The effect drugs and alcohol on memory and thinking
Ingested chemicals in the form of distilled liquors have a way of interfering cognitive functions if not used in the proper amount. Stimulants like coffee, tea, soda and tobacco are known common stimulants which cannot deliver the desired effect we expect when used in minute amounts. We drink coffee to stay awake, yet the less concentrated the coffee combination is; the lesser its chances of keeping us awake. Too little of the stimulant leaves one less capable of cognitive performance while too much makes one jittery and easily distracted (Harrison, 2002: 44). Mind altering chemicals has an immediate effect of impairing cognitive performance and prolonged use may necessitate people to become less adept and less interesting. Likewise the common problems brought about by prolonged cognitive impairment among humans have a resulting factor dependent to psychiatric illness, dementia and brain damage. With this in mind and in preservation of mental faculties, contact and ingestion of chemicals which exhibit a strong causative contribution should be avoided or decreased.
ALCOHOL and Cognitive Performance
In controlled substances like alcohol, cognition and thought process is affected as alcohol tries to depress the central nervous system. Alcohol impairs the working memory and with many years of use slowly destroys the brain tissue, stem and cortex while diminishing the learning capabilities of the brain (Hermann, 2006:154). Tissue loss however stops when alcohol intake is also stopped but tissue regeneration is not promoted nor restored despite medical intervention according to previous studies conducted. With heavy alcohol intoxication, one tends to experience cognitive impairment likely produced by the depressant effects of the diluted ethanol chemical. Likewise with alcohol and other depressants, memories involving semantic and procedural knowledge including past experiences as a combination are deemed temporarily lost (Harrison, 2002:45).
In a test study assessing for delayed memory results among male college social drinkers, the highest alcohol levels which produced differentiated effects of delayed memory functions is at .10mg % (Jung, 2001:322). With increasing doses of alcohol, verbal fluency which is controlled by the cerebrum and motor tasks which are controlled by the frontal lobe is disrupted (Jung, 2001:322). After three dose levels of alcohol, reaction time and pursuit motor tracking abilities are also altered. General intelligence remains however unaffected with slow and minimal ingestion including reaction time. However as the dose is again increased, marked levels of cognitive change is also observed. This procures an idea based on many studies which gave out inconsistencies on the effect of alcohol on cognitive thinking and the heavy disagreement lies in the amount of alcohol drinks that start to impair cognitive skills.
Results in the above study conducted by Jung also found that heavy drinkers and social drinkers varied heavily depending on their habitual use of alcoholic drinks and beverages (Jung, 2001:322). In a concept of accountability and responsibility under a form of treatment applied to heavy drinkers who wished to change and social drinkers who wished to stop, the cognitive process among heavy drinkers showed a strong desire to cease from alcoholism while exhibiting a necessary behavioral approach to change thereby emphasizing a positive element of relearning skills. This method and concept is now used psychologically to treat alcohol offenders in an awareness program that considers alcoholism as a social problem in a positive approach for community re-integration. In effect, alcoholism does not necessarily bring about heavy and long term cognitive impairment among users.
Drugs and Cognitive Performance
In a study, the common cannabis produces a short term memory loss as cognitive deficits are detected at least 7 days after heavy cannabis use (Harrison et al, 2002: 47). The absence of retaining the ill effects of cannabis however cannot hold true for cocaine and other related illegal drugs. Cognitive functions among heavy cocaine users under a cognitive behavioral therapy reported diminished thought processes such as planning, foresight and reaction time (Soares and Gershon, 2003: 352). Upon treatment of the cocaine user through cognitive behavioral therapy, a delay in stimulus translation is observed and can be equated with longer periods of re-adjustment of the neurological communication systems that results to an altered cognitive function. However among heavy amphetamine users, there has been an association with increased vigilance and motor functions among acute amphetamine use as it produces higher levels of alertness and hyper-fluency but a subsequent hypo-excitability is observed upon discontinued use (Kaufmann, 2001:215). Cocaine abusers have shown higher verbal fluency scores under cocaine influence but a subsequent abstinence produces a higher degree of impairment on short term verbal memory (Kaufman, 2001:215).Likewise, users who are not heavily intoxicated with cocaine stand to produce better cognitive performance.
Memory impairment is also observed with amphetamine use with respect to word storage and capabilities of memory retention for sentences and detailed events (Jung, 2001, 222). Although amphetamine use produces non-verbal intellectual capacities, visual memory and auditory senses, chronic use still has an undesirable effect of the cognitive thought process. Eventually the user tends to avoid anything that has to do with learning and memory use and tends to exhibit mood changes upon abstinence.
Pharmacological action
In understanding how alcohol as a depressant and other drugs can produce an immediate effect on cognitive function, the complicated relationship and the pharmacological effects points out to alcohol’s effects on subtypes of 5-HT, NMDA and GABA receptors of the brain (Blow, Willenbring, et al, 2004: 256). Ethanol as an alcohol by-product inhibits the function of GABA receptors which in turn diminishes neural activity upon the receptors translation in the brain. In a normal process, the neurons along with glutamate projections from the amygdala and hypothalamus activate the receptors including GABA. When activated, the receptors allow Ca2 and Na ions to travel and produce neuron excitement (Soares and Gershon, 2003:568). Alcohol interferes with this activity by blocking neurotransmission by inhibiting frontal lobe projections such as decision-making and thought processes (Soares and Gershon, 2003:568).
At the same time, cocaine and other drugs with the same component affects the levels of dopamine in the synapse controls the neurotransmitter of the nerve terminals (Souayah and Khella, 2004: 215). Cocaine which has an active capacity of binding to the dopamine re-uptake transporter works by blocking it in order to produce the desired feelings of euphoria (Souayah and Khella, 2004: 215).
Like cocaine, amphetamines raise the levels of dopamines by blocking the dopamine transporter in order to prolong the dopamine presence in the synaptic cleft (Souayah and Khella, 2004: 215). Feelings of euphoria in amphetamine use is reinforced with the use of alcohol, opiates and benzodiazepines to adapt to heighten heights of the drug as a result of accumulating dopamine in the synapse. In effect, the dopamine receptors are now being studied in order to target developed drugs to control substance abuse and addiction.
Current Treatment for Alcohol and Drug Abuse
Nootropic drugs work by enhancing the Central Nervous System from resisting cellular damage brought about the alcohol and drug abuse. Nootropic drugs works to improve learning and memory and increasing cortical and sub-cortical functions and transfer of information in the brain (Blow, Willenbring et. Al, 2004:242). As a cognition enhancing drug, protect neuronal cells and promote tissue regeneration. This stands to invalidate previous beliefs that tissue destruction in prolonged alcohol and drug use is irreversible. Likewise, nootropic drugs in order to exhibit its desirable qualities require cessation of drug and alcohol use. Unfortunately, the study in relation to alcohol and drug use has just been tested among animals and it is not entirely clear if a desired effect can be portrayed among humans. The efficacy of this drug has still to undergo a battery of tests in order to recognize its successful enhancement effects in the treatment and reversal of cognitive impairment among alcohol and drug users.
Reference
Jung, John. (2001). Psychology of Alcohol and Other Drugs: A Research Perspective. Florida: Sage Publications.
Kaufman, Marc J. (2001). Brain Imaging in Substance Abuse: Research, Clinical, and Forensic Applications. United States: Humana Press.
Blow, F., Willenbring, M., McCormick R. and Brockmann, L. (2004). Substance Abuse. United States: New York: Haworth Press.
Soares, Jair and Gershon, Samuel. (2003). Handbook of Medical Psychiatry. United States: Informa Health Care.
Harrison, G. et al (2002) Cognitive Measures in Long-term Cannabis Users. Journal of Clinical Pharmacology 42, p. 41S-47S.
Souayah, Nizar and Khella, Sami. (2004).Neurology: McGraw-Hill Specialty Board Review Series. New York: McGraw-Hill Professional.
