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

adminhakan 18 Aralık 2023 0 Comments

Still on the neuroscience research horizon are acknowledgment of the heterogeneity of expression of alcoholism’s untoward effects, delineation of substrates of neural change with addiction and further change with alternating periods of drinking and sobriety, and viable approaches for curtailing drinking in alcohol abusers. Over the past 40 years, rigorous examination of brain function, structure, and attending factors through multidisciplinary research has helped identify the substrates of alcohol-related damage in the brain. One main area of this research has focused on the neuropsychological sequelae of alcoholism, which has resulted in the description of a pattern of sparing and impairment that provided an essential understanding of the functional deficits as well as of spared capabilities that could be useful in recovery. These studies have elucidated the component processes of memory, problem solving, and cognitive control, as well as visuospatial, and motor processes and their interactions with cognitive control processes.

Techniques for Studying Alcohol-Related Brain Damage

Family history of alcoholism has been found to be important because it can influence such things as tolerance for alcohol and the amount of consumption needed to feel alcohol’s effects. 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 benzodiazepine withdrawal groups on measures of brain electrical activity (Porjesz and Begleiter 1998). Multiple classes of neuropeptide releasing neurons and neuropeptide receptors have been implicated as critical mediators of drinking behaviors, such as neurotensin [77], neuropeptide Y [78], oxytocin [79], opioid peptides [80,81] and corticotrophin-releasing factor (CRF).

Q: Is alcohol good for heart health?

The impact of alcohol can be observed early on, moderate to heavy drinking during adolescence leads to observable differences to non-drinkers, but this is further confounded by risk factors to unhealthy drinking patterns and alcohol dependence. However, though MRI research will be important in advancing our understanding of the impact of alcohol on the brain we cannot infer harm solely from alterations to brain structure. Alcohol-related functional differences in the brain are not exclusively observed in dependent individuals. When comparing the neural response of light (consuming ~0.4 drinks per day) and heavy (consuming ~5 drinks per day) drinkers to alcohol cues, light drinkers have been found to have a higher BOLD signal in VS, while heavy drinkers show an increased BOLD signal in DS [102].

Want to protect your brain? Here’s what you need to know about alcohol consumption.

  1. Furthermore, genetic analysis in humans indicated that GSK3β is an alcohol dependence risk factor, suggesting a central role of GSK3β in AUD [58].
  2. Just beneath it are the nerve fibers, called the white matter, that connect different cortical regions and link cortical cells with other structures deep inside the brain (subcortical regions).
  3. When pulses are emitted at a particular frequency, the protons briefly switch their alignment and “relax” back into their original state at slightly different times in different types of tissue.
  4. Ultimately, structural abnormalities impose a fundamental change in the choice of cognitive operations possible for the alcoholic (see figure 5).

A major theme of recent alcohol research has been to leverage animal models and circuit-analysis approaches to link neural circuit activity with specific aspects of AUD [95]. For example, in mice, chronic alcohol exposure decreased the excitability of OFC outputs to the DMS [96], and alcohol-induced synaptic plasticity in the OFC has been linked to excessive alcohol use in both mice and monkeys models [97,98]. In addition, using a combination of activity dependent genetic tools and chemogenetic manipulations, a small ensemble of mPFC neurons was shown to serve as a memory to cue induced relapse to alcohol use [99]. Interestingly, like the molecular mechanisms that gate the development of AUD [3], STOP mechanisms also occur on the level of circuitries [100].

Remaining DTI studies of MBD were case studies (e.g., Tuntiyatorn and Laothamatas 2008) showing low ADC along the entire corpus callosum (Bano et al. 2009; Wenz et al. 2014), with FA values diminishing progressively from front to back (Pacheco et al. 2014; Sair et al. 2006). Total infratentorial volume (including pons, cerebellar hemispheres, vermis, fissures, cisterns, and fourth ventricle) is significantly smaller in uncomplicated alcoholics than control subjects. The volume of the pons (Chanraud et al. 2009b; Pfefferbaum et al. 2002b; Sullivan 2003) and cerebellum (i.e., hemispheres) (Boutte et al. 2012; Chanraud et al. 2007, 2009a; De Bellis et al. 2005; Sullivan et al. 2000a,c) is smaller in uncomplicated alcoholics than in normal controls. Alcoholism-related volume deficits are also prevalent in gray and white matter (Shear et al. 1996; Sullivan et al. 2003) of the cerebellar vermis (Antunez et al. 1998; Piguet et al. 2006; Sullivan et al. 2006b, 2010), predominately in anterior superior but not posterior inferior regions (Sullivan et al. 2000a) (see figure 6).

These changes can increase vulnerability to addiction, perpetuating a cycle of trauma and substance use. Research also has found compromised NAA/tCr levels in patients with cerebellar degeneration (Tedeschi et al. 1996; Terakawa et al. 1999). Two MRS case studies of MBD showed reduced NAA/tCr and elevated Cho/tCr in corpus callosum splenium (Gambini et al. 2003; Tuntiyatorn and Laothamatas 2008), findings consistent with demyelination (elevated Cho) and axonal injury (reduced NAA). Although there are no known studies using structural MRI in animal models of ACD, ARD, or MBD, the following section examines animal studies in uncomplicated alcoholism. 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. Schematic drawing of the human brain, showing regions vulnerable to alcoholism-related abnormalities.

Inability to ethically enforce control over drinking and other factors in human alcoholism limits these studies to naturalistic designs. By contrast, animal studies afford control over factors contributing to change for the better or the worse with continued or discontinued alcohol exposure. Animal models of alcoholism may also advance our understanding of the brain volume changes documented in the course of human alcoholism (see figures 7 and ​and88). Increases in FA and decreases in diffusivity have been interpreted as evidence for white-matter recovery with abstinence.

A blood alcohol level of 0.08, the legal limit for drinking, takes around five and a half hours to leave your system. In addition to dementia, long-term alcohol use can lead to other memory disorders like Korsakoff syndrome or Wernicke’s encephalopathy. Building on the new study, Zhang has recommended to healthcare institutions and professional societies that they implement website feedback mechanisms and carry out regular content audits to guard against potentially harmful language. In the 2009 study, Kelly and his colleagues described patients to more than alcohol and the brain 600 clinicians, alternating between “substance abuser” and “having a substance use disorder.” Those in the latter category were viewed more sympathetically and as more worthy of treatment. Chronic use of alcohol and drugs can induce neuroplasticity, the brain’s ability to reorganize itself by forming new neural connections. “Substance use can mimic or inhibit the action of neurotransmitters by disrupting the brain’s normal communication pathways,” Owraghi says. This disruption can cause a cascade of effects, altering mood, behavior, and cognitive function.

In summary, MRI studies have offered invaluable insight into the effects of alcohol and have typically found a loss of volume and reduced myelination throughout the brain. The findings described here fit the notion that alcohol how to tell if someone is on drugs affects healthy brain aging and this effect becomes more pronounced with higher levels of consumption. It also suggests that there may be a greater vulnerability to the effects of alcohol on brain health with old age.

Moderate alcohol consumption is the best strategy for reducing the risk of alcohol-related brain damage. People who binge drink, drink to the point of poor judgment, or deliberately become drunk many times each month have a much higher risk of alcohol-related brain damage. 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.

The reasons for such recommendations are many, but, by and large, they tend to stem from a study someone read about or saw reported in the news. The toll that frequent alcohol use can have on your body can be severe but in some cases, the damage can be reversible. Decide if alcohol is age-appropriate If you decide some alcohol is ok, make sure it’s within the CMOs’ guidelines and stick to the plan. His team is collaborating with Mass General’s Research Patient Data Registry to obtain de-identified patient records, which they plan to review for instances of stigmatizing language. He hopes the process will help researchers quantify the prevalence of such language in clinical notes and identify patterns that can inform interventions. Zhang also said healthcare institutions should look to leverage technology to support adoption of appropriate standards.

An induction in ROS production was observed following alcohol exposure, which peaked after three and six hours of exposure. ROS production was significantly higher in differentiated cells as compared to undifferentiated cells. The reduction in cell viability was more pronounced in undifferentiated cells as compared to differentiated cells. At the lowest tested ethanol concentration of 10 mM, alcohol exposure led to a 6-11% induction in metabolic activity in differentiated cells and 1-10% induction in undifferentiated cells. Alcoholics with Korsakoff’s syndrome have shown a significant decrease in Purkinje cell density in the cerebellar vermis and molecular layer volume (Baker et al. 1999).

For example, naltrexone, a µ-opioid receptor antagonist, can attenuate the increased BOLD response to alcohol-related cues in the putamen and reduce risk of relapse [101]. The use of alcohol and drugs can dramatically alter brain structure and functioning, with far-reaching effects on behavior and cognition. Mielad Owraghi, LMFT lead clinical therapist, explains how these substances impact the brain, leading to profound changes in behavior and mental health. Perhaps the most consistent evidence of greater RH dysfunction has come from studies utilizing electrophysiological measures, although this observation has to be tempered by the poor spatial resolution of ERPs. In one study, ERP abnormalities in alcoholics were particularly evident in the right frontal area (Porjesz and Begleiter 1982).

Alcohol-induced disinhibition is reflected in premature motor preparation based on incomplete stimulus evaluation as measured by event-related potentials (ERPs; Marinkovic et al. 2000). Furthermore, these disinhibitory effects of alcohol are correlated with personality traits related to impulsivity and hyperactivity (Dougherty et al. 2000; Marinkovic et al. 2000). Recent models of vulnerability to alcoholism emphasize the importance of executive functions in mediating, as well as moderating the effects of alcohol (Finn 2002; Giancola 2004).

Conversely, microglial activation and neurodegeneration were clearly shown in rats exposed to intermittent alcohol treatment [91]. Indeed two-photon microscopy has been used to demonstrate the rapid response of microglia to even single acute alcohol exposure [92]. Microglial activation has also been investigated in response to heavy session intermittent drinking in rodents [93].