Other twin studies are investigating the relative magnitude of various influences on alcohol consumption in youth. Identifying the genes that convey risk of alcoholism is a second major goal of genetic research; scans of the human genome reveal evidence of genes in certain chromosomal regions that influence alcoholism. Pioglitazone was found to reduce alcohol drinking, abolish reinstatement of alcohol seeking, reduce alcohol self-administration, and decrease the severity of physical withdrawal symptoms in rats (Stopponi et al., 2011). Taken together, these findings have built substantial evidence for neuroimmune modulation of acute and chronic alcohol consumption and offer unique unexplored targets for therapeutic intervention. Acamprosate, one of the three approved treatments for alcoholism, is proposed to exert at least part of its effect by altering glutamatergic function (De Witte et al., 2005), though the exact mechanism by which it interacts is unclear.
This approach is based on the concept of linkage, which posits that genes located close together on the chromosome are more likely to be inherited together from one parent than two genes further apart. This technique provides a means of locating and measuring the effects of a single quantitative trait locus (QTL) on a trait (i.e., phenotype). One model suggests that people who are characterized by high levels of sensation seeking or who expect that alcohol use will enhance positive mood will be more strongly motivated to drink for this effect (Cooper et al. 1995). Alcohol use to reduce stress or enhance positive mood are not mutually exclusive motivations to drink, however, and they can be observed in the same person. The most severe alcohol problems have been reported in people who are characterized by both high levels of negative affect and low levels of constraint.
THE LANCET STUDY ON ALCOHOL USE AND RISK
Pre-exposure of the animals to high alcohol concentrations by vapour inhalation leads to high levels of alcohol self-administration and can produce BACs of 150–250 mg per dl in rats and 175 mg per dl in mice203. In these animals, alcohol withdrawal produces physical and motivational symptoms of alcohol dependence201, 202. People addicted to alcohol may have a genetic predisposition, like there is some kind of alcoholism gene that determines whether a professional is at risk for alcohol addiction.
Developmental Issues
Many alcoholics suffer from medical complications of alcoholism, such as liver cirrhosis, pancreatitis, cardiomyopathy, or psychosis due to brain damage. The inconsistency with which medical complications occur in alcoholism has led to the hypothesis that susceptibility to these complications is influenced by genetic factors independent of those influencing susceptibility to alcoholism itself. World War II Era Veteran Twin Registry, assessing the co-occurrence of alcoholism, cirrhosis, and alcoholic psychosis (Reed et al. 1996).
Cortico-amygdalar pathways
After detox ends, clients begin a rehab program that teaches them how to cope without alcohol and maintain sobriety. Residential treatment programs provide an immersive healing environment, often necessary for severe AUD cases. These programs typically comprise a multidisciplinary team of health professionals and offer a structured regimen of counseling, medical care, and support services. A personalized treatment plan, may include medication, lifestyle changes, and behavioral therapies.
The Appeal of Relaxation and Stress Relief
- If your liver doesn’t metabolize alcohol efficiently, you might get a buildup of acetaldehyde in your body that makes you feel sick rather than buzzed.
- By focusing on cultivating meaningful relationships, engaging in fulfilling activities, practicing self-care, and developing healthy coping strategies, individuals can work towards a more balanced and sustainable sense of well-being.
- Replication of this study is also needed with members of other ethnic groups and infrequent drinkers.
- As the body develops tolerance, people need increasing amounts to achieve the same relief, potentially leading to dependence.
The pursuit of alcohol-induced happiness can sometimes lead to unintended consequences, including dependence, addiction, and long-term negative impacts on mental health. Although the three leading causes of attributable deaths in this age group were tuberculosis, road injuries, and self-harm, for populations aged 50 and older, cancers accounted for a large number of total alcohol-attributable deaths in 2016. The authors of this large study concluded that alcohol use is a leading risk factor for disease burden globally, accounting for almost 10% of deaths among populations aged 15 to 49. The study demonstrated that the safest level of drinking is none, conflicting with most health guidelines that report up to two drinks per day produces health benefits (GBD 2016 Alcohol Collaborators, 2018).
This article examines these population-level as well as individual influences through a social–ecological framework, which posits that human health and development occur across a spectrum—from the individual to the macro or societal level (Bronfenbrenner 1994). In the context of alcohol use, individuals are nested within their microsystem (their home, work, and school environments), which is nested itself within the larger community. Macrolevel factors, such as exposure to advertising, may influence family and peer what makes alcoholics drink research shows it’s more complex than supposed network attitudes and norms, which ultimately affect individual attitudes and behaviors (see figure).
Silencing the translation of the NK1R using a technique known as RNA interference was found to reduce alcohol drinking in mice, emphasizing the role that NK1R plays in alcoholism (Baek et al., 2010). In fact, an NK1R antagonist (L822429) decreased voluntary alcohol consumption, suppressed stress-induced reinstatement of alcohol seeking, and increased sensitivity to the sedative effects of alcohol in rats (Schank et al., 2011). Similar effects were also seen in detoxified alcoholic inpatients, as an NK1R antagonist suppressed spontaneous alcohol cravings, improved overall well-being, blunted cravings induced by a challenge procedure, and attenuated concomitant cortisol responses. The role of miRNAs in drug addiction139 and, more specifically, in AUD151, 152, 153 is starting to emerge. A pioneering study showed that exposure to alcohol upregulates the levels of miR-9 and, in doing so, downregulates the levels of large-conductance calcium- and voltage-gated potassium channel (BK channel; encoded by KCNMA1), which in turn contribute to alcohol tolerance154.
In addition, the International Agency for Research on Cancer group concluded that acetaldehyde—which is produced when the body breaks down (i.e., metabolizes) beverage alcohol (i.e., ethanol) but also is ingested as a component of alcoholic beverages— itself is carcinogenic. It likely plays an important role in the development of cancers of the digestive tract, especially those of the upper digestive tract (Lachenmeier et al. 2009; Seitz and Becker 2007). Twin studies, which explore the relationship between alcoholism and other traits, continue to contribute to the formulation of a more biologically valid definition of the disease and to the characterization of disease subtypes that may ultimately prove to have differing genetic bases. Further progress toward the precise identification of genes influencing predisposition to alcoholism will depend on the development of improved tools for the gene-discovery enterprise.
- If someone drinks alcohol primarily to reduce stress, then this individual is most likely to drink under times of stress; it is at these times that there is fit between the individual’s personal motives and life situation.
- Then, they were asked how many drinks they usually consumed per drinking occasion (Cahalan et al., 1969; Clark & Midanik, 1982).
- If you carry genes that make it hard for your body to break down alcohol, it decreases your risk (because when your body can’t break down ethanol efficiently, it makes you feel sick).
- Developmentally appropriate strategies are needed to delay initiation of alcohol use, because the family environment may be less influential compared with the influence of peers, social norms, and media among older adolescents and young adults.
Alcohol increases GABAergic neuro-transmission over a wide range of concentrations, with some studies showing that delta-containing receptors are more sensitive than other GABA(A) receptors (Wallner et al., 2003). These molecular and cellular adaptations are thought to be the mechanisms by which neurons adapt to chronic alcohol use. These changes can eventually lead to alcoholism, depending on several factors, such as genetic predisposition, sex and environmental factors such as stress, age of drinking onset, and access to alcohol (Fig. 6.6). Once a person becomes an alcoholic, drinking becomes increasingly compulsive and seems to escapes voluntary control. The heterogeneous nature of alcoholism reflects the complex and multifaceted nature of alcohol’s molecular effects on the CNS.
It is already clear that some vulnerability to developing alcohol-related problems is conveyed genetically, and animal research has indicated that inheritance can take many forms. Studies in mice have demonstrated that various individual genes or groups of genes can shape very distinct responses to alcohol, such as a preference for alcohol over water, sensitivity to alcohol’s intoxicating effects, and the tendency to develop tolerance to it. The alcohol research literature is overwhelmingly focused on risk factors, from the societal level down to the individual. Worldwide, 3.3 million deaths were attributed to alcohol misuse in 2012 (World Health Organization 2014). Excessive alcohol use is the third leading cause of death in the United States, accounting for 88,000 deaths per year (Centers for Disease Control and Prevention 2014).
Thus, it is plausible that an orchestrated balance between go and stop processes, mediated by the mesolimbic dopaminergic signalling cascades, prevents or promotes escalation to pathological alcohol-drinking behaviours. According to the World Health Organization, 10–16% of individuals who consume alcohol and are aged 15 years or older engage in repeated, excessive episodic drinking (WHO, 2014) and are considered to be ‘problem drinkers’ (Enoch et al., 2002). Many of these individuals have a mild to moderate form of alcohol use disorder (AUD) and thus are maladaptively preoccupied with alcohol craving, seeking and consumption, despite the negative consequences of these activities (American Psychiatric Publishing, 2013). A subset of problem drinkers has a severe form of AUD, which is characterized by a dependence on alcohol and is commonly referred to as ‘alcoholism’. It was hypothesized that there would be an interaction between reasons for drinking and environmental circumstances. More specifically, it was hypothesized that, for individuals who reported drinking alcohol to cope with stress, alcohol consumption would be higher if levels of stress were high rather than low.
Another interesting question is whether any of these epigenetic modifications are directly linked to alterations in synaptic transmission and synaptic plasticity. To model excessive drinking, animals undergo intermittent access to 20% alcohol in a two-bottle choice (as described above) and, subsequently, operant self-administration of alcohol, with rats pressing the lever to obtain a 20% solution of alcohol197. Operant responding and alcohol intake are high, and rats typically consume 0.4–1.0 g per kg per 0.5 h, which generates a BAC of 30–90 mg per dl (Ref. 197). In this paradigm, animals typically press a lever to receive a contingent oral reward of alcohol (the premise of this procedure is that drugs of abuse control behaviour by functioning as positive reinforcers196). To obtain lever pressing for a moderate amount of alcohol, the rats are pre-trained on a continuous access to one bottle of water and one bottle of alcohol (typically 10% alcohol in tap water) protocol or undergo a sucrose fading protocol197.
