Did you know that 1 in every 12 adults are alcohol dependent and (or) suffer from alcohol abuse in the United States alone? These statistics put alcohol as the most commonly addictive substance. Shockingly, under-ages as young as 12 years take alcohol with the majority of them taking part in binge drinking and others suffering from alcoholism. Undoubtedly, 12 years is a very young age for one to take part in binge drinking leave alone becoming an alcoholic. Binge drinking is considered as among the major risk factors of alcoholism, although not all binge drinkers end up as alcoholics. Alcoholism, otherwise known as alcohol use disorder, is the condition whereby one is unable to manage his/her drinking habit. If left untreated, alcohol abuse can cause unadorned long-term effects. Most common health side effects include; liver disease, brain defects, increased risk of cancer, diabetes complication, bone loss, and vision damage among many others. Even though these alcohol-related complications are always fatal, it is amusing how numerous people ignore the facts and abuse alcohol anyway. That makes one wonder whether there is more to alcoholism than just as social behaviour, or whether there is something biological that promotes these urges. And if that is the case, are there ways to mitigate them? Maybe then, we might have a chance to bring sanity back into our society.
Seeing that alcoholism is a menace to a society, there is a need to control it or even perhaps do away with it. Several scientists have carried out studies over the years mostly taking a behavioural approach. Desires result in a constricted choice of behavior so that consuming the alcohol mobs out other ordinary actions. Therefore, the best approach to facing out alcohol abuse is to help a patient acquire a set of skills to manage their environment to avoid situations where they are most likely to relapse. Thanks to studies dating several decades, we finally understand the behavior and compulsion of alcoholism at a molecular level (Heilig, 2008).
A researcher by the name Charles O'Brien (1990) and later Stephanie O'Malley (1990) undertook studies showing that an opioid receptor blocker known as naltrexone could help alcohol-depended patients by blocking the opioid signalling chain. They reasoned that when a patient takes alcohol, opioid-like substances known as endorphins are produced by the brain giving a sensation of pleasure and positive reinforcement. The naltrexone blocks this chain and makes drinking less enjoyable. However, over the years there have been arguments concerning the effectiveness of naltrexone in managing alcoholism. A longitudinal controlled study that spanned for 15 years has shown that the magnitude of effectiveness is minimal making it less efficient. It was realized that naltrexone was dependent on broad behavioral criteria of the patient. It just did not work on everybody mainly due to genetics. Ten years ago, Mary-Jeanne Kreek found a genetic variation at the target for naltrexone known as an m-opioid receptor (OPRM 1). Haulers of the variant allele consistently experience more kick with alcohol. Studies on monkeys by the National Institute on Alcohol Abuse and Alcoholism(NIAAA) led by Christina Barr (2006) indicated high doses of alcohol rouse the rhesus OPRM1 allele variant carriers and that they would voluntarily take alcohol if the opportunity was presented. It was also indicated that the carriers of ORPM1 experienced pleasure-mediated reward from alcohol which very important to note.
Over the years, studies on animals have shown that repeated cycles of intoxication and withdrawal have long-term effects on the brain. Chapel Hill, Howard Becker, George Koob and George Breese conducted studies and their data were all consistent and showed that a brain pathology made by an account of dependence has three crucial features. First of all, a record of reliance demonstrated through rehashed cycles of unnecessary liquor admission and withdrawal prompts a perpetual cluster of over the top liquor consumption. Secondly, there is a similarly industrious increment in responses to dread and stress. Finally, while stress does not influence intentional liquor consumption in non-dependent subjects, it does as such powerfully in animals with a background marked by alcohol reliance.
Further studies were untaken to seek out molecular marks inside the neural circuitry of anxiety since anxiety and alarm were the fundamentals of the new alcoholism model. The corticotrophin-releasing hormone (CRH) was targeted, and the studies later showed that the CRH substitute on CRH1 receptors inside the arrangement mediated several social pressure reactions. CRH1 does not have an impact on non-dependent subjects with low liquor admission stages, but eliminates the extreme drinking that follows in the post-subordinate state. That proved to be a very promising target treatment for relief-driven alcoholism. During this investigation, an 11-amino acid peptide known as substance P (SP) was included since it was associated with pain and inflammation. Researchers established a minor molecule that jammed the major human SP receptor for pain communication known as the neurikinin 1 receptor (NKR1). During the trials, mouse subjects that were deficient in NK1R took inferior quantities of liquor and did not get a reward from alcohol. The trials were then conducted on humans where recently detoxified alcoholics were given NK1R inhibitors for a fortnight. The subjects had fewer desires and were evaluated by a blinded physician who used a standardized questionnaire in order to test for their general wellbeing, which was actually noted to have improved significantly. Using an MRI, the degree of oxygen used was monitored to visualize the activity of neurons in reaction to numerous stimuli. Placebo-treated addicts had inflated initiation of neural paths that route undesirable emotions when presented with nasty or scary images. The treatment almost eradicated these undesirable responses. The inhibitors also reinstated activity in the pleasure cores of the brain in reaction to constructive images.
It is my opinion that the new model of alcoholism looks promising. Tremendous improvement has been seen since the early 90's, and this is not the right time to stop. With reduced restrictions on studies and the ever-evolving technology, a permanent solution to alcoholism should be found within the next decade maybe sooner. The NK1R research is the most promising with no side effects, and it may even be used in depression studies since it induces pleasure receptors. These are still the early stages, and with the data already collected, the trials will go a long way to fight alcoholism.
Barr, C. S., Schwandt, M., Lindell, S. G., Chen, S. A., Goldman, D., Suomi, S. J., ... & Heilig, M. (2007). Association of a functional polymorphism in the m-opioid receptor gene with alcohol response and consumption in male rhesus macaques. Archives of General Psychiatry, 64(3), 369-376.
Heilig, M. (2008). Triggering Addiction. Retrieved from https://www.the-scientist.com/uncategorized/triggering-addiction-44592
O'Malley, S. S., Jaffe, A. J., Chang, G., Schottenfeld, R. S., Meyer, R. E., & Rounsaville, B. (1990). Naltrexone and coping skills therapy for alcohol dependence: a controlled study. Archives of general psychiatry, 49(11), 881-887.
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