Author: Alex Thompson

Neuroscience: The Brain in Addiction and Recovery National Institute on Alcohol Abuse and Alcoholism NIAAA

Alcohol lowers inhibitions and clouds judgment, which may lead you to engage in risky behaviors. Research has shown that alcohol can exacerbate symptoms and mood changes in people with mental health disorders like depression or bipolar disorder. People who drink regularly may notice that alcohol does not have the same effect on them as it used to. You build up a tolerance over time and do not feel as good as you once did with the same amount of alcohol. Even low levels of alcohol consumption can harm your health, and high levels have even worse effects.

Hippocampal volume shrinkage in alcoholism is attributed to loss of white matter and decreased axonal diameter (Harding et al. 1997). Glial cell loss (Korbo 1999) or reduced incorporation of newly formed neurons to the dentate gyrus (He et al. 2005; Nixon and Crews 2004), however, could also affect hippocampal volume in alcoholism. Similarly, studies in AUD patients shortly following detoxification have found low levels of Cho (Bendszus et al. 2001; Durazzo et al. 2004; Ende et al. 2005; Fein et al. 1994; Parks et al. 2002; Seitz et al. 1999), although Cho findings in AUD are less consistent (e.g., Hermann et al. 2012; Modi et al. 2011). Because these findings are prominent in white matter, it is thought that the effects of alcoholism are greater in white than in gray matter (De la Monte 1988; Harper et al. 2003). Increases in FA and decreases in diffusivity have been interpreted as evidence for white-matter recovery with abstinence.

Short-term effects

  1. For ACD prevalence, reports based on postmortem evaluation range from as low as 0.4 percent to as high as 42 percent of alcoholics (Riethdorf et al. 1991; Scholz et al. 1986; Stork 1967; Torvik and Torp 1986).
  2. During acute and protracted withdrawal, a profound negative emotional state evolves, termed hyperkatifeia (hyper-kuh-TEE-fee-uh).
  3. This is no more than seven drinks per week for females and no more than 14 per week for males.
  4. Species differences in brain structure and function—among myriad other differences between humans and other animals—can give inadequate information when animal data are applied to human disease.
  5. Also reviewed are neuroimaging findings in animal models of alcoholism and related neurological disorders.

Baseline studies (in the absence of alcohol i.e., EtOH exposure) also suggest that brains of alcohol-preferring rats are different relative to their wild-type counterparts, including reduced gray-matter volume in thalamus, ventral tegmental area, and insular and cingulate cortices (Gozzi et al. 2013). Estimates of HE are derived from estimates of alcoholic cirrhosis, which can range from 8 percent to 20 percent (Bellentani et al. 1997; Mann et al. 2003; Sorensen et al. 1984). Mild HE occurs in up to 80 percent of cirrhotic patients, and overt HE occurs in up to 45 percent of cirrhotic patients (Bajaj 2008; Poordad 2007). One study estimated the incidence of CPM at 0.5 percent among the general population (Newell and Kleinschmidt-DeMasters 1996).

The Cycle of Alcohol Addiction

The following section examines how brain structures and function respond when drinking stops. This article reports key findings in humans, from macrostructural findings using magnetic resonance imaging (MRI), microstructural findings using diffusion tensor imaging (DTI), and metabolic findings from MR spectroscopy (MRS). Studies of alcohol-related central nervous system disorders are used as a framework for findings in uncomplicated alcoholism. The article also examines studies of abstinence and relapse and current imaging studies of animal models of alcoholism and co-occurring brain disorders.

What Effects can Alcohol Have on My Mental Health?

In contrast with early MR studies suggesting that KS affects the mammillary bodies while sparing the hippocampi (Squire et al. 1990), more recent work demonstrates hippocampal volume deficits in KS (Sullivan and Marsh 2003). Other regions affected by KS are the thalamus, orbitofrontal cortex (Jernigan et al. 1991b), cerebellum, and pons (Zahr et al. 2009). Brain imaging technology has allowed researchers to conduct rigorous studies of the dynamic course of alcoholism through periods of drinking, sobriety, and relapse and to gain insights into the effects of chronic alcoholism on the human brain. Magnetic resonance imaging (MRI) studies have distinguished alcohol-related brain effects that are permanent from those that are reversible with abstinence.

This heterogeneity, and the complexity that it introduces, makes it difficult to thoroughly characterize the disorder. Animal models, in contrast to the indefinite natural course of alcohol use in humans, allow researchers to determine alcohol toxicity in a way that allows them to control for multiple genetic, environmental, and alcohol consumption factors. Animal models permit the study of underlying mechanisms, enabling researchers to better interpret findings from human studies. Current rodent models to study HE include models of acute and chronic liver failure (Butterworth et al. 2009; Diaz-Gomez et al. 2011). According to the International Society for Hepatic Encephalopathy, however, “At this time, there are no satisfactory animal models of Type C HE resulting from end-stage alcoholic liver disease or viral hepatitis, the most common etiologies encountered in patients” (Butterworth et al. 2009, p. 783).

The dopamine system and alcohol dependence

The tCr signal, generated by creatine and phosphocreatine, is influenced by the state of high-energy phosphate metabolism (Tedeschi et al. 1995). In spectroscopy studies, it often is used as a reference for other peaks based on the incorrect assumption that its concentration is relatively constant (cf. Zahr et al. 2008, 2009, 2014b). Central pontine myelinolysis (CPM) is visualized as a hypointense T1 (left, sagittal slice) or hyperintense T2 (middle, right axial slices are early and late echo images) symmetric triangle or “bat-wing” lesion in the pons. There’s also more of an effect on your brain and its development if you’re younger — one that can have a lasting impact.

Studies about the relationship of D1 receptors and affinity for alcohol have had inconsistent results. Ethanol is a liposoluble neurotropic substance which penetrates the blood-brain barrier and inhibits central nervous system (CNS) functions; it is directly toxic to the brain. The etiology and pathology of alcohol dependence is the outcome of a complex interplay of biological, psychological and socio-environmental factors. CNS neurotransmitters play an important role in the development of alcohol addiction. Adolescent animals exposed to intermittent EtOH and evaluated postmortem showed no effects on FA but reduced axial diffusivity (hippocampus, cortex, and cerebellum), reduced radial diffusivity (hippocampus and cortex), and reduced MD (cerebellum and corpus callosum) in several brain regions (Vetreno et al. 2016).

Prevalence estimates of alcoholism-related syndromes are difficult to ascertain. Postmortem evaluation indicates a prevalence of 2 percent of WE in the general population; however, as many as 12 to 18 percent of alcoholics can have postmortem evidence of WE (Harper et al. 1988; Riethdorf et al. 1991; Thomson et al. 2002). Based on observations that 80 to 85 percent of patients with WE can develop KS, the estimated prevalence of KS is 11 to 12 percent of the alcoholic population (Day et al. 2013; Victor et al. 1971). Wernicke-Korsakoff syndrome (WKS) is used to refer to the presence of both WE and KS because of the close relationship between the two disorders. Long-term, heavy drinking causes alterations in the neurons, such as reductions in their size.

One of the most consistent findings in alcohol-exposed rodents, ventricular enlargement, varies with timing and method of alcohol exposure. Even repeated binge exposures (i.e., 5 cycles of 4 days of intragastric binge EtOH exposure with 1 week abstinence in between), do not result in persistent effects on the brain detectable with MRI (Zahr et al. 2015). Although ventricular size increases with each binge EtOH exposure, there is rapid recovery during each week of abstinence (Zahr et al. 2015). Such studies suggest that EtOH alone, at least in the exposure protocols evaluated with MRI, does not result in the characteristics observed in human alcoholics.