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group_4_presentation_3_-_alcohol_consumption [2018/03/30 21:15] yarkho |
group_4_presentation_3_-_alcohol_consumption [2018/03/30 22:22] (current) chowds6 |
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| From a top-down perspective of the body, a drinker’s eyes can become blurred and vision can become severely impaired. Their speech can slur and be comprehensible with the added effects of impaired disjointed thought processes (What happened when, 2018). The body can begin sweating become red as well. Ethnicities such as Eastern Asians have exhibited red flush reaction to an extreme because of alcohol due to a condition associated with accumulation of acetaldehyde, a metabolic by-product of the catabolic metabolism of alcohol, and the inability to break it down because of a genetic deficiency of acetaldehyde dehydrogenase in approximately 36% of Eastern Asians (Brooks et al., 2009). Besides flushed skin however, the body can also extremely dehydrated from frequent urination, large mobility issues and imbalance, as well as at more volatile amounts drinkers can experience vomiting, nausea and shallow breathing at higher alcohol amounts (What happened when, 2018). | From a top-down perspective of the body, a drinker’s eyes can become blurred and vision can become severely impaired. Their speech can slur and be comprehensible with the added effects of impaired disjointed thought processes (What happened when, 2018). The body can begin sweating become red as well. Ethnicities such as Eastern Asians have exhibited red flush reaction to an extreme because of alcohol due to a condition associated with accumulation of acetaldehyde, a metabolic by-product of the catabolic metabolism of alcohol, and the inability to break it down because of a genetic deficiency of acetaldehyde dehydrogenase in approximately 36% of Eastern Asians (Brooks et al., 2009). Besides flushed skin however, the body can also extremely dehydrated from frequent urination, large mobility issues and imbalance, as well as at more volatile amounts drinkers can experience vomiting, nausea and shallow breathing at higher alcohol amounts (What happened when, 2018). | ||
| - | <box 60% | >{{ :screen_shot_2018-03-30_at_4.31.39_pm.png?600 |}}</box|Figure 4. Physiological effects of alcohol consumption based on body organ (What happened when, 2018).> | + | <box 45% | >{{ :screen_shot_2018-03-30_at_4.31.39_pm.png?500 |}}</box|Figure 4. Physiological effects of alcohol consumption based on body organ (What happened when, 2018).> |
| **Affected Brain Regions (Lemouse, 2018):** | **Affected Brain Regions (Lemouse, 2018):** | ||
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| Alcohol affects the brain chemistry by altering the levels of neurotransmitters which control thought processes, behavior and emotion. It is known to affect both the “excitatory” and “inhibitory” neurotransmitters. An example of an excitatory neurotransmitter is glutamate. Glutamate normally increases brain activity and energy levels. However, with alcohol intake it suppresses the release of glutamate which results in a delay along the brain’s highways. An example of an inhibitory neurotransmitter is GABA which reduces energy levels and calms everything down. Alcohol actually increases this neurotransmitter. As a result of Glutamate being suppressed and GABA increasing this means your thought, speech. Movements are slowed down. The more you drink the more of these effects you will feel. This is why in this phase there is more stumbling around and falling. Another neurotransmitter that is involved is dopamine, released from your brain’s reward center particularly the ventral striatum that is affected by virtually all pleasurable activity. Alcohol increases dopamine levels making you feel great or at least tricking you into thinking you are better. This produces the euphoric feelings or what otherwise known as the buzzed feeling. Dopamine also activates the memory circuits in other parts of the brain that remembers this pleasant experience and leaves you thirsting for more alcohol. | Alcohol affects the brain chemistry by altering the levels of neurotransmitters which control thought processes, behavior and emotion. It is known to affect both the “excitatory” and “inhibitory” neurotransmitters. An example of an excitatory neurotransmitter is glutamate. Glutamate normally increases brain activity and energy levels. However, with alcohol intake it suppresses the release of glutamate which results in a delay along the brain’s highways. An example of an inhibitory neurotransmitter is GABA which reduces energy levels and calms everything down. Alcohol actually increases this neurotransmitter. As a result of Glutamate being suppressed and GABA increasing this means your thought, speech. Movements are slowed down. The more you drink the more of these effects you will feel. This is why in this phase there is more stumbling around and falling. Another neurotransmitter that is involved is dopamine, released from your brain’s reward center particularly the ventral striatum that is affected by virtually all pleasurable activity. Alcohol increases dopamine levels making you feel great or at least tricking you into thinking you are better. This produces the euphoric feelings or what otherwise known as the buzzed feeling. Dopamine also activates the memory circuits in other parts of the brain that remembers this pleasant experience and leaves you thirsting for more alcohol. | ||
| - | <box 20% | >{{::250px-braincaudateputamen.svg.png?200|}}</box|Figure 6. The ventral striatum; area of the brain where the neurotransmitter, dopamine, is increased as a result of alcohol consumption. ("Striatum", 2018).> | + | <box 35% | >{{ :250px-braincaudateputamen.svg.png?300 |}}</box|Figure 6. The ventral striatum; area of the brain where the neurotransmitter, dopamine, is increased as a result of alcohol consumption. ("Striatum", 2018).> |
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| =======The "Blackout" Phase======= | =======The "Blackout" Phase======= | ||
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| When drinking, a multitude of neurotransmitters are activated, including dopamine, opioids norepinephrine, serotonin, gamma- aminobutyric acid (GABA), and glutamate. It is known that dopamine leads to further reinforcing drinking habits as it leads to the perception of reward, while GABA is associated with the sedative-like effects. Low doses of alcohol act on GABAA receptors while high concentrations of alcohol antagonize glutamate releasing receptors known as N-methyl-d-aspartate (NMDA) receptors (White, 2003). GABAA receptors mediate rapid inhibitory neurotransmission throughout the central nervous system via the release of choloride ions when bound to GABA. These inhibitions lead to decreased anxiety, impaired motor coordination, increased aggressive behaviour, impaired cognitive function, and sedation. It should be noted that not all GABA receptors are activated the same, as some are activated by low-doses of alcohol, while some are specifically activated under high concentrations of alcohol. Alcohol leads to an increase in GABAergic neurotransmission directly (by acting as a GABA agonist) and indirectly via endogenous GABAergic neuroactive steroids (such as allopregnanolone), presynaptic release of GABA, and dephosphorylation of GABAA receptors which in turn leads to an increase in GABA sensitivity (Kumar et al., 2009). | When drinking, a multitude of neurotransmitters are activated, including dopamine, opioids norepinephrine, serotonin, gamma- aminobutyric acid (GABA), and glutamate. It is known that dopamine leads to further reinforcing drinking habits as it leads to the perception of reward, while GABA is associated with the sedative-like effects. Low doses of alcohol act on GABAA receptors while high concentrations of alcohol antagonize glutamate releasing receptors known as N-methyl-d-aspartate (NMDA) receptors (White, 2003). GABAA receptors mediate rapid inhibitory neurotransmission throughout the central nervous system via the release of choloride ions when bound to GABA. These inhibitions lead to decreased anxiety, impaired motor coordination, increased aggressive behaviour, impaired cognitive function, and sedation. It should be noted that not all GABA receptors are activated the same, as some are activated by low-doses of alcohol, while some are specifically activated under high concentrations of alcohol. Alcohol leads to an increase in GABAergic neurotransmission directly (by acting as a GABA agonist) and indirectly via endogenous GABAergic neuroactive steroids (such as allopregnanolone), presynaptic release of GABA, and dephosphorylation of GABAA receptors which in turn leads to an increase in GABA sensitivity (Kumar et al., 2009). | ||
| - | <box 45% | >{{ :gaba.jpg |}}</box|Figure 7. Alcohol actively inhibits the reception of GABA on post-synaptic clefts (Clapp, Bhave, & Hoffman, 2008).> | + | <box 50% | >{{ :gaba.jpg?450 |}}</box|Figure 7. Alcohol actively inhibits the reception of GABA on post-synaptic clefts (Clapp, Bhave, & Hoffman, 2008).> |
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| Though the hippocampus is the main region of the brain that is effected with alcohol, it is not the only part of the brain that does. The medial septum is a structure in the forebrain is critical to hippocampal function as it sends both excitatory and inhibitory signals, known as theta rhythm, to the hippocampus leading to hippocampal pyramidal cell activity changes. This indicates that this theta rhythm acts as a ‘gatekeeper’ to determine if information sent to the hippocampus will be processed. It has been found that the theta rhythm is disrupted with alcohol consumption by suppressing the output of signals from the medial septal neurons to the hippocampus. The frontal lobe is important for short term memory, as well as forming and retrieving long term memories. It has been shown that chronic alcohol use damages the frontal lobe, thus further impairing memory development and recollection. Though not clearly explained, acute consumption of alcohol has been shown to impair frontal lobe functions, such as planning, decision making, and impulse control (White, 2003). | Though the hippocampus is the main region of the brain that is effected with alcohol, it is not the only part of the brain that does. The medial septum is a structure in the forebrain is critical to hippocampal function as it sends both excitatory and inhibitory signals, known as theta rhythm, to the hippocampus leading to hippocampal pyramidal cell activity changes. This indicates that this theta rhythm acts as a ‘gatekeeper’ to determine if information sent to the hippocampus will be processed. It has been found that the theta rhythm is disrupted with alcohol consumption by suppressing the output of signals from the medial septal neurons to the hippocampus. The frontal lobe is important for short term memory, as well as forming and retrieving long term memories. It has been shown that chronic alcohol use damages the frontal lobe, thus further impairing memory development and recollection. Though not clearly explained, acute consumption of alcohol has been shown to impair frontal lobe functions, such as planning, decision making, and impulse control (White, 2003). | ||
| - | <box 60% | >{{ ::brain_regions.jpg |}}</box|Figure 9. Other brain regions involved in the blackout phase of drinking. To highlight, the forebrain, with a focus on the medial septum (White, 2003).> | + | <box 45% | >{{ ::brain_regions.jpg |}}</box|Figure 9. Other brain regions involved in the blackout phase of drinking. To highlight, the forebrain, with a focus on the medial septum (White, 2003).> |
| =======The "Hungover" Phase======= | =======The "Hungover" Phase======= | ||
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| There are many factors that contribute to a hangover. Alcohol may cause the body to produce more urine thus leading to dehydration (Mayo,2017). In addition, alcohol may also cause the blood sugar levels to fall causing weakness and even seizures. Finally, the expansion of blood vessels due to excessive alcohol consumption may lead to headaches (Mayo,2017). However, these symptoms can cause serious problems with memory, concentration, and dexterity which may impact the individual’s life throughout school, the workplace, or completing many tasks. Studies show that men having at least one alcohol hangover a month had a 2.36-fold increased risk of cardiovascular death compared to those with less frequent hangovers (Mayo, 2017). | There are many factors that contribute to a hangover. Alcohol may cause the body to produce more urine thus leading to dehydration (Mayo,2017). In addition, alcohol may also cause the blood sugar levels to fall causing weakness and even seizures. Finally, the expansion of blood vessels due to excessive alcohol consumption may lead to headaches (Mayo,2017). However, these symptoms can cause serious problems with memory, concentration, and dexterity which may impact the individual’s life throughout school, the workplace, or completing many tasks. Studies show that men having at least one alcohol hangover a month had a 2.36-fold increased risk of cardiovascular death compared to those with less frequent hangovers (Mayo, 2017). | ||
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| ====Hungover Physiology==== | ====Hungover Physiology==== | ||
| Although researchers have produced evidence that alcohol can directly promote hangover symptoms. The underlying mechanisms are still not figured out. Researchers are still trying to find out if the effects of a hangover are due to the after-effects of alcohol, the direct effects or a combination of both. One of the hypotheses that has been proposed for the underlying mechanism is the acetaldehyde hypothesis. When alcohol is metabolized in the liver the product is acetaldehyde. This is attacked by the acetaldehyde dehydrogenase enzyme and glutathione which forms the non-toxic form called acetate. However, when large amounts of alcohol are consumed, the liver runs out of glutathione resulting in the buildup of acetaldehyde in the body causing the symptoms of hangovers such as headaches and vomiting. | Although researchers have produced evidence that alcohol can directly promote hangover symptoms. The underlying mechanisms are still not figured out. Researchers are still trying to find out if the effects of a hangover are due to the after-effects of alcohol, the direct effects or a combination of both. One of the hypotheses that has been proposed for the underlying mechanism is the acetaldehyde hypothesis. When alcohol is metabolized in the liver the product is acetaldehyde. This is attacked by the acetaldehyde dehydrogenase enzyme and glutathione which forms the non-toxic form called acetate. However, when large amounts of alcohol are consumed, the liver runs out of glutathione resulting in the buildup of acetaldehyde in the body causing the symptoms of hangovers such as headaches and vomiting. | ||
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| The other hypothesis that has been proposed is the direct-effects hypothesis. This has to do with the direct effects of alcohol. In this hypothesis, it states that gastrointestinal disturbances or symptoms arise since alcohol direct irritates the stomach and intestines which causes inflammation of the stomach lining and delayed. Resulting in upper abdominal pain, nausea, and vomiting. Alcohol causes several alterations in the metabolic state of the liver and organs resulting in low blood sugar. The buildup of the intermediate product of alcohol can actually inhibit glucose production. And since this is the primary energy source it can contribute to symptoms such as fatigue, weakness and mood disturbances. Next, alcohol has been known to have direct sedative effects which result in poor quality of sleep, insomnia, fatigue. All experienced during a hangover. Alcohol intoxication has a direct effect on the vasodilation of blood vessels which may induce headaches. | The other hypothesis that has been proposed is the direct-effects hypothesis. This has to do with the direct effects of alcohol. In this hypothesis, it states that gastrointestinal disturbances or symptoms arise since alcohol direct irritates the stomach and intestines which causes inflammation of the stomach lining and delayed. Resulting in upper abdominal pain, nausea, and vomiting. Alcohol causes several alterations in the metabolic state of the liver and organs resulting in low blood sugar. The buildup of the intermediate product of alcohol can actually inhibit glucose production. And since this is the primary energy source it can contribute to symptoms such as fatigue, weakness and mood disturbances. Next, alcohol has been known to have direct sedative effects which result in poor quality of sleep, insomnia, fatigue. All experienced during a hangover. Alcohol intoxication has a direct effect on the vasodilation of blood vessels which may induce headaches. | ||
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| So far, the most convincing hypothesis as to what causes a hangover is our own immune response. Specifically, it has been shown that cytokines communicate with our brain. Peripherally released cytokines are mediated by the nervus vagus pathway, and thus have an effect on the central nervous system. These cytokine receptors are localized within glial cells and neurons throughout the brain, but are highly concentrated within the hippocampus and signal to the brain to up-regulate the cytokines when needed. As-per the theory, it is thought that the effects of cytokines tend to mimic the symptoms of hangovers, therefore, they may share a similar underlying process. Specifically, cerebral cytokines, including IL-1β, IL-6, and TNF-α are related to the sickness behaviour including weakness, lack of concentration, lowered appetite, reduced activity, lethargic, and loss of interest in common activities. These same cytokines are also associated with a lack of memory (Verster, 2008). | So far, the most convincing hypothesis as to what causes a hangover is our own immune response. Specifically, it has been shown that cytokines communicate with our brain. Peripherally released cytokines are mediated by the nervus vagus pathway, and thus have an effect on the central nervous system. These cytokine receptors are localized within glial cells and neurons throughout the brain, but are highly concentrated within the hippocampus and signal to the brain to up-regulate the cytokines when needed. As-per the theory, it is thought that the effects of cytokines tend to mimic the symptoms of hangovers, therefore, they may share a similar underlying process. Specifically, cerebral cytokines, including IL-1β, IL-6, and TNF-α are related to the sickness behaviour including weakness, lack of concentration, lowered appetite, reduced activity, lethargic, and loss of interest in common activities. These same cytokines are also associated with a lack of memory (Verster, 2008). | ||
| - | <box 75% | >{{ ::immune.jpg |}}</box|Figure 10. The cyclic relationship between neuronal communication and cytokine release (Pacheco, Contreras, & Prado, 2012).> | + | <box 55% | >{{ ::immune.jpg?500 |}}</box|Figure 10. The cyclic relationship between neuronal communication and cytokine release (Pacheco, Contreras, & Prado, 2012).> |
| It has been observed that a significant increase of IL-10, IL-12, and IFN-γ was observed after a cohort of individuals were induced into a hangover state compared to a control cohort. Yet, no changes in IL-1β, IL-4, IL-6, and TNF-α were observed (Kim et al., 2003). This brings forward a key point when it comes to hangover research- the lack of it. As stated in many of the research articles, there is conflicting research observations in this field due to the high variability of hangovers per individual (Verster, 2008). But, it should be noted that IL-10 leads to impaired cellular immunity, IL-12 is a proinflammatory cytokine that leads to cytotoxicity, and IFN-γ further increase cell-mediated immune responses (Kim et al., 2003). | It has been observed that a significant increase of IL-10, IL-12, and IFN-γ was observed after a cohort of individuals were induced into a hangover state compared to a control cohort. Yet, no changes in IL-1β, IL-4, IL-6, and TNF-α were observed (Kim et al., 2003). This brings forward a key point when it comes to hangover research- the lack of it. As stated in many of the research articles, there is conflicting research observations in this field due to the high variability of hangovers per individual (Verster, 2008). But, it should be noted that IL-10 leads to impaired cellular immunity, IL-12 is a proinflammatory cytokine that leads to cytotoxicity, and IFN-γ further increase cell-mediated immune responses (Kim et al., 2003). | ||
| - | <box 50% | >{{ ::kim_results.jpg |}}</box|Figure 11. Changes in cytokine production in control and hangover induce participants of the study conducted by Kim et al., 2003 (Kim et al., 2003).> | + | <box 40% | >{{ ::kim_results.jpg?400 |}}</box|Figure 11. Changes in cytokine production in control and hangover induce participants of the study conducted by Kim et al., 2003 (Kim et al., 2003).> |
| =======Treatments======= | =======Treatments======= | ||
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| =======Conclusion======= | =======Conclusion======= | ||
| - | (conclusion for drunk phys)- Alcohol consumption is known to affect the inhibitory and excitatory neurotransmitters or respectively the glutamate neurotransmitter and the GABA neurotransmitter. Alterations in these neurotransmitters results in the impairment of | + | Alcohol consumption is major activity across the world, enabling states of drunkenness at certain blood alcohol concentration (BAC) levels, as well as blackout and hungover states at excessive degrees. When drunk, the body is in a state of euphoria as the liver works hard to quickly metabolize the incoming alcohol being received. However when there is more alcohol than can be metabolized, the rest is distributed to other bodily organs. Alcohol consumption is also known to affect the inhibitory and excitatory neurotransmitters, or respectively the glutamate neurotransmitter and the GABA neurotransmitter. Alterations in these neurotransmitters results in impairment. When more levels are alcohol are in a dangerously high state a blackout can occur. Recent research has demonstrated that blackouts are the result of alcohol interfering with the hippocampus NMDA receptors, impacting long-term potentiation and thus the ability to process long-term memory. The reason why a loss of memory is observed for those in a blackout phase is due to a downregulation of NMDA and the potentiation of GABAA receptor transmission. This occurs mainly within the pyramidal hippocampal cells, but can occur in other brain regions as well. The next day a hangover can then ensue. An alcohol hangover is defined as unpleasant and adverse physical and mental effects that occur the following morning after the intake of toxic doses of alcohol, and can last up to 24 hours. Symptoms of hangovers may cause serious problems with memory, concentration, and dexterity which may impact the individual’s life throughout school, the workplace, or completing many tasks. The underlying cause of a hangover at the neurochemical level is unknown. There are several hypotheses such as the acetaldehyde hypothesis, after-effects hypothesis, and the immunity hypothesis. The popular hypothesis, Immunity hypothesis, is thought that hangovers could be due to a cyclic communication of ones brain to the immune system, but research is lacking and further understanding is required. |
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| - | (conclusion for blackout phys) - Recent research has demonstrated that blackouts are the result of alcohol interfering with the hippocampus NMDA receptors, impacting long-term potentiation and thus the ability to process long-term memory. | + | |
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| - | (part of the conclusion for neurochemistry of blackout)-The reason why a loss of memory is observed for those in a blackout phase is due to a downregulation of NMDA and the potentiation of GABAA receptor transmission. This occurs mainly within the pyramidal hippocampal cells, but can occur in other brain regions as well. | + | |
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| - | (par of conlcusion for hangover) - Alcohol hangover is defined as unpleasant and adverse physical and mental effects that occur the following morning after the intake of toxic doses of alcohol¬¬ and can last up to 24 hours. Symptoms of hangovers may cause serious problems with memory, concentration, and dexterity which may impact the individual’s life throughout school, the workplace, or completing many tasks. | + | |
| - | + | ||
| - | (part of the conclusion for neurochemistry of hangover)- The underlying cause of a hangover at the neurochemical level is unknown. There are several hypotheses such as the acetaldehyde hypothesis, after-effects hypothesis, and the immunity hypothesis. The popular hypothesis, Immunity hypothesis, is thought that hangovers could be due to a cyclic communication of ones brain to the immune system, but research is lacking and further understanding is required. | + | |
| - | (part of conclusion for treatment)- There are several treatments in regards to the hangover phase, alcohol poisoning that may occur during the drunk or blackout phase, and addiction to alcohol, however, there are no specific treatments for the drunk or blackout phase. To treat a hangover, one must replenish electrolytes and any sodium lost the night before. To treat alcohol poisoning, one must go through supportive care and monitoring and be given fluids intravenously. Finally, to treat alcohol addiction, a physician may recommend, Detoxification, Behaviour Modification, Counseling or Medication. To prevent all of this, one must drink slowly with plenty of water in between and also drink on a full stomach. | + | There are several treatments in regards to the hangover phase, alcohol poisoning that may occur during the drunk or blackout phase, and addiction to alcohol, however, there are no specific treatments for the drunk or blackout phase. To treat a hangover, one must replenish electrolytes and any sodium lost the night before. To treat alcohol poisoning, one must go through supportive care and monitoring and be given fluids intravenously. Finally, to treat alcohol addiction, a physician may recommend, Detoxification, Behaviour Modification, Counseling or Medication. To prevent all of this, one must drink slowly with plenty of water in between and also drink on a full stomach. |
| =======Presentation======= | =======Presentation======= | ||
