NIH findings link aldosterone with alcohol use disorder

A new study led by scientists at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health, demonstrates that aldosterone, a hormone produced in the adrenal glands, may contribute to alcohol use disorder (AUD).

Aldosterone, a hormone produced in the adrenal glands, may contribute to alcohol use disorder (AUD). Image credit: NIAAA

Aldosterone helps regulate electrolyte and fluid balance by binding to mineralocorticoid receptors (MRs), which are located throughout the body.

In the brain, MRs are mainly located in the amygdala and the prefrontal cortex -- two key brain areas involved in the development and maintenance of AUD.

In AUD, amygdala dysfunction heightens activation of brain stress systems resulting in anxiety and other negative emotions, while disruption of the prefrontal cortex impairs executive control systems involved in the ability to make decisions and regulate one’s actions, emotions, and impulses.

The new report describes three separate studies, conducted with non-human primates, rats, and humans, that investigated the potential contribution of the aldosterone/MR pathway to AUD.

In a human study of about 40 individuals undergoing treatment for AUD, the researchers found that blood aldosterone concentrations were higher in individuals who continued drinking during the 12-week period, compared with those who were abstinent during the same time frame.

For those who drank, the researchers found that aldosterone concentrations correlated with the amount of alcohol consumed during the study – higher drinking levels were associated with higher aldosterone concentrations. The researchers also found that increasing blood aldosterone concentrations correlated with increasing levels of both alcohol craving and anxiety.

Taken together, the researchers conclude that the findings provide support across three different species for a relationship between alcohol misuse, AUD, and specific changes in the aldosterone/MR pathway marked by increased circulating aldosterone and decreased mineralocorticoid receptor gene expression in the amygdala. (National Institutes of Health)

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