 1998). Prenatal alcohol exposure can cause brain damage, leading to a range of developmental, cognitive, and behavioral problems, which can appear at any time during childhood. Alcohol can disrupt fetal development at any stage during a pregnancy—including at the earliest stages and before a woman knows she is pregnant. The effects of alcohol on the brain vary depending on the dose and on individual factors, such as overall health. In general, the more alcohol a person drinks, the more likely it becomes that alcohol will damage the brain — both in the short and long term. As safe alcohol consumption varies from person to person, and different sources recommend various intakes, it is important to take an individualized approach.
While the specifics vary between males and females and across brain regions, these adaptations are generally thought to be critical determinants in dysregulated drinking behaviors. Projections from mPFC to the apixaban eliquis striatum have been implicated in mediating specific aspects of drinking behaviors [101–103]. These projections have been targeted to exert bidirectional, long-lasting control of alcohol drinking [103].
Recently, a genome-wide transcriptional assessment of human striatum found that G protein coupled receptors, the primary targets of many neurotransmitters and neuromodulators, were the top canonical pathway affected in striatum of AUD patients [70]. Reverse translation of these findings into a rodent model demonstrated putative therapeutic potential for a positive allosteric modulator of the muscarinic M4 receptor which, when delivered systemically in rats, reduced a wide range of alcohol self-administration behaviors [70]. Over time, excessive drinking can lead to mental health problems, such as depression and anxiety.
Adolescent brains are more vulnerable to the negative effects of alcohol than adult brains. Misuse of alcohol during adolescence can alter brain development, potentially resulting in long-lasting changes in brain structure and function. Although alcohol can cause significant brain damage, an emerging body of research suggests that modest alcohol consumption may be beneficial for the brain. Severe head injuries may even be fatal because they affect the brain’s ability to control essential functions, such as breathing and blood pressure.
