Addiction Science

What Does Alcohol Do to Your Brain?

Susan Tapert — Thu, 02 Oct 2008 19:01:07 +0000

In the United States and most European nations, the majority of people have used alcohol by young adulthood (Substance Abuse and Mental Health Services Administration, 2007). This blog entry will review what is known about how much alcohol use may affect brain functioning long after the intoxication effects have warn off.

About 50% of people who meet diagnostic criteria for alcoholism show some problems in thinking or memory (Oscar Berman & Marinkovic, 2003). The ability to plan ahead, withhold responses, learn and hold information, and work with spatial information (such as following a map) are particularly affected (Fein, Torres, Price, & Di Sclafani, 2006; Sullivan, Deshmukh, De Rosa, Rosenbloom, & Pfefferbaum, 2005; Sullivan, Fama, Rosenbloom, & Pfefferbaum, 2002). Even 15-16 year-olds with heavy drinking histories have shown problems in the ability to recall information that was previously learned (Brown, Tapert, Granholm, & Delis, 2000). However, there is always the chicken and egg problem - what came first? It's possible that alcohol use doesn't actually cause these effects, but instead these problems may have been there before, and may in fact be a risk factor for developing alcohol abuse or dependence. What is important to keep in mind is that we have seen poorer performance over time among young people who continued a pattern of heavy alcohol use (Tapert, Granholm, Leedy, & Brown, 2002). Those who reported drinking so much at times that they experienced negative after-effects, or hangovers, were the most likely to go downhill over time, as compared to those who halted substance use (Tapert et al., 2002).

These findings are not just the results of individuals not trying hard enough on these tasks. The size and shape of brain structures are also abnormal in chronic heavy drinkers. The overall amount of gray matter (brain cells) and white matter (cabling between the cells) are reduced (Pfefferbaum et al., 1995), particularly in the frontal lobes, which are key parts of the brain for planning, withholding responses, making decisions, and regulating emotions. White matter is key for relaying information within the brain, and the coherence or quality of white matter tracts appears poorer in chronic heavy drinking adults (Pfefferbaum, Adalsteinsson, & Sullivan, 2006). In adolescent heavy drinkers, we have seen, on average, smaller sizes of the hippocampus (a key region for learning new information) and portions of the frontal lobes (Medina et al., 2008; Medina, Schweinsburg, Cohen-Zion, Nagel, & Tapert, 2007; Nagel, Schweinsburg, Phan, & Tapert, 2005). Further, our preliminary studies have suggested that white matter quality is poorer in adolescents consuming as little as 20 drinks per month than in non-drinkers.

Taken together, there are clear differences between chronic heavy drinkers and non-drinkers in how the brain works. It appears that the brain of chronic drinkers has to "work harder" to keep things in mind, such as remembering a phone number, an address where you need to go, or a shopping list. In comparison, although we see similar changes in the brains of adolescents with only 1-2 years of heavy drinking, it appears that the young brain can compensate for any subtle alcohol-related disturbances by working other brain regions a little harder (Tapert, Pulido, Paulus, Schuckit, & Burke, 2004). However, if heavy drinking continues, by young adulthood the brain may not be able to compensate as effectively, and performance may begin to decline (Tapert et al., 2001). On the other hand, the brains of adolescent heavy drinkers but not those of individuals who rarely drink spend much processing effort when they look at alcohol advertisements, relative to looking at non-alcohol beverage images (Tapert et al., 2003). Therefore, brains may become "sensitized" to processing alcohol related information once you get involved in drinking.

The bottom line is that research shows clearly that chronic use of heavy levels of alcohol is associated with adverse effects on the brain. The bad news is, if you want to reach your maximum potential with the brain you have, you should limit alcohol use to moderate levels (that is ≤1 drink for females and ≤2 drinks for males per occasion). The good news is that for people in recovery from alcohol problems, many difficulties with concentration and memory will improve substantially in the first month of recovery, and even throughout continued recovery as long as you stay away from alcohol.

References
Brown, S. A., Tapert, S. F., Granholm, E., & Delis, D. C. (2000). Neurocognitive functioning of adolescents: Effects of protracted alcohol use. Alcoholism: Clinical and Experimental Research, 24, 164-171.
Fein, G., Torres, J., Price, L. J., & Di Sclafani, V. (2006). Cognitive performance in long-term abstinent alcoholic individuals. Alcohol Clin Exp Res, 30(9), 1538-1544.
Medina, K., McQueeny, T., Nagel, B., Hanson, K., Schweinsburg, A., & SF, T. (2008). Prefrontal cortex volumes in adolescents with alcohol use disorders: Unique gender effects. Alcoholism: Clinical and Experimental Research, 32, 386-394.
Medina, K. L., Schweinsburg, A. D., Cohen-Zion, M., Nagel, B. J., & Tapert, S. F. (2007). Effects of alcohol and combined marijuana and alcohol use during adolescence on hippocampal volume and asymmetry. Neurotoxicology & Teratology, 29, 141-152.
Nagel, B. J., Schweinsburg, A. D., Phan, V., & Tapert, S. F. (2005). Reduced hippocampal volume among adolescents with alcohol use disorders without psychiatric comorbidity. Psychiatry Research, 139(3), 181-190.
Oscar Berman, M., & Marinkovic, K. (2003). Alcoholism and the brain: an overview. Alcohol Res Health, 27(2), 125-133.
Pfefferbaum, A., Adalsteinsson, E., & Sullivan, E. (2006). Supratentorial profile of white matter microstructural integrity in recovering alcoholic men and women. Biological Psychiatry, 59, 364-372.
Pfefferbaum, A., Sullivan, E., Mathalon, D., Shear, P., Rosenbloom, M., & Lim, K. (1995). Longitudinal changes in magnetic resonance imaging brain volumes in abstinent and relapsed alcoholics. Alcoholism: Clinical and Experimental Research, 19, 1177-1191.
Substance Abuse and Mental Health Services Administration. (2007). Results from the 2006 National Survey on Drug Use and Health: National Findings. Rockville, MD: Office of Applied Studies.
Sullivan, E. V., Deshmukh, A., De Rosa, E., Rosenbloom, M. J., & Pfefferbaum, A. (2005). Striatal and forebrain nuclei volumes: Contribution to motor function and working memory deficits in alcoholism. Biological Psychiatry, 57, 768-776.
Sullivan, E. V., Fama, R., Rosenbloom, M. J., & Pfefferbaum, A. (2002). A profile of neuropsychological deficits in alcoholic women. Neuropsychology, 16(1), 74-83.
Tapert, S. F., Brown, G. G., Kindermann, S., Cheung, E. H., Frank, L. R., & Brown, S. A. (2001). fMRI measurement of brain dysfunction in alcohol-dependent young women. Alcoholism: Clinical and Experimental Research, 25, 236-245.
Tapert, S. F., Cheung, E. H., Brown, G. G., Frank, L. R., Paulus, M. P., Schweinsburg, A. D., Meloy, M. J., & Brown, S. A. (2003). Neural response to alcohol stimuli in adolescents with alcohol use disorder. Arch Gen Psychiatry, 60, 727-735.
Tapert, S. F., Granholm, E., Leedy, N. G., & Brown, S. A. (2002). Substance use and withdrawal: Neuropsychological functioning over 8 years in youth. J Int Neuropsychol Soc, 8(7), 873-883.
Tapert, S. F., Pulido, C., Paulus, M. P., Schuckit, M. A., & Burke, C. (2004). Level of response to alcohol and brain response during visual working memory. J Stud Alcohol, 65(6), 692-700.

Are you at risk for addiction?

Martin Paulus — Fri, 05 Sep 2008 19:54:01 +0000

Sooner or later we all ask ourselves this question. Surprisingly, there are some but no definite answers. This blog entry will discuss some of what is known about risk factors for developing drug addiction.

First and foremost, do we have evidence that individuals are at risk for specific types of addictions, or is there a general tendency to develop addiction?

The answer is that epidemiological studies looking at comorbidities (i.e., the co-occurrence of different types of disorders) favor the idea that individuals have a general tendency to develop drug addictions(Kessler et al., 1997). In other words, people who are addicted to one type of drug often also admit to having used or had addiction to other types before or at the same time. Thus, it appears that our biology can wires us with a general tendency for developing addiction to substances of abuse. The overlap with other forms of addiction (e.g., gambling, binge eating, sex addiction) is present but not as large.

Second, what are the specific factors that increase your risk to develop addictions?

Family: Before examining specific effects of genes, extensive evidence shows that that addiction clusters in families, i.e. there is a higher chance of developing an addiction if one of your blood relatives also has a problem with addiction(Kendler et al., 1997). The closer the family member who has a problem with addiction, the higher the risk. Obviously, this points to both genetic and environmental influences.

Genes: Heritability, i.e. the degree to which genes determine the risk for developing addictions: most of the genetic and shared environmental risk factors for illicit substance use and substance abuse/dependence are nonspecific, i.e. the researchers could not find evidence for genetic factors that increase risk for individuals to abuse substance A and not also to abuse substances B, C, and D(Kendler et al., 2003).

Psychological factors: Two psychological characteristics have been reported repeatedly to be associated with higher risk for various types of addiction - impulsivity and sensation seeking. High levels of impulsivity, i.e. the inability to control premature or inappropriate action, are clearly related to higher levels of use of various drugs(Verdejo-Garcia et al., 2007). Higher levels of sensation seeking, i.e. the need for high levels of external stimulation combined with the urge to seek such stimulation, has also been related to increased risk for drug use(Kelly et al., 2006). In part, this may be due to these individuals experiencing greater subjective effects associated with drug use: feel the drug, like the drug, and experience a high. Finally, the way you look at risk, i.e. whether you focus on the potential benefits or the potential adverse consequences of a situation with uncertain outcome, is also associated with risk for addiction. Specifically, individuals who have a low risk perception, i.e. tend to not see the bad after-effects, are at increased risk for addiction(Ryb et al., 2006).

Psychiatric conditions: Of the many psychiatric disorders, two are noteworthy, one not so surprising, the other one, more so. First, individuals with attention deficit hyperactivity disorder in general are at higher risk for addictions(Biederman et al., 1998). This is probably not surprising because these individuals are also often highly impulsive. However, this increased risk is reduced if these individuals are properly treated - even if it is with prescription stimulants(Wilens et al., 2003). Second, people with anxiety problems irrespective of the type (whether it is panic, social anxiety or post-traumatic stress disorder) are at increased risk for also developing addictions(Sareen et al., 2006). This may be due to the fact that these individuals use substances to reduce their anxious experiences.

So what can you do? Look at yourself, your family background, your own behavior and your previous experience. Do you get hooked on something easily? Are you impulsive? Do you like to be in a highly stimulating environment? Are you anxious? These are simple questions that may raise or lower your concern about your own personal risk. There are many aspects, though, that are not covered here and that I hope to cover and clarify in future blogs, so stay tuned.

For more info:

Biederman J, Wilens TE, Mick E, Faraone SV,and Spencer T (1998): Does attention-deficit hyperactivity disorder impact the developmental course of drug and alcohol abuse and dependence? Biol.Psychiatry 44: 269-273

Kelly TH, Robbins G, Martin CA, Fillmore MT, Lane SD, Harrington NG,and Rush CR (2006): Individual differences in drug abuse vulnerability: d-amphetamine and sensation-seeking status. Psychopharmacology (Berl) 189: 17-25

Kendler KS, Davis CG,and Kessler RC (1997): The familial aggregation of common psychiatric and substance use disorders in the National Comorbidity Survey: a family history study. Br.J.Psychiatry 170: 541-548

Kendler KS, Jacobson KC, Prescott CA,and Neale MC (2003): Specificity of genetic and environmental risk factors for use and abuse/dependence of cannabis, cocaine, hallucinogens, sedatives, stimulants, and opiates in male twins. Am.J Psychiatry 160: 687-695

Kessler RC, Crum RM, Warner LA, Nelson CB, Schulenberg J,and Anthony JC (1997): Lifetime co-occurrence of DSM-III-R alcohol abuse and dependence with other psychiatric disorders in the National Comorbidity Survey. Arch.Gen.Psychiatry 54: 313-321

Ryb GE, Dischinger PC, Kufera JA,and Read KM (2006): Risk perception and impulsivity: association with risky behaviors and substance abuse disorders. Accid.Anal.Prev. 38: 567-573

Sareen J, Chartier M, Paulus MP,and Stein MB (2006): Illicit drug use and anxiety disorders: Findings from two community surveys. Psychiatry Res. 142: 11-17

Verdejo-Garcia A, Bechara A, Recknor EC,and Perez-Garcia M (2007): Negative emotion-driven impulsivity predicts substance dependence problems. Drug Alcohol Depend. 91: 213-219

Wilens TE, Faraone SV, Biederman J,and Gunawardene S (2003): Does stimulant therapy of attention-deficit/hyperactivity disorder beget later substance abuse? A meta-analytic review of the literature. Pediatrics 111: 179-185