Blurred vision on the road Picture credit to Remiss63 (flickr)
Drink and drive increase the risk of automobile accidents dramatically; some may even cause fatal road accidents. While most statutory limits for driving are set at blood alcohol concentrations (BACs) of 0.08 g/dl and higher, human laboratory research has shown that BACs above 0.05 g/dl significantly disrupt performance on some motor tasks such as tracking, tapping, reaction time, and body sway. (Creaser et al. 2007) Performance impairment greatly increases when alcohol levels are above 0.05 g/dl. For instance, more cognitively demanding psychomotor tasks such as inhibiting responses in a go/no-go task, and responding correctly in paradigms employing unrelated choice-response tasks for left and right hands simultaneously are somehow impaired.
Bottles of alcohols Picture credit to INIMAGINE
Ethyl alcohol or ethanol, known commonly as alcohol, a common chemical component within alcoholic beverages whether they are wine, beer, or hard liquor. Alcohol is not digested like other foods. Instead of being converted and transported to cells and tissues, it skips the normal digestive process and goes directly to the blood stream. Approximately 20% of the alcohol is absorbed directly into the blood through the stomach walls while about 80% is absorbed into the bloodstream through the small intestine.
Schematic drawing of the human brain, showing regions vulnerable to
alcoholism-related abnormalities (Image courtesy of National Institute
on Alcohol Abuse and Alcoholism)
Based on the facts above, it can be said that alcoholic beverage is a central nervous system depressant. It acts at many sites, including the reticular formation, spinal cord, cerebellum and cerebral cortex, and on many neurotransmitter systems. Alcohol changes the physicochemical properties of cellular plasma membranes in the adult brain and has more dramatic effects in the developing. The central nervous system (CNS) includes the brain, the spinal cord, and the nerves originating from it. As central nervous system (CNS) is the main part of the nervous system that coordinates the activity of all parts of the bodies, consumption of alcohol can act on the CNS; thus, affecting emotional and sensory function, judgement, memory and learning ability. From here, it is obviously shown that brain is the organ that is most affected by alcohol.
Researchers studying the effects of alcohol use on the brain are aided by techniques that yield images of the brain’s structure and reveal the brain’s activity as it is happening. Tools that produce images of the brain’s structure, such as magnetic resonance imaging (MRI) and positron emission tomography (PET). Whereas, brain activity (rhythms in Hz) can be measured and observed by Electroencephalography (EEG), Event–Related Potentials (ERPs) and Event–related oscillations (EROs) and thus sensory and cognitive functions influenced by brain can be deduced, especially under the influence of alcohol consumption. (Porjesz et al. 2004)
Theta rhythm (3.5–7.5 Hz) is largest in the parietal region of the brain when a person is resting and in the frontal lobes when the person is actively engaged in mental activity. Research showed that the alcohol–dependent group had higher resting theta power at all scalp locations. High tonic theta power in the EEG may reflect a deficiency in the information processing capacity of the central nervous system (CNS). This may also be an electrophysiological indicator of the imbalance in the balance of excitatory and inhibitory neurons in the cortex. (Porjesz et al. 2004) This imbalance causes cortical circuits to be highly recurrent and intrinsically unstable. This leads to disruption the specificity of responses to sensory stimuli. Moreover, these deficits in performance, indexed by low theta power during mental effort, reflect frontal lobe dysfunction in alcoholics. These deficits involve inhibitory processes and are manifested as impairments in working memory and sustained attention.
The alpha rhythm (8.0–11.5 Hz) is an index of relaxation. It is mostly found in occipital region. Extensive research, dating back to the 1940s, confirms that unstable or poor alpha rhythm is found in alcoholics. It is reported that an alpha variant, namely low voltage alpha (LVA) is associated with a genetic variant that leads to low activity in catechol–o–methyltransferase (COMT). (Porjesz et al. 2004) COMT is an enzyme that metabolizes the neurotransmitters such as dopamine and norepinephrine. The effect of altered neurotransmitter levels on activity in the thalamus induces anxiety disorder among alcoholics.
Besides, beta rhythm (12–28 Hz) is obtained in alert subjects. Researchers have identified anterior frontal brain regions (the prefrontal cortex) of alcoholics as the most likely source of this fast beta activity. Increased beta power was superior to severity of illness, depression level, and childhood conduct problems in predicting relapse in abstinent alcoholics.
Neurotransmitters
Neurotransmitters are chemicals which help to send signals from neuron to a target cell. Different neurotransmitters have different effects in the brain. Some may even co-operate to affect the brain activities. The chemical compound acetylcholine (Ach) has the chemical formula C7H16NO2. It is a neurotransmitter in both the peripheral nervous system (PNS) and central nervous system (CNS) in humans. In PNS, it activates muscles. However, under the influence of alcohol, transmission of acetylcholine is retarded by reducing the binding of acetylcholine to acetylcholine receptors on skeletal muscle fibers. This in turn reduces the opening of ligand gated sodium channels in the cell membrane and only little sodium ions can stimulate muscle contraction. This results in staggering, difficulty in walking and uncontrollable movement when one is drunk.
Alcohol causes increased turnover of norepinephrine and dopamine. (Kinney 2006) Norepinephrine, also known as noradrenaline, has both roles as a hormone and a neurotransmitter. Whereas, dopamine, a catecholamine, from which norepinephrine is derived is an important neurotransmitter in brain and CNS involved with the co-ordination of behavior, emotion and movement. When people drink alcohol, they become lively and excited because alcohol raises dopamine levels which lead to excitement and stimulation. As a hormone, norepinephrine stimulates parts of brain by controlling the attention and responding actions. Together with epinephrine, it directly increases heart rate by increases blood pressure. This is why one’s heart beats much faster when consume a lot alcohol in a short period of time.
Serotonin or 5-Hydroxytryptamine (5-HT) is a monoamine neurotransmitter. Serotonin originates in neurons deep in the midline of the brainstem. Because these neurons profile diffusely throughout the brain, serotonin can affect various brain functions. Approximately 20% of the human body's total serotonin is synthesized in serotonergic neurons in the CNS where it has various functions, including the regulation of mood, appetite, sleep, muscle contraction, and some cognitive functions including memory and learning. Alcohol exposure can alter several aspects of serotonergic signal transmission in the brain. As such, alcohol modulates the serotonin levels in the synapses and modifies the activities of specific serotonin receptor proteins. (Lovinger 1999) Abnormal serotonin levels within synapses may contribute to the development of alcohol abuse, severe mood swing and depression.
γ-Aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the brain. It tends to reduce the activity of the signal-receiving neuron. In fact, alcohol produces some of sedation and intoxication effects by enhancing GABA’s inhibitory function. Along with serotonin, the activity of GABAergic neurons can be further enhanced in the hippocampal formation, a part of the brain that is important for memory formation and other cognitive functions. Consequently, alcohol’s effects on serotonin may alter the activity of GABAergic neurons in the hippocampal formation. (Milner et al. 1989) These changes may disrupt cognition and possible contribute to alcohol-induced memory loss and impaired judgment. Furthermore, alcohol’s effects on these GABA receptors also might influence GABAergic signal transmission in the brain. As a result, when some drink alcohol, they feel calm and lose their anxieties because alcohol makes the GABA receptors function more efficiently. The reason that people tend to fall asleep after drinking alcohol is also due to this effect on the GABA receptor.
Alcohol has a painkilling effect like morphine and produces a ‘high’ because it causes a release of beta-endorphins into the brain thus raising the endorphin levels. However, euphoric feeling associated with decreased anxiety and a general feeling of wellbeing can be produced only when low to moderate levels of alcohol is taken. This alters beta-endorphin in the hypothalamus release in the midbrain/Ventral Tegmental Area (VTA) region, producing the pleasant effects through the stimulation of natural opioid peptides in the VTA, which consequently activates dopamine in this critical pathway. (Nauert 2009) On the other hand, high doses of alcohol are known to induce sedative and hypnotic effects, and often increase rather than decrease anxiety. The video below shows the negative effects of alcohol in drunkard's behaviours which is caused by various altered functions of neurotransmitters either combined or alone:
Glutamate is responsible for the formation of new memories as well as for muscular coordination. Alcohol greatly inhibits the functioning of the glutamate receptor which leads to slurred speech, staggering, inability to recall and blackouts. Blackouts, or loss of memory for a period during drinking occur as alcohol cuts off the supply of oxygen to the brain. Lack of oxygen supply to the brain can kill tens of thousands of brain cells every time a person becomes intoxicated. However, glutamate induces muscle relaxation due to loss of coordination.
Hangover Picture credit to INIMAGINE
However, the effects of alcohol on the brain do not end when alcohol is completely metabolized and out of the system. Process followed by is neurotransmitter rebound. GABA system is struggling to overcome the effects of post-alcohol consumption and return to normal functioning. (Anderson 2008) When all the alcohol is finally out of the body, the GABA system overshoots the mark and leaves people feeling restless and wide awake. This is known as post-alcohol impairment (PAI) or in layman term, ‘hangover effect’. A related condition, positional alcohol nystagmus (PAN), refers to the rapid involuntary eye movements and unusual vestibular effects that can persist for several hours after drinking. PAN has been implicated in decreased performance long after Blood Alcohol Concentration (BAC) has returned to a near-zero level.
Chronic drinking can lead to dependence and addiction to alcohol and to additional neurological problems. Typical symptoms of withholding alcohol from someone who is addicted to it are shaking (tremors), sleep problems and nausea. More severe withdrawal symptoms include hallucinations and even seizures due to damage of the connection between nerve cells and irreversible brain damage. All the above can be resulted due to increased size of ventricles and overall reduction in brain size. Long-term chronic alcoholic’s cells become less permeable to alcohol too as they literally become thicker. Vitamin B1 deficiency can be resulted as the digestion system of alcoholics is unable to absorb thiamine. This syndrome is known as Wernicke's Encephalopathy. (Shand et al. 2003) It is characterized by impaired memory, confusion and lack of coordination. Other syndrome known as Korsakoff's Syndrome can be resulted as well due to lack of vitamin B1 which is result in amnesia, apathy and disorientation.
Scanning of fetus’ normal brain (left) and FAS brain using MRI (right)
(Image courtesy of Children’s Research Triangle, Chicago.)
The term ‘Fetal Alcohol Spectrum Disorders (FASD)’ refers to the range of disabilities that may result from prenatal alcohol exposure which have devastating consequences on developing brain and its long-term structural and neurobehavioural consequences indirectly. (Guerri et al. 2009) Numerous brain imaging, neurobehavioural and experimental studies have demonstrated the negative effects of prenatal alcohol exposure on the developing central nervous system (CNS), identifying specific brain regions affected, as well as the range of severity of effects and mechanisms involved.
Alcohol damages the developing brain in a variety of ways. Neuronal loss is one of the most significant alcohol-induced pathologic changes and underlies the microencephaly observed in many children with Fetal Alcohol Syndrome (FAS). Alcohol vulnerability among fetuses may be different due to genetic differences in neuroprotective pathways. One pathway that can protect neurons against alcohol-induced death is mediated by nitric oxide (NO) and nitric oxide-cyclic GMP-protein kinase G (NO-cGMP-PKG) pathway. Within neurons, NO is produced by the enzyme neuronal nitric oxide synthase (nNOS). (Karaçay et al. 2007) Genetically- nNOS deficient fetus is unable to synthesize NO within their neurons, and thus, cannot utilize the NO-cGMP-PKG pathway for neuroprotection. Alcohol exposure during development causes substantially greater microencephaly and neuronal losses in nNOS. Neuronal numbers were quantified in the hippocampal formation and cerebral cortex, two brain regions that are vulnerable to alcohol-induced neuronal death which leads to disruption of structures and functions of CNS.
By the way, the brain is not uniformly vulnerable to alcohol toxicity at all times across development. On the contrary, temporal windows of vulnerability appear to exist, during which time the developing brain is much more vulnerable to alcohol-induced injury, especially cerebellar cells. The parietal lobe, portions of the frontal lobe and specific areas of the cerebellum appear to be especially sensitive to alcohol insult. (Guerri et al. 2009) Specifically, individuals with FASD show reduced cerebellar volume and surface area as well as reduced volume and displacement of the anterior vermis of the cerebellum. As cerebellum is responsible for the execution of motor behaviors such as posture, balance and coordination, the structural abnormalities observed may help to explain motor deficits often seen in individuals with FASD. The cerebellum is also involved in other functions, such as attention regulation and classical conditioning. In accordance with this, deficits in classically conditioned eyeblink responses are noted in children with FAS and cerebellar vermis displacement is negatively correlated with verbal learning and memory in FASD. A volumetric reduction in the basal ganglia, specifically the caudate is disproportionately reduced; thus, this leads to deficits in executive functioning, attention and response inhibition.
Guerri et al. (2009) reported that subtle reduction in glucose metabolism in the thalamus and caudate in young adults with FAS by using PET (Positron Emission Tomography). Cerebral blood flow (CBF) in the left parietoocciptal region has decreased while CBF in the right frontal region has increased in FASD. There were also reduced serotonin levels in the medial frontal cortex and an increase in striatal dopamine transporter binding. According to Malisza and colleagues (2005) conducted an fMRI study using a spatial working memory paradigm to examine haemodynamic brain activation in exposed and non-exposed adults and children, individuals with FASD showed increased functional activity in the inferior and middle frontal cortices when compared with matched controls. In addition, controls showed increased frontal lobe activity with increasing task difficulty, while FASD participants did not. This video shown below summarizes the influences of alcohol on fetus (FAS) and demostrations of how degradation by alcohol happens:
As a result, FAS can be completely prohibited by not drinking any alcohol during pregnancy. In view of the damage caused by FAS, prevention efforts can be focused on educating women not to drink during pregnancy which everyone should be well aware of the potential dangers. Other than that, women who drink alcohol and who are sexually active may benefit from counselling and effective contraception to prevent pregnancy as well as public service announcements and alcohol beverage warning labels help to raise up awareness.
The immediate effects of alcohol consumption vary greatly according to the drinker and the amount that he/she drinks. Sales states that people generally drink for a variety of reasons including relaxation, sleep inducement, stress relief, to feel romantic, for pain relief, or to deliberately become intoxicated. Moderate drinking is not known to cause any long term health problem in most cases and there has even been some research to suggest that light to moderate drinking has a positive effect on overall health. (NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM 2003)
Moderation is the key to the good health. Although the deleterious effects of alcohol on the mind and body are well known, alcohol may have beneficial effects as well. There is epidemiological evidence that moderate, even daily, consumption of alcohol can reduce the risk of heart disease. In a small dose consumed, it can trigger pleasant feeling as well. Alcoholic beverages such as red wines in particular, contain tannins, flavonoids, and other phenolic compounds that play a critical role in modulating important functions, such as oxidation and coagulation to maintain one’s health.
References
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