Effects of alcohol on brain

-Dipti Rani Behera

ଓଡ଼ିଆ ରେ ଏହି ଲେଖା କୁ ପଢ଼ିବା ପାଁଇ ଏଠାରେ କ୍ଲିକ୍ କରନ୍ତୁ ।

Alcohol has been the most lovable beverage since ages. But sometimes choices from taste turns out to be toxic and harmful for health in the long term, such is the case of alcohol, the maker could have never thought of such devastating effect it has on health on long term use. 

Alcohol is absorbed by the lining of the stomach. It reaches the brain within 5 minutes of consumption and starts to show its effect within 10 minutes. Alcohol affects brain function by interacting with neurotransmitter Y-AMINOBUTYRIC ACID or GABA, by facilitating its action alcohol suppresses the CNS thereby disrupting the delicate balance between inhibitory and excitatory neurotransmitters. The substance also directly affects a number of other neurotransmitter systems including those of glutamate, glycine, acetylcholine, and serotonin. This shows symptoms like dizziness, blurred vision, slurred speech etc. 

Short-term alcohol exposure tilts this balance in favor of inhibitory influences. After long-term alcohol exposure, however, the brain attempts to compensate by tilting the balance back toward equilibrium. These neurological changes occur as the development of tolerance to alcohol’s effects. When alcohol consumption is abruptly discontinued or reduced, these compensatory changes are no longer opposed by the presence of alcohol, thereby leading to the excitation of neurotransmitter systems and the development of alcohol withdrawal syndrome. Long-term alcohol intake also induces changes in many neurotransmitter systems like dopamine and endogenous opioids in reward pathways of the brain, which ultimately lead to the development of craving and alcohol-seeking behavior. Apart from these alcohols also causes damaging effects on brain such as:

1. Alcohol related brain atrophy: shrinkage of cerebral cortex, white matter, as well as basal forebrain region due to neurotoxic effects of alcohol. This may cause seizures (burst of uncontrolled electrical activity between brain cells, this causes temporary abnormalities in muscle tone or movements), dementia (loss of memory, language, problem solving and other thinking abilities) and difficulty in speaking.

2. Frontal lobe vulnerability: frontal lobes are connected with all other part lobes of the brain, the parietal, temporal and occipital lobe, and they receive and send fibers to numerous subcortical structures. Neurotoxic effect of alcohol leads to decreased blood flow or metabolism in frontal lobes and also disrupts the normal function of frontal lobe such as executive control, directed behavior, good judgement, and problem solving abilities. 

3. WERNICKE KORSAKOFF SYNDROME: up to 80% alcoholics have thiamine deficiency which lead to serious brain disorder of Wernicke korsakoff syndrome. this condition has two separate syndromes a short lived and severe condition called WERNICKE’S ENCEPHALOPATHY, its symptoms include mental confusion, paralysis of nerves that move the eyes and difficulty with muscle coordination, apart from this people with this disorder are also vulnerable to developed korsakoff psychosis (a long lived and debilitating condition)characterized by learning and memory problems, they are also forgetful and quickly frustrated and have difficulty with walking and coordination. Thiamine is a cofactor for 3 crucial enzymes These enzymes are called transketolase, pyruvate dehydrogenase (PDH) and alpha–ketoglutarate dehydrogenase (α–KGDH); they all participate in the catabolism of sugar molecules (i.e., carbohydrates) in the body, as described in the following paragraphs. Each of these enzymes consists of several components that must be assembled to yield the functional enzyme, and the addition of thiamine is a critical step in this assembly process. As a result, thiamine deficiency causes suboptimal levels of functional enzymes in the cell, in addition to interfering with the activity of those enzymes.

Transketolase is an important enzyme in a biochemical pathway called the pentose phosphate pathway. In this set of biochemical reactions, a molecule called glucose–6–phosphate, which is derived from the sugar glucose, is modified by transketolase, yielding two products—a sugar called ribose–5–phosphate and a molecule called reduced nicotinamide adenine dinucleotide phosphate (NADPH) (see figure 2). Both of these molecules are essential for the production of numerous other important molecules in the cell. Ribose–5–phosphate is needed for the synthesis of nucleic acids, complex sugar molecules, and other compounds. NADPH provides hydrogen atoms for chemical reactions that result in the production of steroids, fatty acids, amino acids, certain neurotransmitters, and other molecules. In addition, NADPH plays an important role in the synthesis of glutathione, a compound that is essential in the body’s defense against oxidative stress. To function properly, all cells require certain levels of NADPH and ribose–5–phosphate, and the biochemical reaction mediated by transketolase is crucial for maintaining the appropriate levels of both molecules.

The other two enzymes requiring thiamine, PDH and α–KGDH, also participate in different steps of the breakdown and conversion of glucose–6–phosphate through two consecutive chains of biochemical reactions called glycolysis and the citric acid cycle (see figure 3). The main function of these pathways is the generation of a molecule called adenosine triphosphate (ATP), which provides energy for numerous cellular processes and reactions. Decreases in the activities of PDH and α–KGDH can result in reduced ATP synthesis, which in turn can contribute to cell damage and even cell death. In addition, proper functioning of PDH is essential for the production of the neurotransmitter acetylcholine as well as for the synthesis of a compound called myelin, which forms a sheath around the extensions (i.e., axons) of many neurons, thereby ensuring the ability of these neurons to conduct signals. The citric acid cycle and α–KGDH play a role in maintaining the levels of the neurotransmitters glutamate, gamma–aminobutyric acid (GABA), and aspartate, as well as in protein synthesis. Thus, the thiamine–using enzymes play numerous vital roles in the functioning of cells, and particularly of neurons.

When thiamine levels decrease, the activity levels of all three enzymes are reduced to some extent. Overall, transketolase activity may be the most sensitive measure of thiamine deficiency. Studies using rats found that transketolase activity may be reduced as much as 90 percent in the brain regions that are most sensitive to thiamine deficiency (Gibson et al. 1984). Substantial decline in transketolase activity resulting from thiamine deficiency has even been found in various brain areas of alcoholics who do not exhibit the clinical and neuropathological signs of WE (Lavoie and Butterworth 1995), suggesting that thiamine deficiency can cause adverse effects even before severe brain damage becomes obvious.

4. Fetal alcohol syndrome: drinking during pregnancy to a range of physical, learning, and behavioral effects in the developing brain, serious of which is a collection of symptoms known as fetal alcohol syndrome(FAS). Children with faces may have distinct facial features, as infants also are smaller than average, their brains have less volume, and may have fewer brain cells or fewer neurons that are able to function correctly leading to long term problems in learning and behavior.

5. Stupor: on reaching a blood alcohol level of 0.25 there may be concerning signs of alcohol poisoning .At this time all mental, physical and sensory functions are severely impaired and risk for passing out, suffocation and injury is high.

There are treatments available for serious diseases like Wernicke korsakoff syndrome. by administering with thiamine to improve brain functions at early stage but in severe cases this is not effective anymore and only solution lies is to be de-addict from alcohol, and for FAS if it is detected at prenatal stage its effect can be reversed by medications and also therapeutic rehabilitate motor training can improve motor performance in children or even adults with FAS. but the major limitation that lie in this path of treatments are DE addiction from alcohol which is toughest due to property of alcohol and its interaction with blood as a drug .so a far more better approach is “prevention being better than cure.” we should always be aware of each and every effect of food and beverages that we consume and should prefer best for our health rather than taste, and should avoid consumption of toxic and addictive substances for our better health.

References:

1. http://www.pubs.niaaa.nih.govt article–alcohol alert) Source material for this Alcohol Alert originally appeared in the journal Alcohol Research & Health, “Alcoholic Brain Damage” (Vol. 27, No. 2, 2003). Alcohol Research & Health is the quarterly, peer–reviewed journal published by the National Institute on Alcohol Abuse and Alcoholism. Each issue of AR&H provides in–depth focus on a single topic in the field of alcohol research. Back issues of Alcohol Research & Health and additional resources can be downloaded from NIAAA’s Web site, www.niaaa.nih.gov. Subscriptions are available from the Superintendent of Documents for $25. Write to New Orders, Superintendent of Documents, P.O. Box 371954, Pittsburgh, PA 15250–7954; or fax 202/512–2250
2. www.webmd.com
3. https://www.nm.org/healthbeat/healthy-tips/alcohol-and-the-brain
4. https://pubs.niaaa.nih.gov/publications/arh27-2/134-142.htm (Peter R. Martin, M.D., Charles K. Singleton, Ph.D., and Susanne Hiller–Sturmhöfel, Ph.D. Alcohol Research & Health. 2003;27(2): 134-42. The Role of Thiamine Deficiency in Alcoholic Brain Disease) 
5. https://en.wikipedia.org/wiki/Alcohol_(drug)#:~:text=Alcohol%20works%20in%20the%20brain%20primarily%20by%20increasing,suppresses%20the%20activity%20of%20the%20central%20nervous%20system.

Written By-

Dipti Rani Behera