Alcohol Related Violence

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Alcohol is one of many factors behind violent behaviour
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Alcohol is believed to be the source of criminal like behaviour, ranging from those that are considered to be petty to those on a much larger scale. Many people do not assume such a common thing as alcohol to be the reason behind why individuals commit crimes, but truth be told, it has an impact on one's brain in various ways. Crime trends even indicate that alcohol related aggression has been increasingly more prevalent over the past 50 years. Alcohol related behaviour is a result of a developed behaviour of consistent drinking. Its dependence is a complex neuropsychiatric disorder characterized by chronic drinking, abstinence, relapse and behavioural impairments. Long-term consumption of alcohol has been reported to have an effect on multiple different factors such as the function of neurotransmitter receptors, intracellular signal transduction systems and biochemical processes in the central nervous system.[2] Currently, it is known that differences in certain receptors and systems in the brain plays a factor in whether or not an individual is more predisposed to alcohol intake and tolerance. It is also known that alcohol impairs memory, affects the development of the adolescent brain, and play a role in aggressive behaviour in both humans and animals.[3] In addition it can further impair executive control, which in turn produces aggressive behaviour.[1]

1. Development of alcohol drinking

Alcohol drinking stems from as early as one's adolescence. It has been reported that excessive drinking, which is classified as 5 or more drinks per occasion, is present in 30% of high school seniors. An analysis done actually shows that individuals who do not drink alcohol on a frequent basis, defined as getting drunk at least once a year are twice as more likely to engage in criminal and domestic violence, including violence to one's intimate partner or loved one. There is convincing evidence in a large segment of the alcoholic population that hereditary factors contribute to a predisposition of excessive alcohol drinking. One experimental approach suggests rat models. Rat models have been used to demonstrate that alcohol drinking can be developed. Selectively bred line of rats that had an initial preference towards alcohol, or noted as P line of rats, voluntarily drank 5 to 8g per kg of body weight of ethanol and maintained a blood concentration of 50~200mg%. [3] In addition, the selectively bred rats will work to earn more ethanol even when food and water are plentiful and will self-administer alcohol intra-gastrically or directly to the VTA (ventral tegmental area). This causes them to develop a metabolic and functional tolerance towards EtOH. It is shown that after time, under regular experimental conditions, the P line of rats will actually develop and display signs of dependence.

2. Neurobiology

There are numerous differences in the neuroanatomy between individuals classified under the P line and the NP, or the non-preferred, line including differences in the neurotransmitter systems and the receptors themselves. The examples that will be focused include the following: DA system, D2 receptors, and 5HT1-A and 5HT2 receptors.

2.1 Mesolimbic DA system

Regarding the mesolimbic DA system and the D2 receptors, lower densities of D2 receptors were found in the nucleus accumbens and VTA in P line individuals than those of the NP line. The lower densities of D2 receptors indicate that there are fewer D2 autoreceptors per neuron in the VTA or even fewer DA neurons in general. The differences in the DA systems' functions were tested by specifically examining the effects of AMPH, or amphetamine, administration on motor activity and ASR response in both P and NP individuals. It is also suggested that the DA system mediating the effects of AMPH is functioning at a lower level in the P line rather than the NP line, thus the capacity of the DA system is much less in a P line individual than an NP individual. This indicates that individuals in the P line are neurobiologically are more impaired than those in the NP individuals thus resulting in abherrant behaviour. [1]

2.2 5HT-system

In the 5HT-system and in several CNS areas, lower contents and immunoreactive fibres were found. In addition, reduced contents of DA and tyrosine hydroxylase immunoreactive fibres projecting from the VTA have also been reported. High densities of 5-HT1A receptors were also found present in the cerebral cortex and hippocampus in individuals of the P line compared to those of the NP line. Compared to NP line individuals 20~40% higher densities of 5-HT1A binding sites were found in the cerebral cortical regions of P line individuals, and 10~20% higher densities of the same receptors were found in the posterior hippocampal regions of individuals of the P line. A reason for the higher densities of the postsynaptic 5-HT1A receptor is that it is a result of the receptor attempting to up-regulate and compensate for the reduced innervation of 5-HT in the neural system. [1]

3. Sensitivity, tolerance, and intake

There are known differences in the tolerance levels of individuals who drink a lot as opposed to individuals who do not drink a lot. Adolescents are less sensitive than adults when it comes to the acute effects of ethanol while adults are more sensitive in other aspects. Adolescents are more vulnerable to to impairments in the hippocampal LTP and changes in the NMDA receptor function than adults are. [4]

4. Vulnerability factors

Even after consumption only a small portion of the individuals actually displays aggressive behaviour which suggests that there must be another factor that triggers such behaviour. These factors are called vulnerability factors, which explain the factors that make one individual more susceptible of expressing a violent act over another individual. For example such factors include gender, personality, sensation seeking, difficult temperament, poor anger control, and even motives for drinking such as to copre or enhance an experience. Situational factors such as provocation, threat, and most importantly social pressure and environmental context can play a role with the other factors to produce and promote alcohol-related aggressive behaviour.[1]

5. Various effects in the brain

5.1 Neurotransmission

Experiments showed that acute alcohol intake stimulates serotonin and dopamine release in the ventral and dorsal striatum. It also induces the release of GABA A and B receptors by blocking glutamatergic neurotransmission thus having an inhibitory effect. However, some of the effects on neurotransmission actually resemble the effects of social stress. For example, alcohol increases the extracellular dopamine in the striatum and stimulates the release of frontal dopamine when applied in small doses. These effects resemble those of stress in which both striatal and frontocortical dopamine release are stimulated. Rodents, in particular, exhibit high levels of dopamine in the PFC, nucleus accumbens and ventral striatum and are associated with the initiation of aggressive attacks and threatening behaviour. Monkeys also display increased concentrations of striatal dopamine. And in cats, dopaminergic stimulation of D1 and D2 receptors in the hypothalamus elicit a defensive behaviour. In addition, animal studies suggest that alcohol itself and fear stress induce the release of dopamine in the amygdala and in humans, these associate to the reaction elicited by aversive visual stimuli. [1]

5.2 Memory mechanism

The gray matter in the temporal lobes do not reach maximum potential until the age of 16~17. Alcohol induces NMDA receptors to be over-expressed in P line individuals and unusually potent levels of ethanol inhibition disrupt neural plasticity and impair spatial memory performance as well. In addition to impairing motor coordination and decision making, alcohol disrupts the ability to form memories that are explicit in nature. For example, one might find it difficult to recall last night's events and the names and phone numbers of the people that individual may have met last night. When the doses of alcohol are small (blood concentration levels below 0.15%), the impairments are not as severe as to those produced by a large dose of alcohol where one will be unable to remember an element of an event or even the entire event that occurred while intoxicated. Evidence shows that alcohol selectively alters the activity of receptor complexes that bind GABA, glutamate, and serotonin, as well as other transmitters. The current view is that alcohol acts on the level of the lipid bilayer. [1]

5.3 Hippocampus

Alcohol impairs memory formation as mentioned previously and it does so by disrupting activity in the hippocampus by preventing the establishment of LTP or long term potentiation. It interferes with the activation of the NMDA receptor and thus preventing the influx of calcium ions and the changes that it induces. Damage to a small region of the hippocampal neurons, known as the CA1, dramatically impacts the ability to form new memories. Small doses of alcohol (~0.5g/kg) decreased the firing output of the CA1 cells and in larger doses, the CA1 were dramatically suppressed and in some cases, completely shut down. [1]

6. Long term consequences of drinking

Adolescent drinking has enduring consequences regarding one's mental and physical health later in life. There have been associations made between early onsets of alcohol usage with increased risk of drug-related problems. In addition, there are effects on the development of the brain as well as behavioural changes that are expressed. [6]

7. Treatments

One of the most common ways to diagnose chronic alcohol consumption and to control the violence and aggression produced by alcohol abuse is cognitive therapy. Other methods that have shown success in treating alcohol use among adolescents include: multisystemic therapy, functional family therapy, and multidimensional family therapy and more. Most of these therapies are psychologically based and are generally outlined by several guidelines. First the individual must be concerned with wanting to facilitate and maintain a healthy, non-abusive lifestyle. Secondly, the unique developmental issues and personal issues of the individual must be taken into account. Thirdly, efforts should be made to identify what can be changed to create positive behavioural change overall.[5]

1. Heinz, A.J., Beck, A., Meyer-Lindenberg, A, Sterzer, P., and Heinz A. (2011) “Cognitive and neurobiological mechanisms of alcohol-related aggression” Nature Reviews Neuroscience 12:400-413.
2. Zhu, Y., et al. (2013) “Differential Phosphorylation of GluN1-MAPKs in Rat Brain Reward Circuits following Long-Term Alcohol Exposure” PloS ONE 8(1):1-12
3. McBride, W.J., Bell, R.L., Rodd, Z.A., Strother, W.N., and Murphy, J.M. (2005) “Adolescent Alcohol Drinking and Its Long-Range Consequences: Studies with Animal Models” Recent Developments in Alcoholism 17:123-142
4. Spear, L.P., Varlinskaya E.I. (2005) “Adolescence: Alcohol Sensitivity, Tolerance, and Intake” Recent Developments in Alcoholism 17:143-159
5. Brown, S.A., Anderson, K.G., Ramo D.E., and Tomlinson K.L. (2005) “Treatment of Adolescent Alcohol-Related Problems: A Translational Perspective” Recent Developments in Alcoholism 17:327-348
6. White, A.M., and Swartzwelder H.S. (2005) “Age-Related Effects of Alcohol on Memory and Memory-Related Brain Function in Adolescents and Adults” Recent Developments in Alcoholism 17:161-176

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