Have you ever woken up in the morning (or afternoon) in a cloud of worry after having a few drinks the night before?
As this holiday season comes to an end — after weeks of Christmas festivities, holiday parties and New Year celebrations — many of you may be nursing some hangover anxiety, or “hangxiety,” after getting just a little too merry.
As a neuroscientist researching how food and drink affect brain function, let me explain how drinking alcohol can trigger hangxiety the next day.
From tequila to endorphins and dopamine
Alcoholic beverages — beer, wine or spirits — disrupt the delicate balance of chemicals in the brain, called neurotransmitters. Alcohol exerts a cocktail of effects on brain function that can be enjoyable at the time, but much less fun the next day.
The pleasurable effects of alcohol are due to the release of endorphins — natural opioid hormones in the brain.
Good feelings also come from alcohol increasing the release of the dopamine by activating the brain’s reward system — the mesolimbic pathway.
Dopamine release reinforces behaviours — making it more likely for us to do whatever caused the dopamine surge again.
So, we quickly learn that the shot of tequila or glass of wine made us feel good, making us want more.
But alcohol affects more than just the rewarding chemicals in the brain. Alcohol alters levels of neurotransmitters that control brain activity and function.
Brain imaging shows that alcohol decreases activity in the prefrontal cortex and temporal lobe — key centres for decision-making, self control and memory.
Feelings of anxiety, unease and stress
Alcohol increases activity of the brain’s main inhibitory chemical GABA (gamma-aminobutyric acid) by mimicking its effects at synapses — the connections between neurons.
GABA reduces a neuron’s activity, and alcohol exaggerates this effect. Increased GABA promotes feelings of relaxation and calmness, making us more sociable and less stressed.
After several more drinks, alcohol blocks the glutamate system. Glutamate is the main excitatory transmitter in the brain, and plays an important role in forming memories and emotions.
Balance between GABA and glutamate is vital for optimum brain functioning. Alcohol shifts this balance. Alcohol is called a central nervous system depressant because it both increases inhibitory GABA and decreases excitatory glutamate.
When your brain senses high levels of GABA and low levels of glutamate it quickly adapts to counteract this imbalance. Compensatory changes result in low levels of GABA and increased glutamate that cause feelings of anxiety, unease and stress, enduring into the next day.
Oh no … did I really do that?
After several alcoholic drinks, glutamate transmission slows down in the medial temporal lobe — the brain region where memories are formed.
Alcohol-induced amnesia, or “blackouts,” are caused by a rapid increase in blood alcohol levels, often due to binge drinking. A binge is defined as more than four or five drinks in two hours for women and men, respectively.
In the sober brain, memories are formed after information is transferred from short-term memory to long-term memory. This process is called memory consolidation. Memories for events can then be retrieved and remembered.
Alcohol interferes with the consolidation and retrieval of memories, leading to confusion and uncertainty the next day. These hazy memories of the night’s events (“Oh no … did I really do that?!”) can cause great anxiety.
Alcohol also dramatically disrupts sleep quality, reducing REM-phase sleep when dreams occur. REM sleep is critical for encoding long-term memories. So, a bad night’s sleep after drinking alcohol can cause memories to become fragmented.
Shy people do suffer more
Not everyone experiences hangxiety, but some may experience it more than others. A recent study found that the intensity of a hangxiety experience varies between people based on personality traits, while controlling for alcohol consumed and blood alcohol levels.
Hangxiety can involve a delightful combination of headache and worry.
Individuals with more reported shyness traits experienced increased levels of anxiety following alcohol consumption than people who had lower baseline levels of shyness.
Can you avoid hangxiety?
The only guaranteed way to avoid hangover anxiety is to not drink alcohol.
You can, however, reduce the adverse effects of alcohol by drinking less. By spacing out drinks with glasses of water, you can avoid the rapid increase in blood alcohol that impairs memory and stay hydrated to lessen the headache the next day.
Funding: Amy Reichelt receives funding from The Australian Research Council and a CFREF BrainsCAN Tier 1 Research Fellowship.
Alcoholism is a chronic relapsing brain disorder with high medical and social importance (1, 2). In accordance to WHO data from 2016, more than 2.3 billion people worldwide, which refers to more than one third of the population, are current drinkers of alcohol (3).
Epidemiological studies indicate the significance of the problem of alcohol dependence and abuse, as globally an estimated 237 million men and 46 million women have alcohol use disorders leading to about 3 millions yearly deaths worldwide (3).
The harmful effects of alcohol are one of the leading risk factors for mental diseases. Alcohol use disorders increase the risk for depression development by a factor of almost five (4). About 80% of patients diagnosed with alcohol dependence develop depression at some periods of their lives (5).
On the other hand, alcohol dependence develops in more than 15% of patients with major depressive disorder (5).
The time course of alcohol use disorder is aggravated by depression, as this interaction enhances the probability of alcohol relapse in patients with these comorbid disorders (6–9).
, even though the comorbidity between depression and alcohol consumption is of high importance, little is known about the potentially common mechanisms determining this dangerous interaction. Moreover, personalized treatment strategies for these comorbid disorders have not been developed yet.
Recent studies have observed that ceramide, one of the crucial sphingolipids in biological membranes, might be link between depression and alcohol use disorder. Clinical studies showed a significant increase in the level of lysosomal and secretory acid sphingomyelinase (ASM) in peripheral blood cells of patients with acute alcohol intoxication (10–13).
Similarly, a rise in the concentrations of total ceramide as well as the products of ceramide metabolism, sphingosine and sphinganine, was observed in the liver of alcohol-fed mice (14).
The levels of ceramide precursor sphingomyelin is found to be reduced in the blood serum of rats exposed to liquid alcohol-containing diet as well as in alcohol dependent patients (15).
A study by Roux et al (16) showed a significant elevation of ceramide, and especially Cer16:0, level in the brain of rodents exposed to long-term alcohol drinking. Altogether, these data indicate that a significant shift in ceramide pattern occurs in peripheral tissues during alcohol treatment (17, 18).
On another hand, ceramide was shown to be involved in the pathogenesis of depressive disorder. Clinical studies revealed an increase in ASM activity in the peripheral blood mononuclear cells of patients with major depressive disorder, which positively correlated with symptom severity (19).
Similarly, post-traumatic stress disorder is associated with elevated ASM activity and ceramide levels in the blood (20). Animal studies have also shown depression-like behavior as well as a reduction in neurogenesis typical for depression in mice with Asm overexpression (tgAsm) (21).
Interestingly, several antidepressants from various chemical groups serve as functional inhibitors of ASM (22–24) suggesting that this enzyme might be crucial for the antidepressant effects (25, 26).
In a recent study in mice, paradoxical antidepressant effects of alcohol were found to depend on Asm activity and the regulation of the sphingolipid rheostat in the brain (27, 28).
Here we asked how a complete reduction of Asm activity, which is the main mechanism of type A and B Niemann-Pick disease, affects the interaction of depression and alcohol in Asm deficient (Asm − /−) mice.
We investigated the behavioral and drinking phenotype of these animals as well as the effects of forced treatment with alcohol on the emotional state.