Chronic Alcohol Addiction caused by Depression

Chronic Alcohol Addiction caused by Depression Dr. Ekasith Kumarnsit Deparment of Physiology,Faculty of Science Prince of Songkla University Depression is a symptom possibly found in mentally ill patients in which the patients are crestfallen, lack enthusiasm and motivation in working. Sometimes they feel like life is worthless. If this symptom becomes intense, it can contribute to committing suicide. For normal people, this symptom can take place but in a short period of time and with causes of depression. When the causes are solved or the persons become tolerant to the problems, the depression will lessen and fade away. Most of mentally ill patients are found that their depression is mainly subject to their abnormal pathology or nervous syste m. One crucial function of neurons is secretion of many of neurotransmitters embracing dopamine, acetylcholine, noradrenaline, serotonin as such. The nervous systems secrete neurotransmitters at the optimal amount to make human or animal bodies work effectively in terms of motion, though, intelligence and emotion. On the contrary, if the secretion is too low or high, it brings about abnormalities. As for the origin of depression, there are a large number of studies with coherent findings that the symptom has relations with disorders of the secretion of a neurotransmitter, called serotonin. For example, insufficiency of tryptophan, which is a precursor to be transformed to serotonin, can cause depression. Furthermore, the study of patients with a record of efforts to commit suicide also finds that those patients have serotonin below standard level. It can be assumed that the efforts to commit suicide possibly come from depression as one of the reasons. For treatment, to give a medicine in order to increase the secretion of serotonin or effects of serotonin can better the depression. An interesting observation is that depression and drug use are usually found in the same population groups or in the same individuals. A study of Mexican population living in California, U.S.A. shows that alcohol addiction is related with pathological conditions significantly. It simply means that people who have mental problems have high risk to become chronic alcohol users. However, the said study only highlights the findings of alcohol addiction in the group of mentally ill patients, but does not indicate in details whether or not alcohol addition is a cause of mental problems, or on the opposite, the mental problems cause alcohol addiction, or both symptoms present simultaneously possibly due to the same causes. The findings are relevant to the situation generally seen in Thailand. Though there is no official data collection, the similar findings are unceasingly discovered that a new mother take alcoholic herbal drinks after parturition in order to rehabilitate here health according to traditional medical patterns. Local herbs believed containing active properties of fitting uterus, fortifying blood or inducing lactation, are fermented in whisky in which whisky will dissolve the active ingredients from the herbs. When the new mother drinks it, she receives both herbal medicinal ingredients and alcohol at the same time. As a result, it is found that a certain number of females after parturition feel good with drinking alcohol unknowingly later on, even though they have never taken alcohol before. This may be explained that after parturition, some females have unbalanced secretion of hormones including neurotransmitters, probably causing depression. Therefore, when alcohol is taken right during the depression, it may account for alcohol addiction. Based on the review of findings from nervous system researches, it shows that depression and alcohol addiction are caused by the secretion of similar neurotransmitters, especially, abnormal secretion found in a part of the brain that controls emotions. This draws an assumption that in the mentioned part of the brain of humans or experimental animals having depression and addicted to drugs, there is abnormally low level of serotonin. This assumption may also account for alcohol addiction since alcohol intake will help increase the

serotonin level, though the serotonin level will increase until close to or equal to the level of normal people in a very short time only. After a while, serotonin will drop quickly and then depression shows as usual. Nevertheless, the heightening serotonin level by consuming alcohol, though in a short time, makes patients experience relaxing feeling. The patients feel good and addicted to it and have a driving force to take alcohol again in order to have that relaxing pleasure. However, the subsequent uses of alcohol do not give pleasure as high as the first use did. This induces both higher amount and higher frequency of alcohol intake in order to gain the satisfaction needed. Finally the patients become addicted to alcohol, cannot stop it and are in the condition of chronic alcohol addiction or alcoholism. In the condition of alcoholism, if the addicts quit drinking, the level of serotonin will be even lower, or minus the existing low level. Consequently, their mental condition would become greatly depressed to critical level. At this stage, it is hard for the addicts to stop using alcohol by themselves. They need to receive medical treatment. An experiment using medicine to increase work level of neurotransmitters by arousing the secretion of serotonin in mice finds that it can make the mice take alcohol less. This unveils that the stimulation of serotonin nervous system could help fulfill the feeling at the satisfying state, and the laboratory mice do not necessarily seek another pleasure from drinking alcohol. Therefore, the mice given the medicine to excite serotonin nervous system have less alcohol intake. This finding reiterates the relations between serotonin nervous system and level of alcohol intake apparently. For human beings, based on the theory that both symptoms of alcoholism and depression share the same pathology or the same cause the low level of serotonin level, another experiment using medicines to activate serotonin nervous system gains a satisfying result that the medicines can reduce the amount of alcohol intake; moreover, they can also ease depression. These findings are considered the foundation of theories used in treatment for alcoholism effectively later on. Nowadays, there is a contemporary ideology of health care applying East concepts or local wisdom, for example, use of herbal extract in replacement of synthetic chemical medicines with the belief that most extracts from plants could give positive results and less side effect than the synthetic medicines do. Likewise, for the effort to reduce the amount of alcohol intake, in1999 a research team of the University of North Carolina School of Medicine, U.S.A. conducted an experiment by extracting a herb called Hypericum perforatum in botanical name or St. John s Wort in a common name. The plant has yellow flowers blossoming during an important religious holiday in commemoration of the Saint after which the plant is named. The extract of this herb has active quality in anti depression by which it can increase a level of neurotransmitters, particularly, serotonin and dopamine. In the experiment, the laboratory mice used are of species that secrete a very low level of serotonin and popularly used as a model of animals addicted to alcohol with depressive character. Generally speaking, these mice are born to be alcohol addicts genetically. The results of the experiment show that the extract from St. John s Wort herb when given to the mice, make the mice lessen their alcohol intake significantly. However, in order to stop alcohol use, the extract must be used continuously since the craving for alcohol remains quite a long time rather than disappears after the first day of abstaining from drinks. The continuing use of this extract for 15 days reveals that the extract can stop alcohol use for the whole period of 15 days. Therefore, the idea to use this plant extract is highly possible. However, though St. John s Wort is a natural plant, it does not necessarily mean that it is 100 percent safe. In practice, analysis must be taken in order to check its toxicity first. For St John s Wort, it has been studied somewhat comprehensively and becomes popular in the last 2 3 decades, especially for depression elevation. Further to other efforts, there are many measures taken for the treatment of alcohol addiction in humans and independent on anti depressive medicines. The most renown measure is a substitution by smoking cigarette probably because a majority of 2

people feel the cigarette is not really dangerous, and most of alcohol addicts are smoking or have smoked before. Hence, they think they should try to smoke heavier when trying to stop using alcohol. This hypothesis is analyzed by using mice based on the observation that depressed persons usually smoke more so that smoking should have some effects in reducing depression and probably the amount of alcohol intake as well. This study started with processes in inducing the mice to have depression and become addicted to alcohol. After addicted to alcohol, the mice are given nicotine which is a main component found in tobacco leaves or in a cigarette. It discloses that nicotine can better the depression and reduces the amount of alcohol use significantly; however, the mice must be given nicotine at a relatively high volume, 1.5 milligram/1 kilogram of the body weight because the lower volume is not effective. Above all, smoking for nicotine during stopping alcohol may not be a good alternative as smokers will inhale smoke detrimental to lungs and causing dangerous diseases, such as, pulmonary emphysema and lung cancer. As for nicotine sticker, to attach the sticker on skin allowing nicotine to absorb gradually can avoid the harms to lungs, is not popularly used mainly possibly because nicotine does not show any impressive healing effects when compared with anti depressive medicines. It ma y also be inferior to the medicines. Apart from the aforementioned alternatives used to stop the alcohol use, one option which is rarely mentioned is promotion of activities beneficial to treatment as some reports find that some activities can help stimulate the secretion of serotonin in the brain, for instance, shopping. If the feeling is carefully observed, it is obvious that most people feel good when going out shopping. Shopping creates pleasant feeling in which depressed persons are soothed unknowingly. As a result, persons who is trying to quit alcohol and feel little depressed should try this recommendation. For those who are not quite in good economic condition, other alternatives would be better, otherwise, shopping might cause them to bankrupt and worse depression. In addition to those studied measures, other activities in routine life should also help reduce depression without massive cost, for instance, playing sports, music or joining family activities. Only activities that bring about enjoyment and do not cause any troubles afterwards are good enough. Nonetheless, our social problem is from that depressed people or drug addicts are normally surrounded by environment unfavorable to the creation of happiness. The other vital factor is the person himself who lacks skills in figuring out solutions or coping with depression. Consequently, it is still essential for him to receive assistance and support from his family and society. Reference List Ballenger J.C.,Goodwin F.K.m, Major L.F., and Brown G.L.(1979) alcohol and central serotonin metabolism in man. Arch. Gen. Psychiatry 36,224 227. Markou A.,Kosten T.R., and Koob G.F.(1998) Neurobiological similarities in depression and drug dependence: a self-medication hypothesis. Neuropsychopharmacolory 18, 135-174. Martinez-Gonzalez D., Prospero-Garcia O., Mihailescu S., and Drucker-Colin R. (2002) Effects of nicotine on alcohol intake in a rat model of depression. Pharmacol. Biochem. Behav. 72, 355-364. Melzer H.Y. (1990) Role of serotonin in depression. Ann. N.Y. Acad.Sci.600, 486-499. Naranjo C.A., Kadlec K.E., Sanhueza P., Woodley-Remus D., and Sellers E.M.(1990) Fluoxetine differentially alters alcohol intake and other consummatory behaviors in problem drinkers. Clin. Pharmacol. Ther. 47, 490-498. Rezvani A.H., Overstreet D.H., Yang Y., and Clark E Jr(1999) Attenuation of alcohol intake by extract of Hypericum perforatum(st.john s Wort ) in two different strains of alcohol-preferring rats. Alcohol Alcohol 34, 699-705. 3

4 Tomkins D.M., Le A.D., and Sellers E.M.(1995) Effect of the 5-HT3 antagonist ondansetron on voluntary ethanol intake in rats and mice maintained on a limited access procedure. Psychopharmacology(Berl) 117, 479-485. Vega W.A., Sribney W.M., and Achara-Abrahams I. (2003) co-occurring alcohol, drug, and other psychiatric disorders among Mexican-origin people in the United States. Am.J.Public Health 93, 1057-1064.

5 Effects of Alcohol on a Part of the Brain that Controls Memory By Dr. Ekkasith Kumarnsit At the present, high competition is found in all fabrics of the society based on the philosophy that human resources should be developed to have high competency leading to exellence in all competitive arenas in which their competency is measured in terms of intellectual quality, thinking and learning capability. Consequently, there are efforts to analyze processes of the brain in learning and storing memory. It is convinced that if the brain is good, learning and memory are also good. Therefore, humans have maneuvered by all means in order to enhance the development of the brain to highest level and to avoid destructive factors or constraints in brain development. A part of the brain called hippocampus has functions regarding learning and process in producing memory cells to collect meaningful and significant experiences. Hippocampus is structurally located in the inner part of the brain right behind 2 sides of the temple, so called temporal lobes. Main functions of the hippocampus is to make information and perceptions such as pictures or sounds memorable in forms of memory though the time passes by. Once pertinent incidents take place, memory will be recalled, enabling humans or animals to respond to stimulants well and promptly without new learning. Periodical studies find that alcohol intake is one of core causes attributed to the destruction of neurons in adults hippocampus. This finding may help answer why chronic alcohol addicts show malfunctions of both physical and mental capacities. However, studies on groups of teenagers of which a higher number become alcohol users are rarely conducted. Importantly, juvenile brains are in the period of growth and development in order to have thinking skills and complete learning skills necessary for living. This period is regarded as a turning point. If brain development in this period does not exist or is not complete, its negative effects shall be worse than those in adulthood. A research done in U.S.A. explored a group of students between 14 17 years old, addicted to alcohol, compared with the other group in the same age but not using alcohol by using the technique called magnetic resonance imaging (MRI). The MRI is the technique that give 8

image of human brain scanned by using magnetic wave to produce several 2 dimension cross section planes throughout the whole length of the brain. Then a computer program will combine all cross section planes and compute the 3 dimension brain image. This study obtained a very shocking result that the alcohol using teenagers have the left hippocampus smaller than the controlled group did, evidenced by a ratio of their hippocampus size per skull spaces. For the right hippocampus and other parts of the brain, both groups are found indifferent. The researcher team tried to reason this finding that the size of hippocampus becoming smaller in the group of alcohol using teenagers was attributed to the toxicity of alcohol on neurons. In general, hippocampus secretes glutamate neurotransmitters from nerve endings in which glutamate will bind non methyl D aspartate receptor located on the cell membrane of another group of neurons. This is a signalling process among neurons which make this brain part active. The neuroscience theory describes that any group of cells in active state will contain more stability, can fix internal cell condition to be healthy and live long because these cells are stimulated to secrete all chemical substances essential for their existence in the meantime. On the contrary, a group of cells in inactive state, for instance, lack of stimulation from neurotransmitters for a long while can lose essential functions of cells, and finally these cells deteriorate and decrease in a large number.. Effects of alcohol both in human or experimental animals are wellknown in manner of suppressive effects on central nervous system (CNS) shown in many symptoms, slower movement, murmuring speech or slower thinking. It is possible that the suppressive effects of alcohol on the CNS include the suppression or the obstruction of glutamate secretion in hippocampus also. As a result, the long term intake of alcohol can make cells in hippocampus deteriorate until the hippocampus becomes smaller in size than that of a normal person is. Why the left hippocampus and the right hippocampus do not have the same effects remains uncertainly answered. Nevertheless, the brain of human or mammal can be evenly divided into 2 hemispheres on average. In details, each brain hemisphere has its own prominent functions by which the left hemisphere is distinctive in language skill. If it shrinks, it may not cause serious harm to language skill as long as the right hemisphere remains in the regular size. These 2 hemispheres may replace each other roughly to a certain extent, since structurally situated in the center between these 2 hemispheres is corpus callosum sending and receiving data from one hemisphere to the other. As shown by the memory test, there is no significant difference between a group of alcoholusing teenagers and a group on non alcohol using teenagers. Even though the abnormality in memory is not detected, the said test might not study in depth and the size of sampled population might not be big enough as a matter of fact that functions of a single hippocampus hemisphere in regular size cannot be so good as those of 2 hemipheres can certainly. During adolecence, the brain can keep on developing and fix its functional 6 9

7 inefficiency occurred in the initial stage. However, if that functional disorders take place for a long time, the brain cannot make it up, and the abnormalities will become noticeable. The aforementioned study is a concrete evidence confirming that alcohol intake has destructive effects on brains of adolescents, in particular, on the part that controls learning and has function on memory process. Damages on the brains of teenagers who can be invaluable human resources or not raise a point of immediate concern that they are urgently required to be protected as soon as possible. A group of adolescent population should be a focus of a campaign to raise their awareness on possible harms of alcohol. Moreover, relevant laws should be issued based on neuroscience theories in order to be most effective in protecting our national human resources from alcohol. Reference List Hawkins,J.D. et al.exploring the effects of age of alcohol use initiation and psychosocial risk factors on subsequent alcohol misuse.j.stud, Alcohol 58, 280 290(197). Grant, B.F.& Dawson, D.A.Age at onset of alcohol use and its association with DSM IV alcohol abuse and dependence: results from the National Longitudinal Alcohol Epidemiologic Survey.J.Subst. Abuse 9, 103 110 (1997). De Vries,T.J.,Schoffelmeer,A.N.,Binnekade,R.,Rasso,H.&Vanderschuren, LJRelapse to cocaine and heroin seeking behavior mediated by dopamine D2 receptors is time dependent and associated with behavioral sensitization.neuropsychopharmacology 26, 18 26 (2002). Oades,R.D. & Halliday,G.M.Ventral tegmental(a10) system : neurobiology.1. Anatomy and connectivity.brain Res.434,117 165(1987). Cunningham,M,G.,Bhattacharyya,S.& Benes.F.M.Amygdalo cortical sprouting continues into early adulthood : implications for the development of normal and abnormal function during adolescene.j.comp Neurol. 453, 116 130 (2002).